black = Kumar, slides purple= Davidson’s green = step up

AKI
Definition A sudden, sustained, and usually reversible decrease in the glomerular filtration rate (GFR) occurring
over a period of hours to days RESULT IN INJURY, cause sudden, life-threatening biochemical
disturbances
Stages Stage 1-Increase in SCr by ≥0.3 mg/dL (26.4 μmol/l) within 48hours Contrast induced nephropathy
-Increase in Scr by ≥1.5 times baseline within the prior 7 days FENa <1%, Give NS 1 cc/kg
-Urine volume <0.5 mL/kg/h for six hours
Stage 2 -2 – 2.9 times UOP < 0.5 ml/kg/hr for > 12Hrs
Stage 3- Initiation of RRT 3 times baseline -eGFR to < 35 in patients <18 -Anuria for > 12Hrs
UOP < 0.3 ml/kg/hr for > 24Hrs
RIFLE a. RISK: 1.5-fold increase in the serum creatinine or GFR decrease by 25% or
Criteria urine output <0.5 mL/kg/hour for 6 hours
b. INJURY: Twofold increase in the serum creatinine or GFR decrease by 50% or
urine output <0.5 mL/kg/hour for 12 hours
c. FAILURE: Threefold increase in the serum creatinine or GFR decrease by 75%
or urine output of <0.5 mL/kg/hour for 24 hours, or anuria for 12 hours
d. LOSS: Complete loss of kidney function ( requiring dialysis) for more than 4 weeks
e. ESRD: Complete loss of kidney function (requiring dialysis) for more than 3 months
Pre renal Intrinsic Post renal
impaired perfusion of the kidneys caused by nephrotoxic drugs, obstruction of the urinary Acute GN hematuria, RBC casts,
Pathophysiology or classification

with blood. This results either from which can cause acute tubular tract proteinuria
hypovolaemia, hypotension, necrosis, interstitial nephritis., or Should be bilateral to renal biopsy, immunosuppressive
impaired cardiac pump efficiency or glomerulonephritis ,vascular dis., produce acute renal failure therapy and steroids
renal artery stenosis, Cirrhosis, NSAIDs, contrast
hepatorenal syndrome, drugs a, recent catheter.
(ACEI, and NSAIDs) leading to
acute tubular necrosis.
FENa < 1% FENa > 1% Hydronephrosis or
Urine osmolality >500 Urine osmolality <350 hydroureters on US , KUB
Urine sodium <20 Urine sodium >40
HF, Dry mouth• extremities are Fever,Rashes Arthralgias, LUTS, flank pain, bladder
cool, Tachycardia, flattened neck seizure, ischemia, hematuria, enlargement
veins, dark urine proteinuria, HTN
Sign, Low Urine Output, HTN, or discolored urine, Weight gain and edema, azotemia (elevated BUN and Rhabdomyolysis high serum CK,
symptoms Cr) weakness and easy fatiguability, anorexia, Vomiting, mental status changes or Seizures pigmented granular casts
1-Blood tests a. Elevation in BUN and Cr levels Acute Interstitial Nephritis,
investigati

b. Electrolytes (K+, Ca2+, PO43−), albumin levels, CBC with differential methicillin, rifampin, NSAIDS,
on

2-Urinalysis (• Muddy brown casts in ATN • WBC casts in AIN • RBC casts in AGN) Fever, Rash , and eosinophilia
- A dipstick test positive for protein (3+, 4+) suggests intrinsic renal failure due to glomerular insult. WBC casts, + Hansel stain
U/S kidneys, Serology and autoimmune
 1-Correct hypovolaemia and optimise systemic haemodynamic status with inotropic drugs if necessary
management 2• Administer glucose and insulin to correct hyperkalaemia if K+ > 6.5 mmol/L
3• Consider administering sodium bicarbonate (100 mmol) to correct acidosis if pH < 7.0 (> 100
nmol/L)
4• Discontinue potentially nephrotoxic drugs and reduce doses of therapeutic drugs .
5• Match fluid intake to urine output plus an additional 500 mL to cover insensible losses once patient
is euvolaemic
Volume overload: esulting pulmonary edema—treat with a diuretic (furosemide)
Hyperkalemia due to decreased excretion of K+ and the movement of potassium from ICF to ECF due
complecation

to tissue destruction and acidosis,

Metabolic Acidosis!(with increased anion gap)—due to decreased excretion of hydrogen ions; if severe
(below 16 mEq/L), correct with sodium bicarbonate,
Uremic Encephalopath y, Uremic pericarditis, if refractory>>dialysis
Hypocalcemia, Hyponatremia ,Hyperphosphatemia !, Hyperuricemia

