Clinical based case reports

By
Dr Azam Arzoo
M.B.B.S (Bangladesh)
Clinical Dissertation of Nephrology
Sheffield Kidney Institute
University of Sheffield

Under Supervision of
Professor A M El Nahas
Professor of Nephrology, University of Sheffield
Sheffield Kidney Institute, Northern General Hospital
Sheffield
United Kingdom

1
 PAGES
CONTENTS
List of abbreviations 4
Acknowledgement 5
Dedication 6
Abstract 7
1 Ward: RUE
1 multiple myeloma associated with hoarseness of voice: case 08-15
report
2 ARF due to alcoholism: a case report 16-20

3 Reflux nephropathy: a case report 21-25

4 Anemia management in CKD: a case report 26-30

5 ARF secondary to fluid overload: a case report 31-35

2 .
Ward: Vickers- 3 .
1 CKD related risk factor for CVD: a case report 36-39

2 IgA nephropathy and management: case report 49-48

3 Acute kidney injury due to insect bite: case report 49-53

4 Diabetic nephropathy and hypertension: case report 54-57

5 P-ANCA positive vasculitis: case report 58-62

3
Ward: Vickers 2 and Transplantation

1 Assessment and management of comorbid diseases in CKD: case 63-68

report

2 Wegener’s granulomatosis: case report 69-74

3 Pulmonary hypertension in patients with ESRD on HD: case 75-78

report

4 Risk of mortality for ESRD patients on dialysis: case report 79-83

5 ADPKD: case report 84-88

2
 6 Ureteric stent( advantages and disadvantages): case report 89-95

7 ATN after Transplantaion report case 96-100

8 Psychotic disorders, after transplant: case report 101-105

9 Delayed graft function and acute tubular necrosis (ATN): case 106-110
report

10 Post-transplant IgA nephropathy: case report 111-115

11 References 116-118

3
List of abbreviations

AKI: Acute Kidney Injury

CKD: Chronic Kidney Disease
ESRD: End stage of Renal Disease
ESRF: End Stage of renal failure
DN: Diabetic Nephropathy
HTN: Hypertension
CRF: Chronic Renal Failure
ANCA: Anti Neutrophil cytoplasmic antibody
ANA: Anti Nuclear Antibody
GFR: Glomerular filtration Rate
ADPKD: Autosomal Dominant Polycystic Kidney Disease
GN: Glomerulonephritis
RRT: Renal replacement Theraphy
HD: Haemodialysis
PD: Peritoneal Dialysis
DM: Diabetes Mellitus
IgAN: Immunoglobulin A Nephropathy
BP: Blood Pressure
IHD: Ischaemic Heart Disease
S.Cr: Serum Creatinine
SKI: Sheffield Kidney Institute
DBP: Diastolic Blood Pressure
SBP: Systolic Blood Pressure
ACEi: Angiotensin Converting Enzyme Inhibitor
ARB: Angiotensin Receptor Blocker
NSAID: Non Steroidal Anti Inflamatory Drug
DGF: Delayed Graft Function
CAPD: Continious Ambulatory Peritoneal Dialysis
ATN: Acute Tubular Necrosis
AR: Acute Rejection
CT: Computer Tomography Scan
CIT: Cold Ischemic Time
US: Ultrasonogram
ASA: American Society of Anesthesiology
KUB: Kidney Urinary Bladder
CVS: Cardiovascular System
PMH: Past Medical History
Hb: Haemoglobin
MCD: Minimal Change Disease
NIDDM: Non Insulin Dependent Diabetes Mellitus
RUE : Renal Unit E floor
WG : Wegerner’s Granulomatosis
JVP : Jugular Venous Pressure

4
ACKNOWLEDGEMENT

First and foremost, praise be to Almighty ALLAH, the creator of the world, the
beneficent and the most merciful. Without his help and guidance, this work, and every
other work, would not be possible

My sincerest appreciation to Prof AM EL NAHAS, for affording me the opportunity to

pursue this thesis in the department of Nephrology, Sheffield Kidney Institute, University
of Sheffield and for his guidance and supervision all through the preparation of this
thesis.

I would like to thank Dr Lutfi, Dr Kossi, Dr Brown, Dr Brenann, Dr Kawar, Dr Othman,

Dr Parvez, Dr Amino Bello and Dr Ghada Said M. Omar

Finally, my deepest gratitude is due to my parents, brothers and sister for their love,
prayer and continues encouragement throughout the course.

5
Dedicated to
My mother

Late Tasliman Nisa who scarifies her whole life to make me a

doctor and dreamt for me to get specialized degree from England
And her wish was that “Before being a good doctor I should be a
good human being”

6
Abstract
Chronic kidney disease (CKD) is a worldwide public health problem with an increasing
incidence and prevalence, poor outcomes, and high cost. Outcomes of chronic kidney
disease include not only kidney failure but also complications of decreased kidney
function and cardiovascular disease. Current evidence suggests that some of these
adverse outcomes can be prevented or delayed by early detection and treatment.
Unfortunately, chronic kidney disease is underdiagnosed and undertreated, in part as a
result of lack of agreement on a definition and classification of its stages of progression

Objective: To distinguish the risk factors leading to kidney diseases through

investigating different patients with kidney diseases (acute and chronic), and to describe
the management of these patients with explaining the natural course of the disease.

Design of the study: 20 in-patients diagnosed either with acute or chronic kidney
disease, were participated in this study. The patients were randomly selected from
Vickers-2, Vickers-3 and RUE in Northern General Hospital, Sheffield Kidney Institute,
Sheffield, England, UK. The patients were fully aware of the objectives of the study. A
complete physical examination for each patient was completed on the first session. A
weekly follow-up and case report recording for each patient was followed for the length
of the study (4 weeks).

Main outcome measures: Most likely that the patients diagnosed with CKD of any stage
converted into ESRD and therefore the patient might need renal replacement therapy in
form of peritoneal or haemo-dialysis (PD or HD) or renal replacement therapy. This is
only meant that patient might improve his or her quality of life but he/she complication
nevertheless.

Conclusion: Risk factors such as hypertension, diabetes mellitus, or aging (age >55)
were the most common leading factors to chronic kidney diseases, however the risk of
end stage renal disease among those patients was very low.

7
A case report: multiple myeloma associated with hoarseness of voice

Introduction:
Multiple myeloma belongs to a group of diseases known as the plasma cell dyscrasias, in
which an uncontrolled proliferation of plasma cells, which elaborates a specific
immunoglobulin molecule. These single clones of cells proliferate diffusely in the bone
marrow, with associated bone destruction, but can give rise to a localized mass in bone,
soft tissues, or both. Multiple myeloma accounts for 1% of all malignancies, with an
incidence of four cases per 100,000, and accounts for 10% of hematologic malignancies.
There are two important variants of multiple myeloma: solitary bone plasmacytoma and
extramedullary plasmacytoma. Solitary bone plasmacytoma (SBP) is a localized
intraosseous lytic lesion without marrow plasmacytosis. Extramedullary plasmacytoma is
a plasma-cell tumor manifesting outside the bone marrow without evidence of systemic
disease. Extramedullary plasmacytoma and solitary bone plasmacytoma have a better
prognosis, and the patients are at least 10 years younger than those with multiple
myeloma. Most authors think that SBP, extramedullary plasmacytoma, and multiple
myeloma are different manifestations of the same disease. Progression of SBP and
extramedullary plasmacytoma to multiple myeloma is the most important feature
affecting the prognosis. The disseminated form, multiple myeloma, is by far the most
frequent and has the worst prognosis of the three types.

Case Summary:
A 59-year-old man admitted to the hospital after a sever deteriorating hoarseness of voice
since 15 days. Patient came in RUE unit with complains of haemoptysis, rigth side
pleuric chest pain and hoarseness of voice associated with shortness of breath. In addition
the patient started coughing up blood since last 2 weeks. The cough is more in the
morning with slight blood coming out with sputum. The patient advised by his general
practitioner (GP) to analyze sputum sample. Bone marrow biopsy showed plasma cells

8
Case Report:
Name of the patient: B B
Sex: male

Age: 59

DOB: 25/09/1947:

Present complain :

Aware of diagnosis

Feeling better

HOPI

Patient came in RUE unit with complain of haemoptysis, side pleuric chest pain and
hoarseness of voice. Patient started coughing up blood since last 2 weeks. The cough
more in morning blood is coming slightly coming with sputum.

Patient went to his GP and GP advised him for sputum sample. Also complained right
side pluraic chest pain. He also has history of shortness of breath, also noticed
hoarseness’ of voice since last 15 days. Weight loss last 3 months but his appetite is
good. No joint pain, no epitaxis no rash, no blood in urine, urine volume normal. No
recent flu like symptom, no orthopnea.

Dietian advised him low phosphorus diet and no added salt diet also fluid restriction.

Reqested medic consider prescribing phosphate binder. Note hypercalcemia. Patient is

now in dialysis using tunnel line on right atrium. No evidence of pneumothorax.
Advising femoral line because tunnel has a complication of low chance of recovery.

9
PMH:

MGUS IgA nephropathy lamda in serum and urine 2001 had bone marrow biopsy

COPD disease with bullae

Emphysema left decoritication

CKD 2

Pleural effusion left mini thoracotomy and plural biopsy, no malignancy found

Personal history:

Life long smoker, stoped in july in 06

Used to smoked 10/15/day

Moderate alcohol consumption 6-8 pints/week

Allergy history

No allergy history

Family history

Not significant

Drug history

Renagel 800mg BD

Frusemide 250mg OD

Na HCO3 50 mg BD

10
Salbutamol 2.5 mg OD

Paracetamol 1gm sos

Recent therapy

CORTICOSTERIODS
CHEMOTHERAPY
STEM CELL TRANSPLANTATION
THALIDOMIDE
BORTEZOMIB
LENALIDOMIDE
RADIATION THERAPY

On examination:

BP- 125 /70 mm of Hg

Pulse- 90

R/R-18 br/min

Euvolumic JVP

No sign of vasculitis

No peripheral Sacral odema

CVS

Heart sound normal

Respiratory

11
Chest clear

Left thoracotomy scar

Abdomen

Soft non tender

Investigation:

17/07/07

HB 11.6
HCT 0.38
WCC 5.3
PLTS 176000
ALK.PO4 109
TOTAL PROTEINS 68
NA 139
K 4.9
UREA 37.6
CR 478
CA 2.62
PO4 2.06

Renal function feb 2007 Urea- 6.4 and Crt-108

Worsening renal failure with

Biopsy report

Plasma cells constitute about 80% of the present and lie in confluent masses, extensive
80% infiltration by myloma

Differential diagnosis:

12
Multiple Myeloma

Amyloidosis

Other Malignancy

DISCUSSION
Multiple myeloma is a plasma cell neoplasia. It is an incurable but treatable disease
characterized by replacement of the bone marrow with malignant plasma cells, bone
marrow destruction and paraprotein formation. This paraprotein is also known as the M-
component. This molecule is a homogeneous, partial or complete immunoglobulin. Based
on the type of the M-component, multiple myeloma can be subdivided into the following
types: IgG, IgA, IgD, IgE and IgM. Common clinical findings in multiple myeloma are
hypercalcemia, anemia, renal damage, impaired production of normal immunoglobulins,
osteoporosis and lytic bone lesions. The patient presented in this case had all of these
symptoms. Additionally, multiple myeloma patients are at an increased risk of bacterial
infections. The most common myeloma types are IgG and IgA, followed by IgD, IgE and
IgM. There is also light chain disease where only light chains are synthesized, either
kappa or lambda. Another variant is a nonsecretory myeloma with no M-component
secretion.

Bone Involvement
The bone lesions are formed as the tumor grows in the bone marrow and invades the hard
bone creating the characteristic multiple small lytic bone lesions. The patient presented in
this case already had back pain and on skeletal survey was found to have multiple lytic
lesions. The severity of these lesions ranges from osteopenia to fractures. This bone
destruction usually presents as bone pain, frequently in the lumbar spine.

Renal Disease
Multiple myeloma causes renal failure in nearly 25% of patients. Hypercalcemia is the
most common cause of renal failure, as it leads to tubulointerstitial disease. There is

13
expression of the calcium receptor in the thick ascending limb of the loop of Henle where
hypercalcemia inhibits reabsorption of calcium, magnesium and sodium chloride. In
addition, hypercalcemia causes hypercalciuria via an increased filtered calcium load and
suppression of parathyroid hormone release with a consequent reduction in calcium
reabsorption.

Myeloma Cells and Bone Marrow Disease

Myeloma cells are of the same type in any given person and produce large
quantities of the same immunoglobulin protein, called monoclonal M protein, or
paraprotein. When blood or urine is processed in electrophoresis, these M proteins
show up as a "spike" in the results. The myeloma cells proliferate in the bone marrow and
do not leave space for the normal B lymphocytes to develop and produce adequate
immunoglobulins. This makes the patient prone to infections. Other cell lines are
produced in smaller quantity. Fewer white blood cells and red blood cells are produced,
and therefore patients present with anemia and susceptibility to bacterial infections.

Hyperviscosity Syndrome
When the protein concentration in blood becomes very high the blood becomes very
viscous, leading to flow problems. This is called hyperviscosity syndrome and some signs
and symptoms of it are shortness of breath, confusion, chest pain, spontaneous bleeding
and blurred vision. IgA myeloma causes hyperviscosity because of the predisposition of
the IgA molecule to form dimers. Increased protein in the blood is what produces the
classical roleaux finding (stacking of red blood cells) in the peripheral blood smear. The
patient in this case was found to have multiple myeloma of the IgA type and she was
experiencing hyperviscosity syndrome with symptoms of bleeding, shortness of breath
and confusion.

Both staging systems are of importance because they give prognostic values and aid in
deciding when to start treatment. Treatment is tailored to each individual depending on
several things, including the stage, physical exam and symptoms. The typical treatment is
high dose chemotherapy and bone marrow stem cell transplantation. Adjunctive therapy

14
for myeloma is radiation therapy. Bisphosphonates are used against skeletal events
because they inhibit bone resorption via action on osteoclasts or osteoclast precursors.
Erythropoietin induces erythropoiesis and can be used to treat anemia from myeloma or
from the chemotherapy. Plasmaphoresis may be done to treat the symptoms of
hyperviscosity syndrome. Hydration sometimes is enough to treat hypercalcemia.
Corticosteroids can be used to reduce swelling in patients with spinal cord compression
due to multiple myeloma. Patients with acute renal failure benefit from dialysis,
plasmaphoresis, management of hypercalcemia and avoidance of nephrotoxic
medications.
The standard chemotherapy regimen (VAD) combines vincristine, doxorubicin and
dexamethasone. Another regimen commonly employed is (VBMCP) vincristine,
bischloroethylnitrosourea, melphalan, cyclophosphamide and prednisone. MP (melphan-
prednisone) has also been used. Treatments currently in research include the use of
interferon alfa to prolong remission. Thalidomide has recently been found to be an active
agent in the management of multiple myeloma. Bortezomib (Velcade) is a reversible
proteosome inhibitor that has also been used with good results.

After several trials, the patient had the best response to a regimen involving regular
hemodialysis and thalidomide-dexamethasone treatment.

1. Radiation therapy, used by some authors to the chest in combination with

systemic therapy resulted in regression in the amount of effusion but no remission
of myeloma.
2. Makino et al used intracavitary interferon-a (given at 5 MIU dissolved in 100 ml
normal saline alternate days), and the patient’s effusion resolved after six
treatments. Unfortunately, the patient died of myeloma about two months later,
therefore this cannot be considered as standard.
3. The mainstay of therapy as of now is systemic chemotherapy.

Reference: [1]

15
Acute Renal Failure (ARF) due to alcoholism accombined with
nonsteroidal antiinflammatory drug (NSAID): a case report

Back ground:
Case of reversible acute renal failure (ARF) following binge drinking together with the
transient use of a nonsteroidal antiinflammatory drug (NSAID) is described. After binge
drinking, the patient experienced hyperdipsia, and the volume of his urine decreased.
Subsequently, he took an NSAID to relieve systemic joint pain associated with low grade
fever, and then he had complete anuria. One day after taking the NSAID, the patient
admitted to the hospital after diagnosed with severe renal dysfunction accompanied by
severe liver damage (blood urea nitrogen and creatinine concentrations were 57 and 5.4
mg/dl, respectively). The impaired renal function progressed over the first three hospital
days, as reflected by an elevated creatinine concentration to ll.6 mg/dl. Nine treatment
sessions of hemodialysis were, therefore, required to recover the loss of renal function.
The present case suggests that binge drinking may be a potential risk factor for ARF.

