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Nephrology Msra

The document outlines key aspects of nephrology, including the diagnosis and management of conditions like bladder cancer, acute kidney injury (AKI), chronic kidney disease (CKD), and hemolytic-uremic syndrome (HUS). It emphasizes the importance of specialist nephrology input for severe AKI cases and provides guidelines for managing complications such as hyperkalemia and anemia in CKD patients. Additionally, it discusses diagnostic criteria for conditions like autosomal dominant polycystic kidney disease (ADPKD) and the role of medications in treatment strategies.

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faisal hussain
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100% found this document useful (1 vote)
45 views3 pages

Nephrology Msra

The document outlines key aspects of nephrology, including the diagnosis and management of conditions like bladder cancer, acute kidney injury (AKI), chronic kidney disease (CKD), and hemolytic-uremic syndrome (HUS). It emphasizes the importance of specialist nephrology input for severe AKI cases and provides guidelines for managing complications such as hyperkalemia and anemia in CKD patients. Additionally, it discusses diagnostic criteria for conditions like autosomal dominant polycystic kidney disease (ADPKD) and the role of medications in treatment strategies.

Uploaded by

faisal hussain
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as TXT, PDF, TXT or read online on Scribd

NEPHROLOGY MSRA

Gold standard for bladder cancer diagnosis is cystoscopy.

In general, antibiotics are not indicated in the treatment of haemolytic-uraemic


syndrome unless the underlying diarrhoeal infection is an indication itself. As his
symptoms have passed there is no indication for oral or IV antibiotics

An uncomplicated stage 1 AKI can be managed without specialist nephrology input.


Referrals of this nature are generally reserved for AKI patients with serious pre-
existing renal comorbidities or with complicated presentations that are refractory
to initial fluid management.

those with post-streptococcal glomerulonephritis develop haematuria approximately 2


weeks following an acute infection.

a patient is deemed in stage 3 AKI if they are commenced on renal replacement


therapy irrespective of creatinine or urine production.

CKD on haemodialysis - most likely cause of death is IHD

a blood film is the most useful initial diagnostic test for HUS

as a general rule plasma exchange is reserved for severe cases of HUS not
associated with diarrhea in HUS

there is no role for antibiotics, despite the preceding diarrhoeal illness in many
patients with HUS

One of the best ways to differentiate between acute kidney injury (AKI) and chronic
kidney disease (CKD) is renal ultrasound

A normal anion gap is 8-14 mmol/L

Ultrasound diagnostic criteria (in patients with positive family history) for ADPKD
two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years

CAGE-variables used in MDRD equation


creatinine
age
gender
ethnicity

stage 1 and 2 CKD require deranged kidney function or proteinurea to diagnose CKD

Causes of nephrogenic diabetes insipidus


genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2
channel
electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney's ability to respond to ADH in the collecting ducts

Investigation
high plasma osmolality (often >295 mOsm/kg), low urine osmolality (often <300
mOsm/kg)
a urine osmolality of >700 mOsm/kg generally excludes diabetes insipidus
water deprivation test
a desmopressin test can help differentiate cranial from nephrogenic DI (an increase
in urine osmolality suggests cranial DI)

When prescribing for routine maintenance alone, consider using 25-30 ml/kg/day
sodium chloride 0.18% in 4% glucose with 27 mmol/l potassium on day 1 (there are
other regimens to achieve this).-maintainence fluids

All patients with severe hyperkalaemia (≥ 6.5 mmol/L) or with ECG changes should
have emergency treatment
IV calcium gluconate: to stabilise the myocardium
insulin/dextrose infusion: short-term shift in potassium from ECF to ICF

The following changes are associated with hyperkalaemia:


peaked or 'tall-tented' T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

drugs: the most common cause, particularly antibiotics


penicillin
rifampicin
NSAIDs
allopurinol
furosemide

Specialist input from a nephrologist is required for cases where the cause is not
known or where the AKI is severe.

All patients with suspected AKI secondary to urinary obstruction require prompt
review by a urologist.

fractional sodium excretion = (urine sodium/plasma sodium) / (urine


creatinine/plasma creatinine) x 100

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma


creatinine) x 100

This is usually a normochromic normocytic anaemia and becomes apparent when the GFR
is less than 35 ml/min (other causes of anaemia should be considered if the GFR is
> 60 ml/min).

Anaemia in CKD predisposes to the development of left ventricular hypertrophy -


associated with a three fold increase in mortality in renal patients

Management
the 2011 NICE guidelines suggest a target haemoglobin of 10 - 12 g/dl
determination and optimisation of iron status should be carried out prior to the
administration of erythropoiesis-stimulating agents (ESA).
oral iron should be offered for patients who are not on ESAs or haemodialysis. If
target Hb levels are not reached within 3 months then patients should be switched
to IV iron
patients on ESAs or haemodialysis generally require IV iron
ESAs such as erythropoietin and darbepoetin should be used in those 'who are likely
to benefit in terms of quality of life and physical function'
ACE inhibitors are first line and are particularly helpful in proteinuric renal
disease (e.g. diabetic nephropathy).

Furosemide is useful as a anti-hypertensive in patients with CKD, particularly when


the GFR falls to below 45 ml/min*. It has the added benefit of lowering serum
potassium.

the evidence base currently supports the use of intravenous 0.9% sodium chloride at
a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure

Patients who are high-risk for contrast-induced nephropathy should have metformin
withheld for a minimum of 48 hours and until the renal function has been shown to
be normal. This is due to the risk of lactic acidosis.

Contrast media nephrotoxicity may be defined as a 25% increase in creatinine


occurring within 3 days of the intravascular administration of contrast media.
Contrast-induced nephropathy occurs 2 -5 days after administration.

bloods:
raised anti-streptolysin O titre are used to confirm the diagnosis of a recent
streptococcal infection

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