Case summary:
A case of middle aged male who developed swelling and weakness of muscles in the
lower limbs following a heavy binge of alcohol is being reported. He had myoglobinuria
and developed acute renal failure for which he was dialyzed. Acute alcoholic myopathy is
not a well recognized condition and should be considered in any intoxicated patient who
presents with muscle tenderness and weakness.

Case report:

Name of the patient: S R G

Age:
DOB: 05/07/68

Present complain:

16
Recent depression
He has on haemodialysis
Feeling well and no pain

HOPI:

Patient came in hospital with history of aneuric and diagnosed ARF due to
Rhabdomyolysis with Crt 598, Urea- 31.6, K-4.5, CK-804040
Early patient admitted in psychiatry dept in Barnsley Hopspital then he transferred in
renal unit due to deterioration of renal function. Patient came back from Thailand had
history of food poisoning over there after he so depressed and taking fluoxetine.
In Thiland for 3 month early this year and he had history of unprotective sexual contact
with female sex worker. No sign of compartment syndrome.

PMH

Depression
Ex alcoholic 5-6 pints/day
Food poisoning while in Thialand early this year
Developed diahorrea last 10 days

Personal history
Smoking 10-20 cigarate per day
Alcohol consume 5-6 pint/day

Family history
Not significant

Drug history:

Omeprazole 10mg od

17
Gliclazide 160mg bd
Lisinopril 2.5mg od
Metformin 1gm bd
Sodium bicarbonate
Calcichew 1.25 gm tds

On examination

BP-160/90 mm of Hg
Pulse: 78/min
R/R- 17 br/min
Peripheral edema present

CVS
Heart sound normal
JVP not raised

Respiratory
Chest clear

Abdomen
Soft non tender

Investigation
14/07/07
HB 10.7
NA 138
K 5.4
CA 2.12
PO4 1.08
ALBUMIN 38
AST 18
HCO3 20

18
USS
Normal size of kidney

Diagnosis
ARF due to Rhabdomyolysis

Discussion:
Acute renal failure has been reported to be induced by alcohol ingestion alone. The case
in this report showed evidence of non-traumatic rhabdomyolysis due to binge drinking.
Severe muscle damage and extremely high levels of serum CK and myoglobin were
observed in the cases of rhabdomyolysis-related ARF. In the present patient, the slight
elevation of serum CKand myoglobin suggests that muscle damage might be less than
that in the above-mentioned cases.

Gabow et al reported that ARF is seen in 33% of patients with nontraumatic

rhabdomyolysis, and dialysis therapy is required in only 15% of the cases They showed
that anion gap (28±14 mEq//) and phosphorus (7.3+3.5 mg/dl) in patients with
rhabdomyolysis-related ARFwere higher than those in patients with non-rhabdomyolysis-
related ARF ( 1 7±6 mEq//, and 4.5± 1.5
mg/dl, respectively)
In the current report, the anion gap and phosphorus were 18.7 mEq// and 3.4 mg/dl,
respectively. These results suggest that the patient had rhabdomyolysis, yet the muscle
damage was not severe enough to induce dependent ARF requiring dialysis therapy. This,
therefore, suggests that the reported case is not typical rhabdomyolysis related ARF.
Experimental and clinical studies have revealed that volume depletion, which leads to
activation of the pressor mechanism, appears to be a crucial factor in precipitating
rhabdomyolysis induced ARF. Dehydration is a frequent consequence of heavy alcohol
ingestion, because it is frequently accompanied by water dieresis, poor food and fluid
intake and vomiting, especially in cases of severe binge alcohol ingestion. Furthermore,
the majority of cases with rhabdomyolysis-induced ARF have manifested apparent body
weight loss. The present patient, however, did not have a poor fluid intake nor suffered

19
from any vomiting or apparent body weight loss before taking the NSAID, but he had
hyperdipsia, dark urine and a decreased urine volume after binge drinking, suggesting
that he was already in a mild dehydrated state before taking the NSAID. The increases in
his hematocrit and total protein levels were slight, and FENa was more than 1%, making
it difficult to suggest that the ARF was due to binge drinking alone. In fact, the patient
had an episode of complete anuria following NSAID ingestion. The present case strongly
suggests a linkage between alcohol-induced rhabdomyolysis and accelerates the
impairment of renal hemodynamics.

In summary, in the present study, it had been reported that a patient with acute renal
failure following binge drinking in which case an episode of complete anuria following
NSAID suggests that NSAID ingestion can accelerate the progression of impaired renal
function induced by mild rhabdomyolysis, mild dehydration, and severe liver damage
resulting in acute renal failure requiring dialysis therapy. It is therefore very important
that physicians and pharmacists be alerted to the potential risk of NSAID induced acute
renal failure when NSAIDs are ingested following binge drinking, even if patients have
no severe muscle damage. In the future, further case reports will surely support our
recommendation that the use of NSAIDs should be avoided.

Reference: [2], [3], [4]

20
Reflux nephropathy : a case report

Introduction:
Reflux nephropathy (RN) as a cause of hypertension and end stage renal disease is being
increasingly recognised. It leads to advanced renal failure in 30% of children and in 15-
20% of adults. The incidence of hypertension in children with RN ranges from 5 to 30%.
It is important to realise that early detection of RN and long-term management of reflux
can prevent both hypertension and end stage renal disease. Therefore, there is a need for
increased awareness of this entity amongst the practising physicians so that cases are
picked up early and by proper therapy adverse sequel of hypertension, chronic renal
failure and end stage renal disease are prevented.

Case summary:
A 63-year-old female suffer from hypertension was brought to Northern General Hospital
with complaints of pain in abdomen, anorexia and was feeling unwell last 2 months. She
had past medical history of urinary tract infection at the age of 5 years. Now she is
feeling lethargy with weight loss. The patient lost her appetite for 3 consecutive days. She
also feeling back pain around the lower spine area. She told that unable to walk much at
home because of leg weakness. She could not movement facial muscle properly and limb
as well. The patient neither was walking or speaking properly due to lethargy. On
examination, she had a high blood pressure of 200/120 mmHg

Case report:
Sur name : G D R
Age: 63, Gender: Female

Present complain:
feeling unwell last 2 months
Lethargic for 2 month
Loss of appetite and does not eat properly last 3 days
Back pain around the lower spine

21
Log weakness unable to walk much at home

History of present illness:

she is feeling unwell with lethargy and also losing weight day by day. She informed me
that she does not ate for 3 days. She also feeling back pain around the lower spine area.
She told that unable to walk much at home because of leg weakness. She could not
movement facial muscle properly and limb as well
She cant speak properly and also have evidence of weight loss.

Past medical history:

Reflux nephropathy, HTN

Medication:

Calcium gluconate 10% i/v

Sodium bicarbonate 200mg tds
15 units actrapid in 50ml 50% dextrose
Gelofusin 500ml i/v
Augmentin 1.25 gms i/v
One alpha .25mcgm od

Social history:

Lives with husband

Not smokes since 27 yrs age
She is working as a shop assistant and also she keeps cat/dog

On examination:
BP: 127/56,
Heart rate: 100 beat per minute

22
CVS:
Heart sound normal

Respiratory system:
Clear both lung

Abdomen: soft tender lower abdomen

CNS:
3, 4, 6 intake
5 intakes
7 intakes
8-12 intakes

Investigation:
11/07/07

HB 12.1
HCT .36
WCC 5.3
PLATELETS 166000
ALK. PHOSPHATASE 105
TOTAL PROTEINS 61
NA 128
K 8.7
HCO3 24
UREA 24.2
CREATININE 428

USG:
Bilateral small kidney, cortical scarring, no hydronephrosis
Urea: 18.2, Creat: 449, K: 5.1

23
ECG: tall T wave, broad QRS

D/D:
Acute rénal fêlure ---- 1. HTN 2. Reflux nephropathy
CKD--- dehydration, sepsis

Discussion:
In the recent literature, a lot of controversy surrounds the exact aetiopathogenesis of
hypertension in RN. In this connection, the role of intra-renal reflux (IRR) should be
emphasised. It has been shown that VUR alone does not lead to renal scarring. Renal
scarring occurs only when VUR is associated with IRR. Factors favouring IRR are (i)
association of UTI, (ii) association of high pressure VIR, (iii) the anatomical factors like
compound and simple papillae. The compound papillae are more susceptible to IRR than
simple papillae, due to anatomy of their orifice.
How, the renal scarring leads to hypertension are still not thoroughly understood. In this
connection the role of plasma renin activity needs to be discussed. In some patients with
RN and hypertension the expected age related decrease in PRA, was not observed
indicating that high PRA levels are contributing to hypertension. Another important
factor is a focal increase in renin secretion and this can be demonstrated by analysing the
segmental renal vein PRA. This segmental hyper secretion of renin may not be reflected
in the renal vein PRA and yet they may be playing vital role in causing hypertension\.
The reflux appears to be primary in our case. Whether this primary reflux is due to
congenial abnormalities of the ureter and ureter orifices such as low ratio of intra-
mucosal ureteric length to orifice diameter (Normal ratio 5: 1) could not be determined in
our case as the parents were reluctant for cystoscopy which is necessary to identify such a
congenital abnormality. For the diagnosis of RN, various imaging techniques have
evolved both to demonstrate reflux as well as scarring. IVP can show scarring, but it can
be normal in few cases. Dimercaptosuccinic acid (DMSA) scan is more sensitive than
IVP in demonstrating scars. Medical Management of hypertension and primary reflux
nephropathy consists of following plan: (a) Keeping the urine sterile by continuous
prophylactic chemotherapy so as to prevent fresh scarring. In this report the patient was

24
put on prophylactic chemotherapy with nitrofurantoin successfully. The drugs most
commonly used are sulphamethoxozole -trimenthoprim, nitrofurantoin and
sulphisoxazole. The prophylactic dose is one half of therapeutic dose. How long to
continue the prophylactic antibiotic therapy? However, there is another view that if the
reflux persists, the age of the patient should be an important determinant in deciding
about the discontinuation of long-term chemotherapy. In late childhood and adolescent
the disappearance of reflux, especially more than Grade III reflux is very much unlikely
and in such a situation, chemo prophylaxis may be discontinued and surgery should be
considered as a choice.
(b) Hypertension should be treated by drugs, which decrease the renin production as the
increased production of renin is shown to be the important factor in pathogenesis of
hypertension. Hence captopril is very useful in hypertension. However, other drugs like
propronol, methyl dopa have also been found useful.
(c) Episodes of intercurrent infection may occur despite prophylactic chemotherapy. This
should be vigorously treated with antibiotics, the type of antibiotics being used depending
upon the culture and antibiotic sensitivity.
The role of surgery in the management of RN is beset with controversy. Surgical success
rate for elimination of reflux is quiet high for all grades of VUR: 90-100% for Grades I
and II, 93-99% for Grade III and 50-60% for Grade IV and V. The patients showing VUR
with or without demonstrable scarring should be given prophylactic chemotherapy to
keep urine sterile (The scar may take several months to be demonstrable either by IVP or
DNISA scan.

Reference: [5]

25
Anemia management in CKD: a case report

Introduction

Anemia is common in chronic kidney disease (CKD) due to a state of erythropoietin

deficiency. Erythropoietin therapy has been used for approximately 20 years to correct
anemia in CKD and to improve both subjective and objective outcomes. Guidelines that
establish a hemoglobin (Hb) goal for anemia correction in CKD patients are largely based
on observational data. Controversy still exists, however, because outcomes have not been
consistent with various degrees of anemia correction. The number of prospective
randomized trials investigating the effects of anemia correction on cardiovascular (CV)
morbidity and mortality in CKD patients, an already high-risk group, is limited. With
respect to improving CV outcomes in the CKD population, the currently available trial
data caution against raising Hb levels in CKD patients to approach more "normal"
physiologic ranges. The disappointing experience with the trial data must be weighed
against the beneficial associations of erythropoietin therapy that have been generated
from observational data. Establishing the ideal target Hb ranges for anemia correction in
CKD patients remains a dynamic process and leaves many gray areas to be further
elucidated.

Chronic kidney disease (CKD) has been linked to higher heart failure (HF) risk. Anemia
is a common consequence of CKD, and recent evidence suggests that anemia is a risk
factor for HF. In this study a case reported to show the association between CKD and
anemia.

Case summary:
A 82-year-old man with hypertension was initially feeling tired and breathless from last
few days. His blood report suggesting severe anaemia 4.6 g/d. renal ultrasound revealed
severe bilateral hydronephrosis. In addition, he had history of prostectomy 5 years back
and CKD-5. He also has Pedal oedema and clubbing. He was referred to our institution

26
for further evaluation and management of his persistent symptom of severe anaemia, dry
cough and mild epitasis for last few months, shortness of breath, loss of appetite and
weight loss.

Case report:

Surname: L H
First name: R
Age: 82 yrs
Male

Present complain:
Feeling tired and breathless from last few days

HOPI:
Normally he is well and no medical illness. Look after his wife for last 2 months who had
a stroke, feel loss of appetite and weight loss. For last few days feeling tired and
shortness of breath..
Today feel more unwell. His blood report suggesting severe anaemia 4.6 g/d. He also
complained about dry cough and mild epitasis for last few months. He also denied
previous renal failure, urinary symptom and peptic ulcer symptom.

PMH:
HTN
Prostate operation 5 years back
CKD stage 5

Drug history:
Venofer 100mg /month
Neorecormon 4000i.u 2/week
Atorvastatin 40mg od
Alfacalcidol 1mcg od

27
Sodium bicarbonate 50mg
One alpha 0.25mcg od
Ramipril 2.5 mg

Allergy history:
NAD

O/E:
Pale looking
BP: 106/55, Pulse: 80, Heart rate-100/min, Sats 96%
Pedal oedema present
Thin comfortable,
Clubbing-present
Dehydration

Lung:
Clear

CVS:
Normal HS

Abdomen:
Soft, non tender
P/R: no melena
Catheter:
Turbid urine

Investigation:
HB 9.1
WCC 10.2
PLTS 182
MCV 87.1
NA 132

28
K 4.6
UREA 10.2
CR 186
Ca 2.0
PO4 2.1
ALK PO4 58
ALBUMIN 38

ECG- No evidence of hyperkalaemia yet

Urine dipstick:
Blood 2+, Protein- 2+, Leu 2+

USS:
Right Kidney measure 10.1 cm and is hydronephrotic renal pelvis measuring 1.5 cm
Left kidney measure 8.9 cm and also grossly hydronephrotic and proximal ureter dialated
as well.
Left renal pelvis measure 3.5 cm.
Bladder catheter in situ
No mass lesion seen

Comment: Bilateral severe hydronephrosis, cortical thinning probably long standing.

Discussion:
Anaemic patients with chronic renal failure should receive treatment with recombinant
human erythropoietin (r-HuEPO, Eéoetin) to maintain hemoglobin levels over 11 g/dL
with an acceptable target of 12 to 12.5 g/dL, according to recommendations from the
European practice guideline for management of anemia in patients with chronic renal
failure [33] and the National Kidney Foundation K/DOQI clinical practice guidelines for
anemia of chronic kidney disease [27]. Benefits of adequate hemoglobin levels had been
established in patients undergoing dialysis, and are supposed to be relevant also in CKD
patients. In addition, anemic patients should receive iron supplementation in order to
maintain serum ferritin levels above 100 μg/L and transferrin saturation above 20%.

29
The CHOIR and CREATE studies, together with previous randomized controlled trials in
patients on dialysis, indicate that we should aim for only partial correction of anemia in
patients with CKD, and that 115 g/l (11.5 g/dl) is a reasonable upper limit for a
hemoglobin target. It is important to recognize that, because of the difficulty of
maintaining hemoglobin concentrations within a narrow window, reducing the upper
limits of hemoglobin targets is likely to increase the proportion of patients with
hemoglobin concentrations less than 110 g/l (11.0 g/dl), and perhaps even the proportion
with levels below 100 g/l (10.0 g/dl). The ongoing Trial to Reduce Cardiovascular Events
with Aranesp Therapy (TREAT), which allows a hemoglobin level as low as 90 g/l (9.0
g/dl) in one treatment arm, should provide important information about acceptable lower
limits.

Conclusion
In conclusion, further evidence was found that the concomitant presence of either CKD
or anemia increased the risk of dying in the hospital or of being readmitted within 30
days among patients hospitalized with heart failure. The association persisted after
controlling for other factors associated with adverse outcomes in these patients.Patients
with anemia caused by CKD are at higher risk of death or cardiovascular events when the
target hemoglobin level is 135 g/l rather than 113 g/l.

Reference: [6], [7]

30
ARF secondary to Fluid overload: a case report

Background:
Fluid overload is a chronic, troublesome problem in many patients on hemodialysis.
These patients suffer from hyperdipsia with inability to excrete water. Angiotensin-
converting enzyme inhibitor (ACEI) has been shown to decrease thirst and interdialytic
weight gain in 2-4 weeks of usage. It was suggested that long-term ACEI may not
continue to suppress inappropriate thirst and fluid intake after 6 months in hemodialysis
patients.

Case summary:
A 19-year-old male patient with untreated seizure disorder, presenting with Nausea,
vomiting, loss of appetite and weight loss for 2 weeks, and impaired renal function –
Urea- 213, Creat 743, K-4.2
Usually fit and well started with nausea, vomiting for 2-3 weeks and also has history of
haemetemesis. He also complain about haematuria and dysuria, He mentioned that he
suffer from decreased urine output. He also was complaining of joint pain but not redness
or swelling of joint.
He had productive cough with slight haemoptysis 2 weeks ago. No recurrent nose
bleeding reported.
Patient was referred with lethargy with increased urea and Creatinine. USS abdomen
showed right kidney 10.1 cm and left kidney 9.3 cm. No hydronephrosis. Renal biopsies
was arranged but cancelled twice because of increase bleeding time in spite of having
DDAVP. Urea and Creatinine remain stable throughout his stay in the hospital. Follow
up is arranged in the low clearance clinic in 3 weeks time.

Case report:

Name: B S M
Age:
DOB:30/08/1988

31
Present complain:
Nausea, vomiting, loss of appetite and weight loss for 2 weeks
Impaired renal function – Urea- 213, Creat 743, K-4.2

HOPC:
Usually fit and well started with nausea, vomiting for 2-3 weeks and also has history of
haemetemesis. He also complain about haematuria and dysuria, He told me that he also
has decreased urine output. He has also complaining joint pain but not redness and
sweeling of joint.
He also informed me has cough with sputum but had slightly haemoptysis 2 weeks ago.
Otherwise no recurrent nose bleeding.
Patient is being refer with feeling unwell and had increased urea and Creatinine. USS
abdomen showed right kidney 10.1 cm and left kidney 9.3 cm. No hydronephrosis. Renal
biopsy arrange but cancelled twice because of increase bleeding time inspite of having
DDAVP. Urea and Creatinine remain stable through out his stay in the hospital. Follow
up is arranged in the low clearance clinic in 3 weeks time.

PMH:
He had episode of constant vomiting for 2 months 2 years ago
No further investigation and treatment at that time has taken.

Drug history:
Frusemide 160mg bd
Prednisolone 15mg od
One alpha 250mcg
Pravastatin 20mg od
Septrin 200mg od
Inj. Eprex 2000 i.u 3/week
Spironolactone 500mg od
Oral antacid syrup from GP either nil else

Allergy history:

32
Nil

Family history:
Lives with parents
Smokes 10/day
Occasionally drinks alcohol. No family history of renal disease and DM
2 cousins have hearing loss and wear hearing aids

O/E:
BP: 153/86, Sats-98%, Weight 71.4, Pulse-104/min

CVS:
Systolic murmur present

Lung:
Clear
Abdomen:
Soft non tender

Investigation: 16/07/07
HB 9.3
WCC 13.1
PLTS 454000
MCV 96.3
ESR 108
PT 16
APTT 40.2
PTH 123
UREA 20.3
CR 319
CA 2.61
PO4 1.8
K 4.7
NA 136

USS:

33
Both kidney measure appro 10.1 cm Right
9.3 cm Left
No abnormality of kidney and no hydronephrosis
Bleeding time: more than 10 minutes

Urine Dipstick
Blood
Protein more than 300 mg/dl
Glucose negative

D/D
ARF
RPGN

Discussion:
Volume overload should be suspected in patients complaining of dyspnea, chest
discomfort, orthopnea, paroxysmal nocturnal dyspnea, or progressive decrease in exercise
tolerance. It may also be asymptomatic. Physical findings could include jugular venous
distention, hepatojugular reflux, pulmonary rales, wheezing (in “cardiac asthma”), and S3
or S4, ascites, and peripheral edema. Patients with chronic kidney failure may also have
significant volume overload even in the absence of the above symptoms and signs. Chest
films may show evidence of pulmonary edema or may be subtle, showing only prominent
pulmonary vasculature. The same findings may occur with heart failure, liver failure and
various other conditions, so the patient’s change in weight over time is critical. Over
weeks to months, these patients may lose lean body mass due to malnutrition and can
develop fluid overload with relatively little change in weight. Therefore, serial
assessment of patients’ lean body mass is also critical.

Contributors include:

34
 • Excess salt intake
• Progressive kidney damage (nephrosclerosis)
• Fluid retention from blood pressure medications
• Inadequate diuretic therapy.

Consider fluid overload for sudden unexplained gains in weight, refractory hypertension,
peripheral edema or shortness of breath. These may be secondary to the above causes.
Hyponatremia, developing as a result of water retention in excess of sodium retention,
may also be a marker for volume overload in the above setting.

Management:

• Patients should be weighed at every visit

• Dietary sodium restriction to 2 gm/d
• Loop diuretics, and if refractory to twice a day dosing, consider adding
thiazide-type diuretics
• If advanced kidney failure, consider initiation of dialysis.

Reference: [2]

35
Chronic kideny disease (CKD) related risk factor for cardiovascular
disease (CVD): a case report

Back ground:
Patients with CKD have many of the traditional risk factors for CVD, including older
age, hypertension, dyslipidemias, diabetes mellitus, and physical inactivity (Menon, Gui,
& Sarnak, 2005). Age is the only one of these traditional risk factors, shared by many
patients with CKD, that is not modifiable. Other nonmodifiable CVD risk factors include
gender, family history, and hereditary factors such as race. Hypertension, dyslipidemias,
diabetes mellitus, smoking, and physical inactivity, risk factors, that adversely affect
other risk factors, such as obesity and hypertension, can all be managed or treated, thus
are considered modifiable risk factors (Grundy et al., 1999).

In addition to traditional CVD risk factors, individuals with CKD must also be assessed
for nontraditional risk factors. Many of the complications of CKD, when not adequately
treated, may lead not only to more rapid progression of kidney disease but, also, to
increased cardiovascular morbidity and mortality (NKF, 2005). These unique CKD-
related risk factors for the development of CVD include anemia,
proteinuria/microalbuminuria, disturbances of mineral metabolism, extra cellular volume
overload, malnutrition, inflammation, elevated homocysteine levels, and elevated c-
reactive protein levels (Abramson, Jurkoutz, Vaccarino, Leveintraub & McClellan, 2003;
Cullerton et al., 1999; Sarnak et al., 2003; Shlipak, Fried, Stehman-Breen, Siscovick, &
Newman, 2004). The Kidney Disease Outcome Quality Initiative (K/DOQI) Guidelines
recommend consideration of all of these unique risk factors and suggest that efforts to
reduce CVD risk should be initiated early in the course of CKD to reduce morbidity and
mortality (NKF, 2005).

Case summary:
A 75-year-old man of British origin, was admitted to renal unit at Northern General
Hospital for further evaluation of chronic kidney disease (CKD). He has no history of

36
diabetes mellitus or hypertension but nocturia 4 times per night. He had history of CKD
with progressive incline of creatinine from 136 mmol/l in 2005 to 200 mmol/l in
December 2000. Lately a creatine of 153 mmol/l and GFR 38ml/min (CKD) was
reported.

Case report:
Name: D P
Age: 75
Occupation: retired
Gender: male

HOPI: The patient suffer from shortness of breath, wheeze, hotness, sweaty and
dizziness upon standing. Also he felt chest tightness across the chest.
There is no history of DM, haematuria but nocturia 4 times per night. Pheripheral oedema
is intermittently a problem through is currently well control with just 2 mg of
bumetanide.
There is no definitive history of orthopnea or paroxymal nocturnal dyspnea. Though he is
markedly dyspnea on walking a few yards.
H/O CKD with creatinine climbing from 136 mmol/l in 2005 to 200 mmol/l in
December. From this clinic visit he had a creatine of 153 mmol/l and GFR 38ml/min
(CKD)

Past history: CKD, AF, CF

No history of DM, stroke, weakness, numbness, coughs, diarrohea, vomiting and leg
swollen.
Medication:
there is recent NSAID used, no allergy drugs.
Bisoprolol fumarate 3.75 mg tab
Bumetanide 1 mg tab
Ramipril 5 mg

37
Bumetanide 1mg
Warfarin WBS 1mg
Simvastatin 20 mg
Omacor 1g

Personal history: Ex smoker who drink 5 pints 2 times weekly through was previously a
heavier drinker. He lives a lone but has a stair

O/E:
Pulse
BP
CVS: S1 and S2 heart sound normal. JVP not visible.
Respiratory: Trachea centrally. Few basal crepitation present.
GIT: abdomen is soft , no tender and rigidity.

Investigation: Na- 139, K- 4, Urea- 10.1, Creat- 147, HCO3- 33, Ca- 2.32, PO4- 1,
CaPO4- 2.32, AlkPO4- 87,
AST- 40, Bilirubin- 17

Hb- 15.4, WCC- 10.2, MCV-94.3, MCH- 31.1, MCHC- 32.9

Discussion:
There are guidelines available to direct the practitioner in reducing a patient's
cardiovascular risk factors. The National High Blood Pressure Education Program of the
NIH presented its Seventh Report of the Joint National Committee (JNC) on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure in 2004 (USDHHS, 2004).
Like its predecessors, these JNC 7 Guidelines provide an evidence-based approach to the
prevention and management of hypertension, a major risk factor in the development of
CVD as well as CKD (Chobanian et al., 2003).

The American Heart Association (AHA) Guidelines for Primary Prevention of

38
Cardiovascular Disease and Stroke: 2002 Update: Consensus Panel Guide to
Comprehensive Risk Reduction for Adult Patients without Coronary or Other
Atherosclerotic Vascular Diseases provides a framework to assist primary care providers
in assessment, management, and follow-up of patients who may be at risk for but who
have not yet manifested cardiovascular disease (Pearson et al., 2003). Although the JNC
7 Guidelines and the AHA guidelines provide a framework for comprehensive care for
the general population of patients at risk for CVD, they do not specifically address all of
the CKD-related nontraditional CVD risk factors.
The Third Report of the National Cholesterol Education Program (NCEP) Expert Panel
on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III)
Executive Summary was released in 2001 (ATP III, 2001). Based on the ATP I and APT
II, these were updated, evidenced-based clinical guidelines. They provided direction for
cholesterol testing and management that expanded the indications for intensive
cholesterol-lowering therapy in clinical practice and applied findings from the most
recent clinical trials. While ATP III maintained attention to intensive treatment of
patients with CHD, its major new feature was a focus on primary prevention in persons
with multiple risk factors. Because of the focus on individuals with multiple CHD risk
factors, the guidelines can be applied to the population of patients with CKD. However,
they do not specifically address this group or CKD-related risk factors.
In 2005, in an effort to more effectively address the risk of CVD in patients with CKD,
the National Kidney Foundation (NKF) developed the K/DOQI Guidelines for
Cardiovascular Disease in Dialysis Patients (NKF, 2005). The K/DOQI Guidelines
recommend that CVD risk factor reduction should be initiated early to reduce morbidity
and mortality associated with CKD. The guidelines for treatment and prevention are
specific to individuals with Stage 5 CKD, and the extent to which they can be applied to
persons in the earlier stages is unclear.

Reference: [8], [9], [10]

39
IgA nephropathy management: case report

Back ground:
IgAN is the most common type of glomerulonephritis in the world. Between 15 and 40
percent of adults and children diagnosed with IgAN eventually progress to (ESRD).
Despite the need for effective treatment strategies, very few Randomized Control Trial
for IgAN have been performed. The most effective therapies for IgAN appear to be
corticosteroids, ACEi, that contain a high concentration of omega 3 fatty acids. While
ACEi are generally well tolerated with minimal side effects, the use of high dose steroids
over a long course of therapy is often associated with significant morbidity

Case summary:
A 36-year-old man was referred to the Department of Nephrology at the Northern
General Hospital (Vickers 3) because of an episode of asymptomatic gross proteinuria
suggesting nephritic syndrome with a serum albumin of 21, serum protein of 51.2;
clinically she had edema in mild shin on review clinic. The patient’s Alanine Transferase
which returned back to normal. In addition her Anti Nuclear Antibody and Ig A antibody
were positive. The patient had no family history of renal disease. Biopsy results showed.

Case report:

Name: B P
Age 60 yrs

Chief complain:
post biopsy, passing urine
HOPI:
The patient was feeling unwell recently. She also complained of back pain of dullache
nature over the last year and, taking pain killer. She attached anxiety last year and last

40
night she had physiotherapy. After holiday in Turkey in October 2006 she began to
complain arthralgia, ankle swelling and severe lethargy.
She did have transient upper GI symptom which settle with OPI. She had went a normal
OGD and colonoscopy in 2006. Her urine dipstick was positive for protein in a 24 hrs.
urine collection at 3.22 for in 24 hrs of protein.
Suggesting nephritic syndrome with a serum albumin of 21, serum protein of 51.2,
clinically she had odema in mild shin on review clinic. Her ALT which her now settle
back to normal.
In condition, her ANA was positive, Crt-54, Na- 136, Urea-4.8.
She also positive Ig A antibody, low Ca 2.17
She denies any diarrohea, haematuria, previous recurrent UTI, renal stone, flank
abdominal pain, she denies facial rashes, red dry eyes, sore throat. She has not had a
blood transfusion in past. She denies an any past history of IHD, DM,CVA, malignancy,
asthma, COPD
Family history: there is no history of kidney disease. She only smoke for a year or when
she is very young but has not smoke last 50 yrs. She takes very minimum amount of
alcohol. She did biopsy and waiting for biopsy report.

HPH: hypothyroidism, proteinuria, microscopic haematuria, HTN

Treatment

Alfacalcidol 1 mcg od
Gliclazide 40mg od
Neorecormon 4000i.u / week
Clonazepam 50 mcg od
Lactulose + senna

O/E:
Pulse 72 beats/min
BP 130/70 mm of Hg
CVS: S1 and S2 heart sound normal. JVP not visible.
Respiratory: Trachea centrally. Chest clear

41
GIT: abdomen is soft, no tender and rigidity

Investigation:
HB 10.8, WCC 12.1, PLTS 196, MCV 91.6, NA 136
K 4.6, UREA 10.2, CR 199, HCO3 21, CA 2.1
PO4 1.45, ALK.PO4 58, ALBUMIN 38

Discussion:
Patients with IgAN usually present with hematuria. Approximately 40% to 50% of
patients have macroscopic hematuria frequently accompanied by an infection of the
upper respiratory tract and, less often, pneumonia, gastroenteritis, or urinary tract
infection. The episode is usually brief—about 24 hours—but can last as long as 1 week.
This feature usually occurs in children and in patients under 40 years of age, and loin
pain often accompanies the hematuria. Microscopic hematuria, usually with proteinuria,
constitutes the other common initial presentation in another 30% to 40% of patients.
Macroscopic hematuria can complicate the course of about 20% to 25% of patients in this
subgroup. This presentation is more common in older patients but is observed in patients
of all ages. As many as 20% of patients with IgAN present with severe azotemia that
represents long-standing disease. Acute renal failure occurs in less than 10% of patients,
and the nephrotic syndrome is uncommon, occurring only in approximately 5% of all
patients, usually children and adolescents.
The diagnosis of IgAN currently can be made only by kidney biopsy. The spectrum of
light microscopic findings ranges from minor mesangial changes to focal and diffuse
mesangial proliferation to crescentic glomerulonephritis. In addition to glomerular
lesions, various tubulointerstitial and vascular lesions also can be seen, including tubular
atrophy, interstitial fibrosis, interstitial cellular inflammation, and vascular sclerosis.
However, the histopathologic criterion for IgAN is the dominance or co-dominance of
IgA deposition in the mesangium. Although many other diseases also are associated with
glomerular IgA deposits5, I will not consider their prognosis and treatment in this review.

42
 Table 1. Clinical risk factors for progression in IgA nephropathy (IgAN)
Impaired renal function at discoverya
Magnitude and duration of proteinuriaa
Hypertension at presentationb
Older age at onset
Absence of recurrent macrohematuria
Persistent microscopic hematuria
Male gender
Obesity
Hyperuricemia
Hypertriglyceridemia
Smoking
Familial disease

Table 2. Histologic risk factors for progression in IgA nephropathy (IgAN)

Glomerular
Advanced glomerulosclerosisa
Mesangial hypercellularity
Segmental necrotizing lesions
Extensive crescents (>30%)
Capillary wall deposits of IgA
Tubulointerstitial
Marked tubulointerstitial fibrosisa
Intense interstitial infiltration
Arteriosclerosis/arteriolosclerosis

The magnitude and character of proteinuria are powerful clinical indicators of an adverse
outcome. At present, it is believed that no sharp dividing point relates the magnitude of
proteinuria to prognosis. Most investigators, however, believe that more than 1 g/day is a

43
reasonable threshold for concern11,15. Universal consensus exists that proteinuria >3
g/day is associated with a high likelihood of a subsequent progressive decline in renal
function
Less concordant are the data for the prognostic value of arterial hypertension at
presentation. High blood pressure (>140/90 mm Hg) can be an important factor
associated with a more rapid progression in adults with IgAN. However, when this
clinical factor was evaluated using multivariate analysis in several studies, it appeared to
be significant in some but not all
Treatment
The patients with IgAN with normal renal function, minimal (<1.0 g/day) or no
proteinuria, normal blood pressure, and minimal or mild lesions on renal biopsy should
not be treated as benign course of patients, they should be kept under periodic review. On
the other hand, patients with one or more adverse prognostic features such as
hypertension, proteinuria >1 g/day, slowly progressive renal failure, and moderate to
severe changes in renal biopsy histology could be candidates for one or even several
therapeutic modalities. There are many approaches to treat adults with primary IgAN
includes the following:

ACE inhibitors
Control of blood pressure remains the cornerstone of treatment as for patients with other
types of kidney disease. The therapeutic benefit of antihypertensive drugs is thought to be
a putative reduction of glomerular hypertension that provides protection against
glomerular injury. Because of their ability to specifically reduce intraglomerular pressure,
ACE inhibitors have attracted the most attention as the ideal antihypertensive drugs for
the treatment of hypertension in renal disease, including IgAN. The effectiveness of ACE
inhibitors in reducing progression of renal dysfunction is posited to be a consequence of
their antiproteinuric effect rather than attributable to their blood- pressure-lowering effect
alone. Moreover, ACE inhibitors also might attenuate the effect of angiotensin II on renal
cell growth and proliferation and might inhibit extracellular matrix component release
that culminates in sclerosis.

44
Steroids
Steroids were among the first agents used for the treatment of IgAN. In an early,
randomized, prospective, controlled trial in adult patients with IgAN and the nephrotic
syndrome, 4 months of therapy with moderate doses of oral steroids did not produce any
benefit except in patients with very mild histologic lesionsAlso, Kobayashi et al reported
beneficial effects of steroids given in moderate doses for periods of 1 to 3 years in
patients with moderate or heavy proteinuria. In both studies, renal function was preserved
in patients with an initial creatinine clearance of >70 mL/min but not in those with more
severe impairment of renal function. The same authors also have demonstrated that daily
steroids for 18 months in IgAN patients with normal renal function and moderate
proteinuria produced a better preservation of renal function and a greater reduction in
proteinuria 10 years after therapy when compared with an untreated group.

Immunosuppressive drugs
There is limited experience with the use of azathioprine in the treatment of IgAN in
adults. Goumenos et al published a retrospective study that used long-term azathioprine
combined with low-dose prednisone in patients with progressive renal disease
accompanied by proteinuria and moderate to severe histologic changes. Eighty percent of
patients receiving azathioprine exhibited stable renal function, but only 36% of the group
treated conservatively. There was no effect on proteinuria..

Cyclophosphamide has been used in a limited number of trials. Some of these studies
used a combination of cyclophosphamide, dipyridamole, and warfarin and chiefly showed
a reduction in proteinuria.

Cyclosporine was tested in a randomized single-blind trial conducted by Lai, Lai, and
Vallance-Owen. The drug was given for 12 weeks to 24 patients with proteinuria of at
least 1.5 g/day and reduced renal function. They showed a modest reduction in
proteinuria, unfortunately often accompanied by a rise in serum creatinine. These
changes were reversed after cessation of the treatment. Thus, while cyclosporine is likely
to display an antiproteinuric effect in IgAN, the risk of nephrotoxicity limits its
usefulness.

45
Limited trials of mycophenolate mofetil (MMF) have been reported. In a few case reports
and a small uncontrolled trial, MMF, 1 to 2 g/day alone or combined with steroids for
several months, decreased proteinuria and stabilized serum creatinine in patients with
severe IgAN

Fish oil
Interest in fish oil as a treatment of IgAN has recently intensified. Fish oil is rich in -3
fatty acids, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). These
compete with arachidonic acid and produce biologically less-effective prostaglandins and
leukotrienes that might retard renal damage by decreasing glomerular and interstitial
inflammation, platelet aggregation, and vasoconstriction. In the United States, a
randomized controlled trial is underway comparing fish oil, alternate-day prednisolone,
and ACE inhibitors in children and young adults with IgAN. The results of this trial
should considerably clarify whether steroids or fish oil is better for patients at risk for
progressive renal disease.

Anticoagulant and antiplatelet drugs

Anticoagulant and antiplatelet therapy have long been used in the treatment of IgAN.
Most of the early trials were uncontrolled and small in size.

Other treatment considerations

Tonsillectomy also has been recommended for patients with IgAN, but its role remains
controversial. Removal of the tonsils in patients with chronic or recurrent tonsillitis
reduces serum IgA levels, circulating immune complexes, proteinuria, and episodic
hematuria. Patients most likely to benefit from tonsillectomy had preserved renal function
(serum creatinine <1.4 mg/dL) and mild changes on histology. These benefits were not
observed in patients with more advanced renal disease.

Tonsillectomy in combination with pulse steroid therapy might produce higher rates of
clinical remission. However, no study to date has shown long-term preservation of renal
function in patients who have undergone tonsillectomy. Tonsillectomy has not yet been

46
tested in a controlled randomized trial, so this approach should be reserved for recurrent
episodes of macroscopic hematuria or relief of chronic recurrent tonsillitis.

Conclusions
For the moment, no consensus exists on the best treatment of IgAN. Before making any
therapeutic decisions, clinicians should keep in mind the chronic nature of the disease and
the possibility of a good outcome without therapy. Treatment, therefore, should be
relatively nontoxic and probably limited to patients who have reasonable evidence of a
poor long-term prognosis.

Hypertension should be treated aggressively, mainly with ACE inhibitors or ARBs.

General agreement exists that patients with normal renal function, no or trivial
proteinuria (<0.5 g/day), normotension, and minimal or mild lesions on renal biopsy
should be managed conservatively with regular follow-up. It is not known whether
patients with proteinuria > 0.5 g/day but <1 g/day should be treated. In my opinion, even
if they are normotensive, one should attempt to lower proteinuria to <0.5 g/day by giving
these patients fish oil and an ACE inhibitor or an ARB.

Patients with greater proteinuria (>1 g/day), normal or mildly impaired renal function
(serum creatinine <1.4 mg/dL), and mild-to-moderate renal lesions should initially
receive fish oil in combination with an ACE inhibitor or ARB in an attempt to lower
proteinuria to <1 g/day. If this reduction cannot be achieved, then a course of low-dose
steroids on a daily or alternate-day basis for 3 to 6 months is indicated. Whether the
combination of these two therapies is more effective is not clear as yet.

Patients with persistent proteinuria >1 g/day, impaired renal function (serum creatinine
>1.4 mg/dL), and moderate to severe histologic changes are less likely to respond to
steroids. Again, these patients could be successfully treated with fish oil in combination
with ACE inhibitors or ARBs, as indicated by the international experience and our own.
Alternatively, azathioprine or MMF and low-dose alternate day prednisolone could be

47
considered. When contraindications to prednisolone or immunosuppressive drugs exist,
low-dose warfarin combined with dipyridamole could be used.

Patients with NS and minimal glomerular changes appear to respond to steroids. For
nephrotic patients with more severe histologic changes, a combination of steroids with
immunosuppressive drugs is indicated, as they appear to respond less favorably to
steroids alone. Fish oil also might be effective in some of these patients.

Patients with rapidly progressive crescentic glomerulonephritis can benefit from steroids,
either pulse therapy or oral prednisolone in combination with cyclophosphamide, and
sometimes supplemented by plasma exchange. High-dose intravenous immunoglobulin
therapy also might be of benefit in this group. Patients with acute renal failure after a
bout of macrohematuria demonstrating a paucity of crescents (<30% segmental crescents)
on renal biopsy but predominantly tubulointerstitial changes seem to spontaneously heal
and recover even if dialysis is required. Patients with chronic renal failure (serum
creatinine > 3 mg/dL) should be treated symptomatically. Fish oil combined with an ACE
inhibitor or an ARB might stabilize progression in some of these patients. For the
moment, there is no specific therapy for recurrent IgAN in renal allografts. The use of
ACE inhibitors might be beneficial and MMF might prevent recurrent disease.

Reference: [11], [12]

48
Acute kidney injury due to insect bite: case report

Back ground:
Insect stings and bites are known to cause a variety of allergic reactions and direct toxic
effects. Stinging insects are classified as hymenoptera which includes apids (honey bees,
Africanized bees) and vespids (wasps, yellow jackets & hornets). Hornet stings are
generally followed by minor allergic reactions and rarely anaphylaxis.
However multiple stings can sometimes lead to angioedema, vasculitis, encephalitis and
acute renal failure. Usually acute renal failure is due to acute tubular necrosis secondary
to intravascular hemolysis, rhabdomyolysis or shock .Rarely it can be due to the
development of tubulo-interstitial nephritis . In this report we describe an aged male who
had insectt stings and developed acute renal failure as a result of tubulo-interstitial
nephritis.

Case summary:
A 60-year-old British man had a history of a insect bite on the anterior aspect of his left
leg resulting in cellulitis. Several days later, the patient presented to the emergency room
complaining of fevers, severe itching, swelling, and blistering of the left leg. The past
history was unremarkable. There was no history of asthma or use of medications.
Physical examination at that time was consistent with a bullous cellulitis of the left leg.
Laboratory investigations revealed: white blood cell count (WBC), 10.3 differential: 54
neutrophils, 15 lymphocytes, and 31 eosinophils. The platelet count was 225,000/mm3. A
blood chemistry profile was within normal limits. Blood cultures and stool examination
for ova and parasites were negative.
Leg X-ray: no boney abnormality Chest X-ray- clear
C/S: green sputum,USS of left leg: no evidence of DVT (Distal calf vessels not arrested)
According to the patient statement he had leg erythema with swelling for the last 2
months which was increased overtime. He reported first leg swelling and redness
appeared 29/6/07 then it turned to dark color with swollen persist. He also added some
blister lifting off from the infected area. But patient clinically looked well.

49
Patient also has history of insect bite on ankle and that time he was treated with anti
histamine. Then he developed increase blood pressure for few years and take atenolol.
Patient mentioned that he has had chronic right ankle pain, hip and shoulder pain with
arthritis.

Case report:

Name: R D S
Age 60

Presenting complains:
Pain in the let lower leg
Swelling of lower left leg
Redness with some blister is lifting off from affected leg

HPI:
According to patient statement he was leg redness for 2 months swelling increased as day
passes. He is reported first leg swelling and redness appeared 29/6.07 then it become dark
swollen. He also added some blister lifting off from the infected area. But patient
clinically well look
Patient also has history of insect bite on ankle and that time he was treated with anti
histamine. Then he developed increase blood pressure for few years and take atenolol.
Patient tells me he has had chronic right ankle pain, hip and shoulder pain with arthritis

PMH:
Renal failure, insect bite, HTN, Arthritis

Personal history: Ex smoker,

Medication:
Metaclopramide 5mg tds
Salbutamol 5mg od
Nefoman 30mg od

50
Quinine sulphate 300mg od
Fluoxetine20mg od
Sodium bicarbonate 50mg

O/E:
Leg erythoma extending to just below knee
Mild wheeze
Good foot pulse
Leg look like cellulitis
Splinter haemorrage on hand nail
P/A:
Soft non tender epigastrium
Vascular bruit
CVS:
Heart sound normal, JVP (-)
Right ankle odema
RS
Very few basal crepitation

Investigation: 06/07/07

HB 11.6
WCC 19
CRP 370
NA 139
K 4.5
UREA 28.7
CR 701
HCO3 28
CL 105

Leg X-ray: no boney abnormality

Chest X-ray- clear
C/S: green sputum
USS of left leg: no evidence of DVT (Distal calf vessels not arrested)

51
Discussion:

This case demonstrates that multiple bee stings may cause rhabdomyolysis and hemolysis
with consequent ATN. Components of venom responsible include toxic surface-active
polypeptides (mellitin and apamin), enzymes (phospholipase A 2 and hyaluronidase) and
low molecular weight agents (histamine and aminoacids). Mellitin and phospholipase are
important components causing rhabdomyolysis following a toxic action on striated
muscles and also act on red cell membrane and provoke hemolysis. The elevated levels of
enzymes CPK and aspartate-aminotransferase suggest the existence of rhabdomyolysis
and hemolysis is suggested by anemia, unconjugated hyperbilirubinemia, reticulocytosis,
increased serum LDH and hemoglobinuria.

Rhabdomyolysis and hemolysis can induce ARF, particularly in hypovolemic or acidotic

individuals. It has been postulated that myoglobin and hemoglobin released from muscle
or red blood cells cause ARF by toxic effects on tubule epithelial cells or by inducing
intratubular cast formation. Hypovolemia or acidosis may contribute to pathogenesis of
ARF in this setting by promoting intratubular cast formation. In addition, both
hemoglobin and myoglobin are potent inhibitors of nitric oxide bioactivity and may
trigger intrarenal vasoconstriction and ischemia in-patient with borderline renal
hypoperfusion.

The primary therapeutic goal is to prevent the factors that cause ARF, i.e. volume
depletion, tubular obstruction, aciduria and free radical release. Patients are administered
saline for intravascular volume expansion and sodium bicarbonate for urine alkalization
(to urine pH level above 7). The ideal fluid regimen for patients with rhabdomyolysis
consists of half isotonic saline (0.45%, or 77 mmol/L sodium), to which 75 mmol/L of
sodium bicarbonate is added. Once overt renal failure has developed, the only reliable
therapeutic modality is extracorporeal blood purification. The treatment of severe ARF
following Africanized bee stings with repeated hemodialysis, hemofiltration, or
peritoneal dialysis has been described. Exchange transfusion or plasmaphresis has been
found useful because it acts through a direct effect of reduction of the massive circulating

52
venom or removal of the circulating mediators of inflammation caused by the venom
itself. Taking into account the potentially lethal risks of plasmapheresis, this should be
reserved for the treatment of life-threatening multisystem organ failure due to stings of
members of the order Hymenoptera (honeybee, bumblebee, wasp, hornet, yellow jacket).

In conclusion, acute renal failure after bee stings is probably due to pigment nephropathy
associated with hypovolemia. Early recognition of this syndrome is crucial to the
successful management of these patients.

Reference: [13]

53
Diabetic nephropathy and hypertension: case report

Back ground:
Hypertension and diabetes mellitus are interrelated diseases, which, if untreated, strongly
predispose to atherosclerotic cardiovascular disease. Lifestyle and genetic factors are
important in the genesis of both conditions The prevalence of hypertension and type II
diabetes, or non-insulin-dependent diabetes mellitus (NIDDM), increases with age.
Hypertension occurs more frequently in persons with type I diabetes, or insulin-
dependent diabetes mellitus (IDDM), than in those with type II diabetes after adjustment
for age.

Essential hypertension accounts for the majority of hypertension in persons with diabetes,
Particularly in those with type II diabetes, who constitute more than 90 percent of those
with a dual diagnosis of diabetes and hypertension. Diabetic nephropathy, which
occurs after 15 years of diabetes in one of three persons with type I diabetes and one of
five persons with type II diabetes, appears to be an important cause of hypertension.

Hypertension can exhibit several kinds of pathophysiology in patients with diabetes.

Hypertension associated with diabetic nephropathy is a form of renal hypertension with
sodium and fluid retention, increased peripheral vascular resistance, and increased
cardiac output, especially if anemia is present. Isolated systolic hypertension can occur at
any age and is considerably more common in persons with diabetes than in those without
diabetes.Hypertension contributes to the leading causes of morbidity and mortality in
persons with diabetes, including coronary heart disease, stroke, peripheral vascular
disease, lower extremity amputations, and end-stage renal disease. Hypertension also
contributes to diabetic retinopathy

case summary:
71 years, british man admitted in Northern General Hospital with complain of difficult in
micturation, Cough with sputum for 6 days,

54
SOB for 2 days, Chest pain 2 or 3 days patient admitted for renal biopsy and waiting for
biopsy report. According to the pt he was alright then after 4 days he devolved shortness
of breath which was associated with chest pain and followed by cough with sputum. Also
he is complaing of nausea and vomiting and anorexia for last 7 or 8 days.
Now patient has had catheterization in situ for 2 days as he suffering from oliguria.
Patient also had past history of MI, HTN, Asthma, Pleural effusion, DM, Epilepsy

Name: B B
Age 71

Presenting complains:
Currently feeling well, difficult in micturation,
Cough with sputum for 6 days,
SOB for 2 days,
Chest pain 2 or 3 days
Patient has had catheterization in situ.

HPI: patient admitted for renal biopsy and waiting for biopsy report.
According to the pt he was alright then after 4 days he devolved shortness of breath
which was associated with chest pain and followed by cough with sputum. Also he is
complaing of nausea and vomiting and anorexia for last 7 or 8 days.
Now patient has had catheterization in situ for 2 days as he suffering from oliguria.

PMH:
MI, HTN, Asthma, Pleural effusion, DM, Epilepsy

Personal history: live with wife, ex smoker.

Drug history:
RENAGEL 800mg bd
Alfacalcidol 0.25mcg od
Mixtard 30 u (m) 45u (e)

55
Ciprofloxacin 250mg bd for 7 days
Frusemide 160mg bd
Metalozone 5mg bd
Lopramide 2mg od
Paracetamol 1gm sos
NSAID, Beclomethasone BD

O/E:
Leg oedema and sacral oedema present
JVP is raised.

RS:
Chest clear
CVS:
Heart sound is normal
P/A:
suprapubic tender, soft and non tender abdomen.

Investigation: 20/07/07
HB 11.6
WCC 8.6
PLTS 387000
NA 132
K 4.3
HCO3 23
UREA 24.2
CR 434
CA 2.28
POA 1.89
TOTAL PROTEIN 77
ALBUMIN 31
AST 19
BILIRUBIN 10

US: 5/7/7- No hydronephrosis

56
Discussion:
A medical history should include family history of hypertension, diabetes, renal disease
and CVD; patient history of CVD, cerebrovascular disease, renal disease, and
retinopathy; known duration and levels of elevated blood pressure and blood glucose;
results and side effects of previous antihypertensive and hypoglycemic therapy; use of
drugs that may influence blood pressure or diabetes; history of weight gain or loss,
proteinuria, sodium intake, other dietary factors, exercise habits, and alcohol use;
symptoms suggesting secondary hypertension; psychosocial and environmental factors
(e.g., emotional stress, cultural food practices, economic status) that may influence blood
pressure or blood glucose control; other cardiovascular
risk factors including obesity, smoking, and hyperlipidemia; and date of last eye
examination. With regard to diabetes, information should be sought about
the history of polyuria, polydipsia, polyphagia, fatigue, blurred vision, hypoglycemic
reactions, sexual dysfunction, paresthesia or other signs of peripheral neuropathy in the
extremities, and leg and foot ulcers.Diabetes With Renal (Parenchymal) Hypertension

A persistent increase in albumin excretion rates on at least three occasions and/or a

progressive decline in renal function suggest a diagnosis of renal (parenchymal) disease.
Hypertension in patients with diabetic nephropathy is manifested by sodium and water
retention (extracellular fluid volume expansion), increased cardiac output, and increased
peripheral vascular resistance. Although these mechanisms do not differ from those
usually encountered in patients with hypertension who do not have diabetes, special
consideration must be given in choosing antihypertensive agents for
patients with diabetes and renal disease.
Others have included persons with diabetes who do not have hypertension and have used
microalbuminuria as a surrogate for alterations in renal function. Some, but not all,
studies with calcium antagonists have suggested a reduction in albumin excretion, and at
least one study has suggested an additive benefit when an ACE inhibitor and a calcium
antagonist are used together.

Reference: [14]

57
P-ANCA positive vasculitis: case report

Background:
The perinuclear antineutrophilic cytoplasmic antibody (p-ANCA) is closely associated
with rapidly progressing glomerulonephritis, microscopic polyangiitis, and allergic
granulomatous angiitis. While mononeuropathy due to vasculitis is a well- known
neurological manifestation of these conditions, manifestations involving the central
nervous system (CNS) have rarely been reported.

Case summary:
A 78 year old man admitted in northern general hospital to make AVF for dialysis
purpose but unfortunately failure of left brachiochephalic AVF happened.
The patient of Pakistani origin that has been refers to the clinic for abnormal renal
function. He was recently admitted for episode of angina, P-ANCA positive, 24 hrs urine
excretion 1.3 gm, Creatinine Clearence 30 l/min, suggesting renal failure. Complement
level is normal.
He had a right eye cataract removal. He was well himself and fairly asymptomatic. He
occasionally complains of angina on exertion. His blood pressure was well with in
normal range. Investigation so far showed a significantly impair renal function with
serum creatinine show below and a GFR of around 20ml/in. this is most likely due to
long standing HTN, Ischemic nephropathy. There is no haematuria to suggest a
glomerular nephritis. However as mention in the previous level his P-ANCA serology has
been slightly rise. We are keep an eye on his immunology, advice for 24 hrs urine
collection to estimate proteinuria as has +++ albumin in Dipstick analysis.
Over the last 2-3 is a reflection of good blood pressure control, possibly ACEi and the
fact that he is a non smoker. I have also stated him in a statin even his serum cholesterol
is with in normal range

Case report:
Name: M M
Age: 78 years

58
Present Complain:

Failure of left brachiochephalic AVF (Exploration of left radio cephalic AVS done)

HPI:
78 yrs, Pakistani origin that has been refers to our clinic for abnormal renal function. He
was recently admitted for episode of angina, P-ANCA positive, 24 hrs urine excretion 1.3
gm, Creatinine Clearance 30 l/min, suggesting renal failure. Complement level is normal.
He had a right eye cataract removal. He was well himself and fairly asymptomatic. He
occasionally complains of angina on exertion. His blood pressure was well with in
normal range. Investigation so far showed a significantly impair renal function with
serum creatinine show below and a GFR of around 20ml/in. this is most likely due to
long standing HTN, Ischemic nephropathy. There is no haematuria to suggest a
glomerular nephritis. However as mention in the previous level his P-ANCA serology has
been slightly rise. We are keep an eye on his immunology, advice for 24 hrs urine
collection to estimate proteinuria as has +++ albumin in Dipstick analysis.
Over the last 2-3 is a reflection of good blood pressure control, possibly ACEi and the
fact that he is a non smoker. I have also stated him in a statin even his serum cholesterol
is with in normal range.

PMH:
CRF, HTN, P-ANCA positive, IHD

Personal History: Ex smoker

Drugs history:
Currentl he is taking Na Bicarb Norton – 500mg cap
Glyceryl trinitrate 400 micrograms
Quinine Sulfate 300 mg
Furosemide 40mg

59
Isosorbide mononitrate 60mg
Simvastatin 20mg
Ranitidine 150 mg
Amlodipine 5 mg
Aspirin 75 mg

O/E:

Failure AVF left hand

P/A:

Soft non tender abdomen

CVS:

Heart sound normal, JVP (-)

RS:

Clear chest wall

Investigation: 08/08/07
HB 11.3
HCT 0.35
WCC 5.3
PLTS 168000
NA 139
K 4.9
UREA 37.6
CR 474
HCO3 17
CA 2.21
PO4 2.17
ALK.PO4 105

60
TOTAL PROTEIN 61
ALBUMIN 33

The date of investigate is 10/07/2007

Urea-30.3
Creatinine- 506

Discussion:
The pathogenesis of ANCA-related vasculitis is very complicated, and several
mechanisms are considered to be involved together in its development. In the present
case, Damage to the endothelium may lead to an increase in vascular permeability and
extravasation which can break the blood-brain barrier and eventually result in
uncontrollable vasogenic edema. In this regard, we feel that the dilatation of intracranial
vessels seen in the present case especially that of the peripheral small arteries must be
significant.Vasospasm has often been seen in RPLS associated with hypertension, but the
MRA findings suggest vasodilatation in the present case. This disease entity represents a
relatively new concept and its pathogenesis remains to be determined, though coronary
artery spasms, myocarditis, an over-response to catecholamine and stress have been
postulated as causes. The present case suggests that it can also be associated with p-
ANCA-positive vasculitis.

The treatment of renal limited systemic vasculitis usually involves a combination of

cytotoxic drugs and steroids. As shown by randomised prospective controlled trial,
plasmapheresis may be of additional benefit for the management of patients with renal
involvement severe enough to require dialysis support. Recently, growing evidence has
suggested that autoantibodies to neutrophil cytoplasm (ANCA) may play a role in the
pathogenesis of the primary vasculitides by promoting neutrophil mediated endothelial
cell cytotoxicity. This has led to new strategies for treatment based on firstly, the use of
semi-specific immunoabsorption (IA) devices to remove circulating autoantibodies, and
secondly, the use of 'Humanised' monoclonal antibodies (MAbs) with specificity for
lymphocytes, particularly T lymphocytes. We have treated four patients, two with ANCA
specificity for proteinase 3 (PR3), and two with specificity for myeloperoxidase (MPO).

61
Semi-specific IA was carried out by plasmapheresis through extracorporeal online
devices, using L tryptophan as the immobilised immunoabsorbant. Of the four patients
who received IA, three showed substantial depletion in ANCA titres and resolution of
clinical symptoms. The MAbs were subsequently used to attempt to obtain long-term
control of ANCA synthesis. These results suggest that an optimal strategy for treatment
of systemic vasculitis might consist of specific IA, using immobilised ANCA antigens to
deplete circulating vasculotoxic antibodies, combined with MAb therapy to restore
immune homeostasis.

Reference: [15], [16]

62
Assessment and management of comorbid diseases in CKD: case report

Background
Chronic kidney disease (CKD) is common and can be found in up to 23% of patients with
diabetes. The recommended hemoglobin A1c goal for these patients is also < 7.0%.
Medication therapy for diabetes may require dose adjustments or may be contraindicated
in patients with CKD. Assessment and management of comorbid diseases, including
hypertension, hyperlipidemia, anemia, hyperphosphatemia, and hyperparathyroidism, is
important in the care of patients with diabetes and CKD. Multidisciplinary care may
provide the optimal system for maximizing care of these complex patients.

Case summary:
A 84 years old British man get admission in Northern General Hospital with complain of
pain on upper abdomen for 4/5 days, loss of appetite, nausea, vomiting for 4-5 days.
Patient was seen 1 week back in gastric clinic for investigation of his microcytic anemia.
He slept well overnight but his morning he has vomited for 5 times and had an episode of
diarrhea as well.
He has epigastric pain which was mild to moderate in intensity. Blood test in the OPD
showed K increased 6.4 mmol/l
Patient denies any chest pain on his discomfort or shortness of breath. No haemoptysis,
malena, bleeding PR noticed. He also denies any urinary symptoms what so ever. Also he
had past history of MI-.1992
Angina for more than 15 yrs ,CKD stage Diabetes for 20 years

Case report:
Patient name: S G
Age: 84 yrs
Sex: male

63
Present complain:
Pain on upper abdomen for 4/5 days
Loss of appetite, nausea and vomiting for 4-5 days
Bodyache for 1 week
Also informs me increased potassium level.

HOPI:
Patient was seen 1 week back in gastric clinic for investigation of his microcytic anaemia.
He slept well overnight but his morning he has vomited for 5 times and had an episode of
diarrhea as well.
He has epigastric pain which was mild to moderate in intensity. Blood test in the OPD
showed K increased 6.4 mmol/l
Patient denies any chest pain on his discomfort or shortness of breath. No haemoptysis,
malena, bleeding PR noticed. He also denies any urinary symptoms what so ever.

PMH:
MI-.1992
Angina for more than 15 yrs
CKD stage 3
Diabeties for 20 yrs

Social history:
Non smoker
Non alcoholic

Drug history
Omeprazole 10mg
Aspirin 150 mg
Gliclazide 160 mg
GTN

64
Lisinopril 2.5 mg
Metformin 1 gm

On examination
Patient is well co-operative oriented with time, place and person

CVS:
BP- 150/80
Pulse 96 b/min
JVP- not raised
HS: normal
No pedal odema

RS:

Decreased air entry in both lungs

No cough sputum, wheeze, Crepitation,
O2 saturation 94% on air

GIT:
Soft non tender
No sign of viseromegaly or peritonitis.
Bowel sound is audible

CNS
GCS 15
Cranial nerve intact

Investigation
Hb 9.7

65
Na 138
K 6.4
Ca 2.44
PO4 –1.01
TSH- 1.14
B12- 377
Ferritin-32.0
HbAIC- 6.7%
HCO3- 18

Diagnosis:
Normocytic anemia
MI
Type 2 DM

Impression
Sepsis

Discussion:
Management of cardiovascular comorbid Disease

Hypertension:
Hypertension is commonly found in patients with DKD and is diagnosed by a blood
pressure measurement > 130/80 mmHg, as defined by the Seventh Report of the Joint
National Committee on the Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure. Prevalence of hypertension is estimated to range from 30 to 96%, with
higher prevalence found to be associated with greater levels of proteinuria Hypertension
that is not controlled leads to a higher risk of cardiovascular events including death,
increasing proteinuria, and progression of kidney disease. The cornerstone of medical
therapy for hypertension, especially in patients with CKD, is treatment with angiotensin-

66
converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). ACE
inhibitor or ARB therapy has been demonstrated to slow the progression of proteinuria in
patients with either type 1 or type 2 diabetes and microalbuminuria; however, no
randomized clinical trials have shown impact on development of more advanced CKD or
mortality in this population.

Hyperlipidemia
Cardiovascular disease is common in patients with both diabetes and kidney disease. Risk
factor modification, including management of dyslipidemia, is a key component of care
for this patient population. Lipid levels should be measured annually, with a target LDL
cholesterol level < 100 mg/dl for patients with CKD stages 1-4. In a study of nearly
20,000 patients, those with diabetes and CKD who received pravastatin compared to
placebo were found to have a 25% relative risk reduction of cardiovascular disease
events. Consideration of dosing of drugs for dyslipidemia therapy must also take into
account severity of kidney disease. No dosage adjustments are required for bile acid
sequestrants, niacin, ezetimibe, atorvastatin, or pravastatin. Reduced dosing of fibric acid
derivatives, fluvastatin, lovastatin, rosuvastatin, and simvastatin should be considered in
patients with Stage 4 or 5 CKD

Complication:

Anemia in CKD is defined as a hemoglobin value < 13 g/dl for males and < 12 g/dl for
females, and annual evaluation is recommended. Correction of anemia to levels of 11-12
g/dl in dialysis patients has been associated with improved quality of life, fewer
hospitalizations, and a lower risk of mortality; however, studies in patients with CKD
(pre-dialysis) are lacking. Two recent clinical trials, the Cardiovascular Risk Reduction in
Early Anemia Treatment With Epoetin Beta study and the Correction of Hemoglobin and
Outcomes in Renal Insufficiency study, suggested that hemoglobin levels > 12 g/dl did
not improve measures of quality of life and may increase the risk of cardiovascular
events. Additional clinical studies are ongoing to try to provide guidance in this complex
area.Abnormal calcium and phosphorus metabolism may also be present in patients with
CKD. These measures, along with measurement of intact-parathyroid hormone (i-PTH),

67
may identify bone disease related to CKD. Bone disease may lead to poor bone structure
resulting from high or low turnover, and this may result in a higher risk of fracture.
Frequency of measurement of calcium, phosphorus, and i-PTH is described in The target
serum phosphorus goal is < 5.5 mg/dl in patients with Stage 5 CKD and < 4.6 mg/dl in
Stage 3-4 CKD. In

Conclusion:

CKD and diabetes are common diseases that affect a large proportion of the population.
Depending on the severity of the CKD, drug regimens, including those for glycemic
control, and dietary intake may require adjustments . Aggressive identification and
treatment of risk factors for cardiovascular disease as well as complications of CKD are
recommended given the very high risk of adverse cardiovascular events in patients with
both diabetes and CKD..

Comments:

Chronic kidney disease (CKD) is common and can be found in up to 23% of patients with
diabetes.The recommended hemoglobin A1c goal for these patients is also <7.0%.
Medication therapy for diabetes may require dose adjustments or may be contraindicated
in patients with CKD. Assessment and management of comorbid diseases, including
hypertension, hyperlipidemia, anemia, hyperphosphatemia, and hyperparathyroidism, is
important in the care of patients with diabetes and CKD..

Reference: [17], [18], [19]

68
Wegener’s granulomatosis: case report

Background
Wegener's granulomatosis is one of the pauci-immune small vessel vasculitides. It
classically presents with the triad of upper and lower respiratory tract granulomas and
necrotising focal segmental glomerulonephritis. It is associated with the presence in the
serum of autoantibodies against components of neutrophil cytoplasm–antineutrophil
cytoplasmic autoantibodies (ANCA). The illness can develop at any age but is more
common in patients in their 50s and 60s and in men. The incidence of vasculitis is
increasing, with about 10-20 people per million affected. We present a case that in
retrospect had many clues at the initial time of admission, but it took five months and six
different hospital teams to make the diagnosis.

Case Summary
A 71 year old woman, admitted to Northern General hospital at Vickers 2 with a
complain of shortness of breath. According to the patient she was alright 5 yrs back then
she was diagnosed as a case of Wegners Granulomatosis. WG has been well controlled
and relatively symptom free but over last 6-8 months she has been getting sinus
symptoms and hearing loss. But now for last 2-3 days the symptoms are very much
problematic. As she told me that she cant walk too long as she developed shortness of
breath and tiredness. As by saying that yesterday evening she was unbable to go up stair
one at a time, she took about an hour to do so and needs her husband assistance to get up
and dressed this morning, feeling so lethargic and weak.
She feel hot and sweaty does not feel unduly well in herself if breathing was better.
She also says that she has mild pain at the right breast for 3 weeks or so but was relieved
by sitting forward. She have not take any analgesic for that. She does not give me any
history of urinary abnormality like haematuria and increased urinary frequency, nausea,
vomiting, abdominal pain or indigestion

69
Case Report
Name: E C
Age: 71 yrs

Presenting complain:
Shortness of breath for 4 days

HOPI:
According to the patient she was alright 5 yrs back then she was diagnosed as a case of
Wegners Granulomatosis. WG has been well controlled and relatively symptom free but
over last 6-8 months she has been getting sinus symptoms and hearing loss. But now for
last 2-3 days the symptoms are very much problematic. As she told me that she cant walk
too long as she developed shortness of breath and tiredness. As by saying that yesterday
evening she was unbable to go up stair one at a time, she took about an hour to do so and
needs her husband assistance to get up and dressed this morning, feeling so lethargic and
weak.
She also noticed blood in spit she think that blood causes from post nasal site. She feel
hot and sweaty does not feel unduly well in herself if breathing was better.
She also says that she has mild pain at the right breast for 3 weeks or so but was relieved
by sitting forward. She have not take any analgesic for that. She does not give me any
history of urinary abnormality like haematuria and increased urinary frequency, nausea,
vomiting, abdominal pain or indigestion

PMH:
WG
PD in past but stopped because renal function improved.
Hypothyroidism after partial thyroidectomy

Drug history:
Prednisolone 15mg
Azathioprime 150mg

70
Septrin 480mg
Pravastatin 20mg
One alpha 250mg
Levothyroxine 75mg

Allegies history:
NAD

Social history:
Retired
Never smoked
No alcoholic
Live with husband and sons

On examination
Co operatiove well oriented comfortable looking

CVS
JVP- not raised
BP-130/90
Pulse 86 b/min
Warm peripheries
Slightly pitting oedema left foot

Respiratory system:
Bilateral crepts R>L
Bronchial breathing
Wheeze
Decreased air entry on right mild zone
R/R- 20 br/min
Sat 100% on 40 O2 (92% on air)

71
GIT:
Soft no tender
Bowel sound audible

Eyes
Swollen eyelids
Left eye may be conjunctivitis
Eye movement normal
According to her vision is normal

Investigation

Urine dipstick: Gl- negative, Ketones-negative, Blood ++ ve, Protien: +++ ve

Leucocyte trace, nitrate- negative

Hb- 9.3, WCC-13.1, MCV-96.3, N-12.3 increased, L-0.4 decreased, ESR- 108
PT- 16, APTT- 40.2, PTH-123
Cr- 209
Urea 20.3
Alb- 25
AST-27
Ca- 2.71

Chest X-ray:
Dense opaciy right mild zone
Well defined opacity left mild zone
Right hemidiaphragm elevated

Impression
Right middle lobe pneumonia

72
Hypercalcemia
Renal impairement
Progression of WG

Discussion
Vasculitis can be categorised by the size of vessel affected (small, medium, or large).
Wegener's granulomatosis is a small vessel vasculitis classically involving the upper and
lower respiratory tracts and kidneys. A limited form involving the upper respiratory tract
has been described in a quarter of cases. The most common presenting symptoms include
most upper airway respiratory symptoms, but particularly rhinorrhoea, oral ulcers, nasal
discharge, polyarthralgias, myalgias, and sinus pain. Lower airway complaints such as
cough, dyspnoea, haemoptysis, and pleuritic pain are also early features. More rarely,
Wegener's granulomatosis can present with tumour-like masses distant from the lung.
The renal disease often presents with haematuria, red cell casts, proteinuria, and renal
failure. Other systems that may be involved include joints, eyes, skin, nervous system,
heart, and gastrointestinal tract. Serological testing for ANCA is a useful diagnostic aid
for small vessel vasculitis,2 although caution is needed as the sensitivity may be as low as
66% when the disease is not severe.3 The diagnosis should be suggested from clinical as
well as laboratory findings and where possible confirmed with a tissue biopsy. Treatment
in Wegener's granulomatosis can be life saving. It is usual to obtain a tissue diagnosis
before starting treatment, but if the patient is too unwell, as in this case, treatment should
not be delayed. Untreated Wegener's granulomatosis has a poor prognosis, with most
patients dying within two years.1 With cytotoxic treatment, this has improved, and the
eight year survival is about 80%.1 Up to 90% of patients respond to cyclophosphamide,
and three quarters have a complete remission,4 but pulmonary haemorrhage remains a
potentially life threatening complication. Induction treatment is usually given as
combined treatment with cyclophosphamide and corticosteroids. Use of corticosteroids
alone is associated with a higher relapse rate.5 The specifics of induction regimens vary
with the drugs used, doses, routes of administration, and duration. Patients with severe
disease are treated with either plasma exchange or pulsed intravenous

73
methylprednisolone. The results of a randomised study comparing these two treatments
when used as an additional early treatment in patients with severe kidney damage are
awaited (MEPEX trial, European Vasculitis Study Group). Recovery from dialysis
dependence is common; 55% to 90% of patients recover their renal function, and 40% to
70% manage without dialysis for three years or more.

This case illustrates the importance of considering vasculitis in differential diagnosis of

patients with multi-system disease. The clinical manifestations of small vessel vasculitis
can be very varied because they are influenced by the sites of involvement and disease
activity. ANCA testing is highly sensitive for detecting pauci-immune small vessel
vasculitis, although its specificity depends on the patient population tested. Early
diagnosis allows appropriate treatment to be started before serious and potentially life
threatening complications have developed.

Reference: [20]

74
Pulmonary hypertension in patients with ESRD on HD: case report

Background
Kidney transplantation is now recognized as the treatment of choice for patients with
chronic renal failure. Despite the extension of indications to patients suffering severe
hypertension, ischemic heart disease, and chronic heart failure, the worldwide results are
superb. However, perioperative cardiac complications occur in 6% to 10% of
transplanted patients. Aggressive intraoperative volume expansion is still recommended
to maximize graft functional recovery (up to 30 mL/kg/h, central venous pressure [CVP]
> 15 mm Hg), but patients with preexistent cardiac disease or poor myocardial function
are exposed to the risk of fluid overload, acute respiratory failure, and prolonged
ventilationAge above 50 years was the only significant risk factor. Supranormal volume
loading is probably not always warranted in kidney transplantation.

Case summary:
A 51 years old woman, came in Northern General Hospital with complain of shortness of
breath for 3 weeks strangery for 1 week. Patient came through sorby room 1 with
complaint of dyspnea or shortness of breath for 2 weeks while doing some work. She also
has got muscle tenderness which gradually increased intensity by walking but got
relieved by taking rest.
Urine output was reduced for last 10days and also has strangury but no haematuria. She
also noticed increased leg swelling. Lower abdominal wall edema also complaint of pain
at biopsy performed. He had past history of NIDDM for 12 yrs
MCD for since 1987, Cadaveric renal transplant on 1993, Renal biopsy on 1999
Asthma and HTN for 10 yrs, He also history of sleep apnoea

Case Report
Name: R J K
Age: 51 yrs

75
Presenting complain:
Shortness of breath for 3 weeks
Bodyache for 1 week
Strangery for 1 week

HOPC:
Patient came through sorby room 1 with complaint of dyspnea or shortness of breath for
2 weeks while doing some work. She also has got muscle tenderness which gradually
increased intensity by walking but got relieved by taking rest.
Urine output was reduced for last 10days and also has strangury but no haematuria. She
also noticed increased leg swelling. Lower abdominal wall edema also complaint of pain
at biopsy performed.

PMH:
NIDDM for 12 yrs
MCD for since 1987
Increased BMI
Cadaveric renal transplant on 1993
Renal biopsy on 1999
Asthma and HTN for 10 yrs
He also history of sleep apnoea

On examination
Patient is well oriented and co-operative
BP-163/90 mm of Hg
HR-96 b/min
R/R- 18 br/min
SpO2- 88% on air
94% with 2 liters O2

76
CVS
JVP increased
Sacral edema positive

Respiratory system
Few crackles on right side to mid zone
No wheeze
Good air entry to bases

Abdomen
Soft and non tender
No redness around groin

Right leg biopsy site 1.5 cm densely non healing size necrotic pussy discharge

Investigation
Hb- 8.4
WCC- 9.2
Platelets- 348
Ca- 0.98
Cl- 95
ECG- normal

Chest X-ray
Huge cardiomegaly with biventricular enlargement. Interstitial edema with edema with
evidence of upward diversion of pulmonary vessels

Impression
Fluid overload failing renal transplant
No healing influenced biopsy site

77
DISCUSSIONS:

Various contributing factors are involved in the pathogenesis of pulmonary hypertension

in patients with ESRD on HD. Volume status, diastolic dysfunction, pulmonary vascular
disease, and high cardiac output from a left-to-right shunt across the arteriovenous fistula,
can all contribute to pulmonary hypertension either singly or in combination. Delineating
these 4 etiologies can be difficult without invasive hemodynamics. Our patient had
evidence of diastolic dysfunction and fluid overload at initial catheterization as suggested
by the elevated wedge pressure. However, the fall in pulmonary vascular resistance by
64% with marked improvment in cardiac index is strongly suggestive of pulmonary
vascular disease as the primary underlying etiology for her pulmonary hypertension.

CONCLUSION:

The reversal of pulmonary hypertension with dual endothelin-receptor antagonist in our

patient supports the hypothesis that in patients with ESRD on HD, there is an alteration in
endothelium-mediated vasodilators causing vasoconstriction and pulmonary
hypertension. The pharmacokinetics and safety of bosentan in ESRD has already been
demonstrated. This is the first reported case of improvement of pulmonary hypertension
associated with ESRD on bosentan therapy.

Reference: [21]

78
Risk of mortality for ESRD patients on dialysis: case report

Background
Patient survival after renal transplantation (RT) is markedly better than that seen with
either haemodialysis (HD) or peritoneal dialysis. Transplantation is also associated with a
better quality of life and a higher degree of rehabilitation .Some of the benefits associated
with transplantation are related to patient selection, since dialysis patients with the most
serious co-morbid conditions are not accepted for the transplant waiting list and hence
remain in the dialysis group. Some previous comparative studies of dialysis vs renal
transplant survival have considered that the transplant group is favoured by inclusion of
these high-risk patients in the dialysis group.

The present study uses the Cox proportional hazard regression model to compare the
relative risk of mortality for ESRD patients on dialysis vs after transplantation. Analysis
was adjusted for the variables that were significantly and independently related with
mortality

Case summary:
A 39 years old man get admission in northern general hospital with complain of shortness
of breath and weekness. According to patient he was alright 1 week back then he
develops dyspnea which was associated with generalized weakness and bodyache also
followed by nausea, vomiting and anorexia for 3-4 days. Patient is diagnosed as ESRF on
hemodialysis since 2003
He had past history of ESRF on HD since 2003, Pauci immune necrotizing GN feb 2003,
HTN, Obese BMI 38, Previous left DVT, Type 2 DM, Left AVF made on 9/5/03,
Cadaveric renal transplant, H/O fracture collar bone and finger

Case report:
Name: S M E
Sex: male
DOB: 5/11/68

79
Present complain
Shortness of breath for 1 week
Generalized weakness for 4 days
Nausea vomiting for 3-4 days

HOPI:
According to patient he was alright 1 week back then he develops dyspnea which was
associated with generalized weakness and bodyache also followed by nausea, vomiting
and anorexia for 3-4 days. Patient is diagnosed as ESRF on hemodialysis since 2003

PMH:
ESRF on HD since 2003
Pauci immune necrotizing GN feb 2003
HTN
Obese BMI 38
Previous left DVT
Type 2 DM
Left AVF made on 9/5/03
Cadaveric renal transplant
H/O fracture collar bone and finger
Active bleeding piles 8/10/03

Social history:
Lives with parent
Unmarried
Ex manager in computer firm
Never smoked
Take alcohol in moderation

Drug history:

80
Venofer 100mg
Alfacalcidol 1 mcg
Gliclazide 40 mg
Neorecormon 4000 i.u
Clonazepam 500mg
Aforvastatin 40 mg
Lactulose + senna
Clopidrogel 75 mg
Basiliximab 20 mg
MMF from 500mg-750 mg

On examination
Patient is well oriented with time place and person and is co-operative

BP: 160/90 mm of Hg
Pulses: 86 b/min
R/R: 20 br/min

CVS:
Heart sound normal
JVP not raised

Respiratory:
Decreased air entry right lung and left lung
Mild crepitation on right middle lobe
Also crepitation on left side as well
Abdominal
Soft and non tender
Bowel sound audible

81
Investigation
Hb: 10.5
WCC:12.1
Platelates: 189
MCV: 87.3
Urea: 10.2
Cr- 186
PO4- 1.3
Chest X-ray
Shows cardiomegaly
Small left plural effusion

Discussion

Several studies have examined survival rates for ESRD patients and compared results of
patients treated by dialysis vs patients treated by transplantation. However, many of these
studies did not consider patient selection bias or time-to-treatment bias . The dialysis
treatment before transplantation of most of the transplant patients was carried out in other
dialysis centres. On the other hand, most of the patients who lost their transplants
restarted dialysis in other dialysis centres. The importance of the co-morbidity added
during dialysis treatment in RTR survival has been evaluated by the relationship between
RTR survival and the length of time on dialysis before transplantation. It has been
reported that increased time on dialysis prior to renal transplantation is associated with
decreased survival of RTR .. The knowledge of the different outcomes in haemodialysis
and after transplantation between diabetic and non-diabetic patients may be useful to
health-care professionals when advising patients that they would be acceptable as
transplant candidates. Diabetic ESRD patients would have a high long-term benefit when
they receive a successful transplant, after a period of higher risk. The benefits for non-
diabetic patients are less evident: transplantation would offer little additional survival
benefit on average. Moreover, the relative scarcity of cadaveric organs for the high

82
demand and the increasing frequency of diabetes in the new ESRD patients must be
considered. Diabetes is now the most common cause of new patients requiring renal
replacement therapy, accounting for as many as 37% of the cases in the United States and
about 15 or 20% in Europe, Latin America and Japan . These findings about survival need
to be put into perspective, with the consideration of a better quality of life observed in
transplant recipients compared with dialysis patients , although the quality-of-life results
should also be adjusted to the significant risk factors for a better comparison

Reference: [9]

83
ADPKD: case report

Background
Shortage of cadaver kidney donors has prompted occasional use of abnormal kidneys
such as those affected by autosomal dominant polycystic kidney disease (ADPKD) with
preserved renal function. ADPKD is a hereditary disorder characterized by slow
progressive deterioration of renal function due to cystic changes. Upon serious
consideration of quality-of-life improvement with a functioning kidney graft, there is
justification for use of cadaveric polycystic ADPKD kidneys when the intervals between
progression to end-stage renal disease and graft survival period are compared. We report
our experience of transplantation of two ADPKD kidneys with normal graft function.

Case summary:
A 46 years old man get admitted in Nothern General Hospital with complain of Fever
with rigors for 1 week, Nausea, vomiting for 3-4 days, Anorexia for 10 days Constipation
for 2 days. According to patient he was alright 2 weeks back then he develops fever with
rigors with sweating also associated with nausea, vomiting and anorexia also has
constipation as well. He takes paracetamol for fever which works. He says that he had
mild headache and lethargic. He had no history of dyssuria, haematuria or uregency. He
had a cadaveric renal transplant in 3/1/2000 due to ADPKD with renal failure.

Case report:
Name: Rodgers David
Age :46 yrs
Sex : male
NGH no: 600820

Presenting complain
Fever with rigors for 1 week
Nausea, vomiting for 3-4 days

84
Anorexia for 10 days
Constipation for 2 days

HOPI:
According to patient he was alright 2 weeks back then he develops fever with rigors with
sweating also associated with nausea, vomiting and anorexia also has constipation as
well. He takes paracetamol for fever which works. He says that he had mild headache and
lethargic. He had no history of dyssuria, haematuria or uregency

PMH:
HTN for 1 yrs
Familial renal disease
DM
Asthma
Strokes
TB
Past surgical history:
He had a cadaveric renal transplant in 3/1/2000
Left AVF formed on 2/3/98
He received kidney from 21 yrs old male died of head injury
Cold ischaemic time 24 hrs
Arrest time 50 mins
Re-perfussion time 45 times

Drug history:
Mycophenolate mofetil 500mg BD
Neural 125mg BD
Amlodipine 5 mg

Allergy history:
No allergy history

85
Social history:
Lives with his family
Coping at home indecently
Ex smoker smoked for 4 yrs
Rarely drink alcohol

Family history:
He had a family history of CKD (mother and brother)
ADPKD

On examination
Well oriented comfortatble co-operative
JVP not raised
Temperature 38.8
BP: 130/65 mm of Hg
R/R: 16 br/min
HR: 90 b/min
Ankle edema: neck stiffness

Respiratory:
Chest clear

CVS:
Normal heart sound

Abdomen:
Soft non tender
No viseromegaly
Normal bowel sound

86
Urinary tract:
He had got repeatedly UTI for 2 occation although treated with Augmentin for 14 days

Investigation:
Urine dipstick
Protein - +
PH- 5.0
Blood- +++
Leuco-+
Sp.gravity- 1.015

Hb: 12.2
WCC: 15
Platelates- 223
MCV-86.9
Urea 9.4
Cr-148

Impression
UTI

Discussion:
ADPKD is a hereditary nephropathy characterized by multiple renal cysts, with slow
progressive deterioration of renal function. It often terminates in renal failure and
accounts for 2–9% of this population. The symptoms of ADPKD do not generally
develop until adulthood; 85% of carriers are asymptomatic until the fourth decade of life .
In Dalgard's retrospective study, the mean age for diagnosis of ADPKD was 47.2 years,
while Singh reported that the mean age at the start of ESRD treatment was 47.3±15.2
years. There is often a period of more than 10 years when patients with polycystic
kidneys develop symptoms of end-stage renal disease. Howard et al. reported that an

87
ADPKD donor kidney with cysts size up to 34 mm may take 12.5 years to develop end-
stage renal disease after transplantation. Based on the age of a 21-year-old cadaver donor
there should be at least a 10-year period of kidney function. Over the past 40 years, great
improvements have been made in graft survival with some forms of cyclosporin-based
immunosuppression. One-year and 3-year graft survivals of 85 and 75% respectively are
possible for normal kidney donations. Furthermore, previous reports showed that
polycystic kidneys with normal renal function and preserved renal cortical mass could be
used for transplantation and disappearance of the cysts may even occur, as reported by
Spees . Ettenger et al. compared mortality between renal cadaveric transplant patients and
patients on dialysis who were or were not waiting for transplantation. He found that the
mortality rate is lower in the renal transplant patients after 2 years follow-up. In
consideration of quality of life with a good functioning kidney and the shortage of donors,
a polycystic kidney with good renal function may be used as a donor kidney based on the
estimated time for the donor kidney to fail and the graft survival period on
immunosuppression.

Reference: [22]

88
Ureteric stent( advantages and disadvantages): case report

Background

Increasing attention has focused on improving the acceptability and morbidity of

antegrade renal and urologic procedures. Separately, a number of refinements of
percutaneous nephrolithotomy have addressed the issue of the tube-related morbidity
after surgery . For such surgery, a large track (30 F) is created for the percutaneous
working sheath and stone removal. After the procedure, the track is exchanged for a 24–
30-F percutaneous tube—a nephrostomy catheter—to ensure satisfactory renal drainage
and to tamponade the track. Because of the size and rigidity of the nephrostomy tube,
postoperative pain control can be a problem. Some workers have attempted to minimize
this tube-related morbidity and advocate tubeless percutaneous nephrolithotomy ; they
report that in many cases the protective nephrostomy tube is unnecessary, and the sheath
could be removed after the procedure if satisfactory ureteral drainage was assured and
bleeding was only minimal.
For antegrade ureteral stent insertion, attention has focused on shortening the duration of
the procedure. Traditionally this was a two-stage procedure. After relief of ureteral
obstruction with a nephrostomy catheter (8–10) and a few days of satisfactory external
drainage, an antegrade stent was inserted in a second procedure. Thus, an individual stent
insertion episode may last 2–5 days in total. This two-stage procedure or secondary
ureteral stent placement is being increasingly superseded by primary antegrade stent
placement. In primary antegrade stent placement, primary renal access and stent insertion
are performed as a single procedure, and this single procedure has an 80% reported
success rate . As originally described , even this procedure required a covering
nephrostomy catheter to guard against poor stent function and was removed after 12–24
hours of satisfactory ureteral drainage. From the patient’s perspective, an antegrade
ureteral stent procedure was still relatively prolonged—a stent was inserted on day 1 with
a nephrostomy tube left in situ, and the covering nephrostomy tube was removed on day
2; the patient either stayed in the hospital overnight or required two outpatient visits to the
interventional radiology department. However, if the encouraging experience of tubeless

89
percutaneous nephrolithotomy could be extended to the antegrade ureteral stent
procedure, the latter promises to be a true one-stage or tubeless stent service, and the
patient would visit the interventional suite only once. The attraction of such a one-stage
procedure is obvious, but advantages may be outweighed if they are accompanied by an
increased risk to the patient or a higher complication—in particular increased bleeding or
septicemia—rate.

The purpose of our study was to evaluate the technical success and complications of one-
stage antegrade ureteral stent placement

Case summary:
A 28 years old female student, get admitted in Northern General Hospital with complain
of UTI and for removal of ureteric stent. Live kidney related transplant recurrent
hydronephrosis of transplanted kidney which nephrotomy done
Balloon dialatation of ureter on 13/06/07 and nephrostomy taken out and ureteric stent
inserted 13/06/07

Case report:
Name: D S
DOB: 27/3/79, 28 yrs, female student

Presenting complains:
Elective admission for removal of ureteric stent

PMH:
Live kidney related transplant recurrent hydronephrosis of transplanted kidney which
nephrotomy done

Balloon dialatation of ureter on 13/06/07 and nephrostomy taken out and ureteric stent
inserted 13/06/07

90
Psychriatric problems
No cough, shortness of breath, fever, chest pain, vomiting, diarrhea,
Had history of transplant kidney for that account hydroureter with impaired kidney
function Cr 195 25/5/07

Transplant nephrostomy was performed under LA and it started to drain 5 litres and level
of creatinine down to 117
Also admitted for ballon ureteroplasty stent placement on 12/06/07

Had C/0 dysuria 21/6/07

Urine MCS 14/06/07- enterococcus
S---trimethoprine, amoxicillin, nitrofurantoin, cefuroxime
R---fefalexin, feroroxime

Urine MC+S--- mixed growth suggesting contamination

Allergy history:
NAD

Drug history:
Loratadine 10mg
Olanzapine 5 mg
Tacrolimus 1 mg
Nystatin 100,000 U/ml suspension
MMF- 250 mg
Omeprazole 20 mg
Levothyroxine sodium 50 mcg
Prednisolone 2.5 mg
Seena 7.5 mg
Atenolol 25 mg

91
Investigation:
Hb: 10.9, K- 4.1, HCO3- 21, PO4- 1.2, Alk PO4- 74, albumin- 34
WCC: 6.8
Urea-7
Cr-115
Urate: 322
On examination:
Oriented co-operative but very anxious about her disease and removal of ureteric stent.
BP- 116/73 mm of Hg
Pulse- 78 b/min
Sats- 98% on air
Afebrile

CVS:
JVP not raised
Heart sound normal

Respiratory:
Trachea centrally placed
No added sounds

GIT:
Soft non tender abdomen
Bowel sound is audible

Stent is still in
Enterococcus recently UTI

92
Discussion:

Ureteral stent placement is a routine safe procedure for the maintenance of ureteral
patency. A stent can be inserted through either the antegrade or retrograde route through a
cystoscope. Antegrade insertion is successful in 88%–96% of cases , but the two routes
have not been critically compared in an unselected randomized fashion. Although the
retrograde route is usually the preferred first option because the potentially serious
complications related to renal puncture may be prevented, the final choice often depends
on local skills and equipment. However, in some patients, antegrade stent insertion is
more likely to succeed, particularly if the ureteral orifices are poorly visualized—for
example, in patients with pelvic, bladder, or prostate malignancy. In one study, retrograde
stent insertion failed in 14% of all cases, but the failure rate was higher in those with
malignant or external obstruction than in those with benign obstruction—27% versus 6%,
respectively . In our institution, there is a policy of first attempting antegrade stent
placement in all patients with malignant obstruction, whereas patients with benign
obstruction, in particular pelviureteric junction obstruction, undergo retrograde stent
placement.

The major disadvantages of antegrade ureteral stent insertion are that it requires
percutaneous renal puncture and traditionally was a two-stage procedure. With
improvements in guide wires and stent design, stent placement in obstructed but
noninfected ureters can be performed safely as a single procedure and is becoming the
preferred option of many interventional radiologists. The clinical value of this so-called
primary antegrade ureteral stent procedure (ie, renal access and stent insertion carried out
as a single procedure) has been demonstrated in a separate group of patients , and it was
successful in 80% of selected cases with a 2.5% major complication rate. However, even
this modification required an overnight or approximately a 12-hour hospital stay, as a
drainage nephrostomy tube was left in situ, and so patients still visited the radiology
department a second time for tube removal.

Complication:

93
The major complication was septicemia, and both patients in whom this complication
occurred had received gentamicin alone intravenously as a single infusion before the
procedure. Some consider gentamicin alone to be inadequate , and we are discussing a
new policy regarding antibiotics with our hospital microbiology and infection control
department. There were further predisposing factors in both cases—the first patient had
undergone bladder surgery recently, and the second patient had undergone unsuccessful
retrograde ureteral instrumentation. An indwelling bladder catheter was in place in both
cases.

Apart from sepsis, another major risk after percutaneous renal intervention is bleeding.
No patient in the present study developed major bleeding, and we have not yet seen major
bleeding that required embolization after ureteral stent placement in our practice, although
one patient who was not part of this study required transfusion. In a standards-of-practice
document from the Society of Cardiovascular and Interventional Radiology, a serious
hemorrhage risk of 1%–4% is noted, although this risk refers to nephrostomy tube
insertion alone . Before the start of this study, bleeding was our particular concern, as a
freshly created 8–9-F renal puncture was to be left without a catheter to tamponade the
track. However, we were persuaded that tubeless percutaneous urologic procedures were
safe because of the encouraging experience after so-called tubeless percutaneous
nephrolithotomy. It has long been clear that the large nephrostomy catheter—typically 24
F—left as a drainage catheter after even uncomplicated percutaneous nephrolithotomy
results in marked minor postprocedure morbidity, which is related to discomfort and pain
caused by the tube. To improve procedural morbidity, interest has focused on elimination
of the postoperative nephrostomy tube if the procedure is uncomplicated.

Conclusion:

One-stage tubeless antegrade ureteral stent placement is feasible in carefully selected

patients and will be successful in more than 80% of all patients, including outpatients. It
is now our policy to attempt one-stage stent placement in all suitable cases. Until there is

94
further experience, this technique should be reserved for stable and otherwise fit patients
with normal results of hematologic studies. In our study, major complications were all
infections. Patients who are clinically suspected of having infection should be excluded,
as should those with a predisposition to infection (eg, history of recent retrograde ureteral
instrumentation, failed retrograde stent insertion, or genitourinary tract surgery). We
continue to be conservative in our approach to clinically unstable patients or those who
are suspected of having infected systems. In our view, these patients should still undergo
secondary antegrade stent placement after initial nephrostomy tube drainage has resolved
the pyonephrosis and the clinical status improves. In any case, careful technique is very
important, and all patients should receive preliminary antibiotic therapy. If a patient is
suspected of having any periprocedural bleeding or substantial clotting is seen in the
collecting system on a postprocedural nephrostogram, then a temporary nephrostomy
catheter should be inserted. Even if one-stage stent placement has been successful, cases
should be reviewed daily for the next few days either in the ward or by means of a
telephone interview if the person is an outpatient

Reference: [23]

95
ATN after Transplantation:report case

Background

Kidney transplantation is the best option for all patients with terminal renal failure.
Kidney transplantation is not only associated with an improved quality of life in
comparison to all other renal replacement therapies, this method also offers a
significantly extended lifespan. Therefore, the option for transplantation has to be
verified for every patient with renal failure. Graft and patient survival is best when
transplantation is carried out just before starting dialysis treatment. Realistically, only
living donor transplantation offers the option of sparing the recipient a long waiting
period on dialysis. Although transplantation from living donors is superior to cadaveric
kidney transplantation, a small risk remains for the donor. Kidney transplantation and the
immunosuppressive therapy are associated with an increased risk for certain types of
infection, an increased tumour risk and an increased risk for carciovascular
complications. To address these problems, specific recommendations for patient
surveillance have been provided by different transplantation societies.

Case summary:

A 44 years female admitted in Northern General Hospital with complain shortness of

breath, ankle swelling, cough with sputum. Patient been well recently then suddenly
developed cough with sputum and shortness of breath. She also complained ankle
swelling and chest pain some times. Recently she is anuric for 1 week she has no history
of MI or angina. Her past medical history was significant for systemic lupus
erythematosus (SLE) for 7 years when she presented with fever, rash, polyarthralgia and
anasarca and Cadaveric renal transplant had done on 2003. she started hemodialysis on
RUE 9/02/99.

96
Case report:

Name: G J
Sex: female
Age: 44 yrs
Hospital no: 604391

Present complain:
Shortness of breath
Ankle swelling
Cough with sputum

HOPI
Patient been well recently then suddenly developed cough with sputum and shortness of
breath. She also complained ankle swelling and chest pain some times
Recently she is anuric for 1 week she has no history of MI or angina

PMH
Cadaveric renal transplant 2003
SLE- for 7 yrs
HTN- 10 yrs
Deteriorating renal function for 5 yrs
Hemodialysis on RUE 9/02/99
Right elbow AVF on 2/2/99
Transplanted right kidney biopsy 25/6/03

Family history:
Nothing significant

Social history:

97
Lives with son
Works in electronic firm
Smokes 10/day cigarettes

Drug history:
Venofer 100mg
Calcium resorum 15mg
Alfacalcidol .5microgram
Prednisolone 5 mg
Renagel
Descloradine 5mg
Calcium acetate
Lansoprazole 15 mg
Quinine sulphate 300mg
Fluamcorhzone 100 microgram
Clonazepam 500 microgram
Aspirin 75mg

On examination
BP-121/84 mm of Hg
Pulses: 74 b/min
R/R: 16 br/min
Sats 90% on air
Heart sound normal
Pedal odema
ECG
Sinus rhythm

Blader no obvious distension

Mild sacral odema
Drain site healthy

98
Bruit over transplanted kidney
Bowel sound normal

Investigation
Hb 9.9
WCC: 7.1
Platelates- 349
Urea- 9.4
Cr- 409
HCO3- 31
Ca- 2.18
PO4- 1.49

Had renal transplant on 31/7/07 by Mr Halawa then after she has no pain MAG scan 3
and anuric

Input- 3.7 lts

Output: nil

Investigation after surgery

Hb : 14.3, WCC: 7, MCV: 102, K: 5.4, urea: 4.1, Cr- 406

Diagnosis
ATN–

Discussion:

Previous studies aimed at identifying the causes, risk factors, and outcome of kidney
transplant recipients with delayed graft function (DGF) have yielded controversial
results. We retrospectively analyzed the causes and risk factors for DGF in 263 cadaveric
kidney transplantations from November 1988 to March 1997 in one center. Causes of

99
DGF were assessed by postoperative graft evolution and graft biopsy. Univariate and
multivariate analysis were used to investigate the risk factors for DGF induced by acute
tubular necrosis (ATN). Seventy-six patients (29%) had DGF, which was caused by ATN
in 70 patients (92.1%) and acute rejection (AR) in 6 patients (7.9%). Therefore, we
focused on risk factors and consequences for ATN-induced DGF. In monofactorial
analysis, ATN was significantly associated with greater weight and presence of an
atheromatous disease in both donor and recipient. Other risk factors for ATN were older
age of donor, recipient American Society of Anesthesiology (ASA) physical status
category IV, cold ischemia time (CIT), and transplantation using the right kidney. The
multivariate analysis showed that donor and recipient weight, donor age, transplantation
using the right kidney, preservation in Eurocollins solution, ASA score, and CIT were
associated with ATN. The incidence of rejection and renal function were not different at
3 months or 1 and 5 years. ATN is the main cause of DGF in kidney transplant recipients.
ATN is caused by donor and recipient vascular background, grafting the right kidney, and
CIT. ATN does not appear to have an adverse effect on long-term kidney function,
hydrocarbon solvents, organic solvents, herbicides, bacterial and viral infections

In conclusion, recurrent disease, although rare, can occur at any time after transplantation
and should be considered with late graft dysfunction. There is often, but not always, an
identifiable precipitating factor. A high index of suspicion is the key for early diagnosis
because it has been shown that prompt treatment can salvage the graft.

Reference: [24]

100
Psychotic disorders, after transplant: case report

Background

Patients with psychotic disorders have been considered appropriate candidates for
transplantation but are expected to have special needs. Nonetheless, the special needs of
these patients are unclear and will most likely depend upon the individual circumstances
of each patient and their previous psychiatric history. In a 1993 survey of transplant
programs, only 33% of heart, 15% of liver, and 6% of renal transplant programs indicated
that controlled schizophrenia was an absolute contraindication to transplant..

Case summary:
A 21 years old girl admitted in Northern General Hospital with complain of feeling
sickness and admitted here for renal biopsy. Patient had history of maternally donated
renal transplant on 2/7/03. she was living with parents and also attend college. She had
long and complex medical history that she first presented in 2002 with ESRD cause
unknown.
A renal biopsy showed ESRD without any evidence of glomerulonephritis. There was an
intriguing past history of her having been investigated as an infant with dysmorphic
feature and apparently abnormal looking kidney of ultrasound. A repeat USS performed
by an expert paediatric radiologist was however normal. At initial presentation with end
stage of renal disease, Tegan also had an extremely severe dialated cardiomegaly with
profound symptomatic hypotension and severe reduced ejection fraction.
She under went a living related donor transplant after 18 months on peritoneal dialysis,
however unfortunately she had a number of very major and debilitating problems. Early
post transplant she developed acute psycosis that was sufficient in severity. She had to be
transferred for in patient psychiatric management.

101
Case report:
Patient name: T C
Age: 21 yrs
Sex: female

Present complain:
Feeling sick today
Also have little sickness
Admitted here for renal biopsy.

HOPI:
Patient had history of maternally donated renal transplant on 2/7/03. she was living with
parents and also attend college. She had long and complex medical history that she first
presented in 2002 with ESRD cause unknown.
A renal biopsy showed ESRD without any evidence of glomerulonephritis. There was an
intriguing past history of her having been investigated as an infant with dysmorphic
feature and apparently abnormal looking kidney of ultrasound. A repeat USS performed
by an expert paediatric radiologist was however normal. At initial presentation with end
stage of renal disease, Tegan also had an extremely severe dialated cardiomegaly with
profound symptomatic hypotension and severe reduced ejection fraction.
She under went a living related donor transplant after 18 months on peritoneal dialysis,
however unfortunately she had a number of very major and debilitating problems. Early
post transplant she developed acute psycosis that was sufficient in severity. She had to be
transferred for in patient psychiatric management.

PMH:
ESRF due to unknown cause. 2002
CAPD 2002-03
Dialated cardiomyopathy 2002
Spontaeniously live transplant from mother 2003
Psychosis post transplant

102
Personal history:
She is living with parents

Social history:
She is no smoker and non alcoholic

Drug history:
Amlodipine 10 mg OD
One alpha 0.25 mcg OD
Frusemide 160 mg OD
Calcichew 1.2gm TDS
NaHCO3 50 mg BD
Neorecormon 4000 IU 2/week

On examination
Ill looking,
BP-121/84 mm of Hg
Pulses: 74 b/min
R/R: 16 br/min

Respiratory:
Chest clear

CVS
Heart sound normal

Abdomen
Soft non tender

103
Investigation:
Hb 10.8 gm
WCC- 5.6, Plts- 168000, HCT- 0.38
Na-138, K-4.9, Urea-38.6, Crt-474, HCO3-18, Ca 2.21, PO4- 1.8

Bone mineral density report:

Osteopenia
Fracture history nil

Discussion:

This patient with acute psychosis was felt to be an appropriate candidate for a renal
allograft. She had a good adjustment to dialysis, and despite his chronic psychiatric
disorder the medical and psychiatric staff felt that he could comply with the
transplantation medications. Overall, the transplant team decided that the benefits of renal
transplantation outweighed the potential problems in the case of this high-risk patient.

Since patients with chronic psychotic disorders rarely present as candidates for renal
transplantation at our institution or elsewhere in the nation, few transplant programs have
developed a process to specifically address their complex psychosocial needs.

The only other published report regarding transplantation recipients with schizophrenia
discusses two patients who underwent elective removal of a transplanted organ. One
patient received a cadaver renal transplant, which was removed when the patient refused
to take his ant rejection medication or permit laboratory studies. This patient was known
to have ongoing alcohol dependence and was felt not to understand the diligence required
for ongoing transplant care. The second patient was a man with insulin-dependent
diabetes mellitus who received a cadaver pancreas transplant. The patient requested
removal of the transplanted pancreas because he felt it compromised his quality of life.
The transplant was not removed, and the patient followed up with outpatient psychiatric
care. This patient was felt to be compliant with ant rejection medications. The authors

104
report that in both of these cases, family members had pressured the patient to receive the
transplant.

In my case, there was no family pressure on the patient to accept the transplant. She had
been advised that long-term dialysis presented greater risk of long-term medical
complications than transplantation. She had consented to undergo transplantation based
on these considerations plus his desire not to spend time receiving dialysis. The limited
family support was evidently replaced by the considerable support from medical and
nursing staff at the medical center clearly; patients must make their own informed
decision about a procedure of this magnitude. It is our assertion that patients with
schizophrenia benefit from transplantation but may require additional monitoring and
treatment planning to address their psychiatric, medical, and psychosocial needs. The fact
that this patient developed a bond with the dialysis staff is very promising because it
demonstrates his ability to develop a therapeutic relationship. In this case, I believe that
her positive adaptation to dialysis bodes well for his participation in a supervised,
supportive group therapy program while adhering to his post transplant medical care

Reference: [25]

105
Delayed graft function and acute tubular necrosis (ATN): case report

Background
Delayed graft function (DGF) is a common clinical problem occurring after cadaveric
renal transplantation. DGF occurs in more than half of the cadaver grafts Acute tubular
necrosis (ATN) is one of the main causes of the DGF with an incidence varying from
20% to 50% in the cyclosporine era. Protracted recovery of ATN may continue for
several weeks. Persistence of oliguria in ATN is an ominous sign that usually results in
allograft loss or chronic renal insufficiency. Here, we describe a case of prolonged
oliguric ATN that lasted for more than three months with complete recovery of renal
function.

Case summary:
A 32 years girl, get admission for biopsy purpose. Today at evening will go for HD and
will plane to go home foe a break then come back Sunday for HD. She informed that she
has been adviced to drink more water to pass urine, she went under cadaveric transplant.
Since starting CAPD in January 1998. she has had two episode of peritonitis although
these have both clear up well. It would seem time to put her on the transplant operation.
We have mentioned in passing to her family that there is always the possibility of a live
related donor but have not looked in to this any further. She under transplant 15/7/07. she
had biopsy last Monday 23/07/07
She had past medical history of Two small kidney, Recurrent UTI in children
HTN, CAPD, recurrent peritonitis

Case report:
Name of the patient: N C
Age: 32

Present complain:

106
Today she is feeling fine and well.
Feeling bored in hospital

HOPI:
Today at evening will go for HD and will plane to go home foe a break then come back
Sunday for HD. She informed that she has been adviced to drink more water to pass
urine, she went under cadaveric transplant.
Since starting CAPD in January 1998. she has had two episode of peritonitis although
these have both clear up well. It would seem time to put her on the transplant operation.
We have mentioned in passing to her family that there is always the possibility of a live
related donor but have not looked in to this any further. She under transplant 15/7/07. she
had biopsy last Monday 23/07/07

PMH
Two small kidney
Recurrent UTI in children
HTN
CAPD, recurrent peritonitis

Personal history
She is living with parents

Social history
She is smoker and drink regularly

Family history
NAD

107
On examination
BP- 135/94 mm of Hg
Pulse- 90
Left Sacral odema

CVS
Heart sound normal

Respiratory
Chest clear

Abdomen
Soft non tender

Investigation
USS kidney shows 24/7/07 normal

Diagnosis
ATN
Tx
AVF

Discussion:
Renal failure persisting after renal transplantation is called delayed graft function (DGF).
The definition of DGF is varied in different studies, but generally refers to anuria or
requirement for dialysis after the first week post transplantation. Less than 5 percent of
the kidneys with DGF never function (primary nonfunctioning). The frequency of DGF
may be as low as 10% and as high as 70% in some series.

108
The major causes of DGF are acute tubular necrosis (ATN), hyperacute rejection, accele-
rated rejection superimposed on ischemic ATN, urinary tract obstruction or, very rarely,
atheroembolic or thrombosis of the renal artery or vein.

ATN is the most common cause of DGF with an incidence varying from 20% to 50% in
the cyclosporine era. Causes that have been implicated in the etiology of ATN include
renal ischemia due to hypoperfusion in the donor, prolonged warm and cold ischemia
times, harvesting conditions, surgical procedures and cyclosporine given immediately
following transplantation. Cyclosporine (especially at doses above 10 mg/kg per day) and
prior sensitization in the retransplanted patients have been shown
to increase the incidence and duration of ATN.
Some investigators have reported an increased risk of delayed graft function following
transplantation in the cyclosporine treated patients. However, others have failed to
document any difference in the rate of DGF with the conventional immunosuppressive
drugs. ATN tends to become prolonged when cyclosporine is used in these settings.

Administration of calcium channel blockers can prevent the acute renal vasoconstriction
induced by cyclosporine., The long-term reno-protective effects of these agents have yet
to be proven. Chung et al treated 13 patients with DGF and ATN with a low dose
cyclosporine and found no significant decrease in the one-year survival rates. However,
he found that poor functional recovery of ATN or non-ATN condition could predict poor
one-year allografts survival rate.
The most dangerous potential risk of the low dose cyclosporine used in the patients with
DGF was the increased incidence of rejection that results in poor graft survival. On the
other hand, the episodes of infection were significantly lower.
In our patient, the prolonged ischemia time resulted in primary nonfunctioning allograft.
Cyclosporine was not included in the induction regimen in an attempt to decrease the
duration of the DGF. The initial ischemic tubular injury was worsened by the contrast
media-induced nephrotoxicity. Angiogram had to be performed to rule out vascular
occlusion as was evident on Doppler ultrasound. The fulminant chest infection with

109
pulmonary failure obligated the use of aminoglycosides, adding further to the tubular
injury. Furthermore, the biopsy of renal allograft was resorted to on three different
occasions to evaluate the delayed function and to rule out acute rejection. These repeated
and continued insults to the allograft might have contributed to the lengthy ATN that
required the prolonged dialytic support.

Reference: [24]

110
Post-transplant IgA nephropathy: case report

Background

Currently, post-transplant IgA nephropathy (IgAN) is considered to include recurrence of

IgAN, de novo IgAN, or transmission of IgA deposit from donor kidney . Yamaguchi et
al. reported that the prevalence of post-transplant IgAN was 34% in renal biopsies of
allografts surviving more than 5 years. Berger et al. were the first to describe recurrence
of IgA deposit, and subsequent studies showed 50–60% prevalence of recurrent IgAN.
Graft loss due to recurrent renal diseases has been reported to be a rare event, estimated
as less than 5% However, it has recently been shown that deteriorating renal function and
substantial graft loss were observed in 55% of renal allograft recipients with recurrent
IgAN at long-term follow-up

It appears that normal blood pressure is a good marker of graft survival and that an
effective antihypertensive treatment reduces the progression of graft damage. Protection
of allografts from long-term functional deterioration is one of the major goals of treatment
of post-transplant patients. In primary IgAN, hypertension and proteinuria (more than 1
g/day) are considered to indicate a poor prognosis.

Numerous studies have shown that angiotensin-converting enzyme (ACE) inhibitors

interfere with progressive deterioration of many chronic renal diseases, including IgAN.
Only one report so far has shown the antiproteinuric efficacy of ACE inhibitors in patients
with post-transplant glomerulonephritis. The beneficial effect of ACE inhibitors still
remains obscure for post-transplant IgAN, and to date there are a few in-depth studies in
renal transplantation that have analysed the relationship between histological lesions and
response to ACE inhibitor treatment.

111
Case summary:
A 58 years british male, admitted in Northern General Hospital with complain of Mild
diarrhea for 5 days 8-10 times per day. Patient admitted for a renal transplant which he
had on the 18/05/07. Post operation cause was relatively uneventful. His pre operative Cr
was 870.
He had a DVT following air journey and was found to have impaired renal function. He
has had a biopsy in Nottingham with a possible histological diagnosis of IgA
nephropathy. He was admitted with uremic pericarditis, dialysed briefly and was put on
CAPD. He did not get adequate dialysis through it and he has been switched back HD on
renal RUE through a tunnel line neck since may 2003
He was clinically fairly fit and well with no history suggestive of IHD or peripheral heart
disease. He also informed that time shortness of breath at about 100-150 yars
He had past medical history of ESRD- hospital haemodialysis
IgA nepthropathy, Controlled HTN, renal transplantation

Case report:
Name of the patient: C C
Sex: male
Age: 58

Present complain:
Mild diarrhea for 5 days 8-10 times per day
Feeling well

HOPI
Patient admitted for a renal transplant which he had on the 18/05/07. post operation cause
was relatively uneventful. His pre operative Cr was 870.
He had a DVT following air journey and was found to have impaired renal function. He
has had a biopsy in Nottingham with a possible histological diagnosis of IgA

112
nephropathy. He was admitted with uremic pericarditis, dialysed briefly and was put on
CAPD. He did not get adequate dialysis through it and he has been switched back HD on
renal RUE through a tunnel line neck since may 2003
He was clinically fairly fit and well with no history suggestive of IHD or peripheral heart
disease. He also informed that time shortness of breath at about 100-150 yars

PMH
ESRD- hospital haemodialysis
IgA nepthropathy
Controlled HTN
Transplantation

Personal history:
Not smoking since 2003
Ex security guard

Allergy history
No allergy history

Family history
NAD

Social history
He was regular alcoholic but now he informed occasionally drink

On examination:
BP- 135/94 mm of Hg
Pulse- 90
Left Sacral odema

113
CVS:
Heart sound normal

Respiratory
Chest clear

Abdomen
Soft non tender

Diagnosis
IgA nephropathy

Discussion:

In the present study we have studied the histological characteristics of post-transplant

IgAN and primary IgAN. As far as we are aware, this is the first systematic analysis of
histopathology of post-transplant IgAN. The main findings are as follows: (i) acute
lesions such as mesangial proliferation, crescent formation were rarely found in post-
transplant IgAN; (ii) chronic lesions such as glomerular obsolescence and interstitial
fibrosis were observed irrespective of the severity of the glomerular changes; (iii) in post-
transplant IgAN, glomerular hypertrophy was observed at any grade of glomerular
obsolescence. These histopathological characteristics may result from the
pathophysiological conditions of the allograft kidneys.

In renal allografts, glomerular hypertrophy was reported to be a risk factor of focal

glomerulosclerosis and a predictor of risk of late allograft dysfunction .Focal and
segmental sclerosis is also thought to result from glomerular hypertension/hyperfiltration
and is also considered to be related to proteinuria. In addition we found that segmental
sclerosis was more frequently found in the patients with heavier proteinuria (more than
1.0 g/day).

114
It has become evident that several non-immunological factors such as systemic
hypertension, glomerular hypertension, and heavy proteinuria may affect long-term graft
outcome .In patients with a renal allograft, a state of hyperfiltration, one of the main non-
immunological factors, can occur secondarily to a reduction in the functioning renal mass
by various circumstances (e.g. repeated acute rejection episodes, CsA nephrotoxicity,
small renal graft size, or post-transplant glomerulonephritis). Thus, hyperfiltration is
considered to play an important role in the progression of renal insufficiency in the late
post-transplant period.

Conclusion

In conclusion, in post-transplant IgAN, histopathological lesions indicative of acute

inflammatory insults were suppressed; but glomerular hypertrophy, which relates to
haemodynamic burden such as hyperfiltration, was prominent. These histological features
support the use of ACE inhibitors in the treatment of hypertension/hyperfiltration in post-
transplant IgAN.

Preliminary study of ACE inhibitor treatment in 10 patients showed favourable effects.

Future long-term follow-up studies are required to establish the effectiveness of ACE
inhibitors in the treatment of post-transplant IgAN

Reference: [11]

115
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