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 CKD
longstanding (more than 3 months), and usually progressive, impairment in renal function.
stages stages What to do? As screening of kidney
1 Normal or ↑ GFR ≥ 90 Treat comorbidities function:
Kidney Damage with Mild ↓ Slow progression Urinary albumin to creatinine
2 60-89 ratio (ACR)
GFR
3 Moderate ↓ GFR 30-59
Causes:
4 Severe ↓ GFR 15-29 Prepare for RRT
a. Diabetes is the most
5 Kidney Failure < 15 Dialysis
common cause (30% of
cases).
b. HTN is responsible for 25%
of cases.
c. Chronic GN accounts for
15% of cases.
d. Interstitial nephritis,
polycystic kidney disease,
obstructive uropathy
e. Any of the causes of AKI
may lead to CKD if prolonged
and/or if treatment is delayed.

s/s Symptoms are common when the serum urea concentration exceeds 40 mmol/L, Malaise, loss of energy, Loss of appetite,
Insomnia, Nocturia and polyuria due to impaired concentrating ability, Itching, Nausea, vomiting and diarrhea, Paraesthesiae due
to polyneuropathy, Bone pain due to metabolic bone disease, Paraesthesiae and tetany due to hypocalcaemia, Symptoms due to
salt and water retention – peripheral or pulmonary oedema, Symptoms due to anaemia, Amenorrhoea in women; erectile
dysfunction in men. neurological:!confusion, peripheral neuropathy
 Urinalysis: Haematuria, proteinuria, Urine culture: including early-morning urine samples for TB.
Urine microscopy: White cells UTI, papillary necrosis or renal tuberculosis, Eosinophiluria :allergic 
tubulointerstitial nephritis or
cholesterol embolization. Casts. Granular casts indicate active renal disease. Red-cell casts are highly suggestive of
glomerulonephritis. muddy brown cast = ATN,.
investigation

Urine biochemistry urinary sodium , Urine osmolality

Serum biochemistry 
urea and creatinine. Calculation of eGFR. Electrophoresis and immunofixation for myeloma.
Elevations of
creatine kinase and a disproportionate 
elevation in serum creatinine and potassium compared with urea suggest rhabdomyolysis 

Haematology, Immunology:Complement components, Autoantibody screening
Radiological investigation: Ultrasound. (for renal size and to exclude hydronephrosis), and plain abdominal radiography and
CT (without contrast) to exclude low-density renal stones or nephrocalcinosis, which may be missed on ultrasound.
Renal biopsy performed in every person with unexplained CKD and normal-sized kidneys,
1- diet restrict Na, K, low protein, Ph, Mg. 2- ACE inhibitors—dilate efferent arteriole of glomerulus
Treatemnt

3- BP control 4- Target HbA1c ~7.0% • 5- Smoking cessation • 6- Exercise 7-Weight reduction •8- Lipid lowering therapy
9- Correct hyperphosphatemia with calcium citrate (a phosphate binder).!b. long-term oral c! alcium and vitamin D for secondatry
hyperparathyroidism a! nd uremic osteodystrophy.!c. Acidosis—treat the underlying cause (renal failure) or oral b
! icarbonate
replacement. ! 10- Anemia—treat with erythropoietin.
1-Anaemia : Erythropoietin deficiency (the most significant) , Bone marrow fibrosis secondary to 
hyperparathyroidism 

Haematinic deficiency – iron, vitamin B12, folate , Increased red-cell destruction, Abnormal red-cell membranes causing
increased 
osmotic fragility ,Increased blood loss – occult gastrointestinal bleeding, 
blood sampling, blood loss during
haemodialysis or 
because of platelet dysfunction, ACE inhibitors (may cause anaemia in CKD )

2- renal osteodystrophy 
 Phosphate retention owing to reduced excretion by the >> release of fibroblast growth factor 23,
Elevated FGF 23 levels are the strongest independent predictor of mortality >> 1-Reduced activation of vitamin D>> gut calcium
malabsorption> 2- secondary hyperparathyroidism>> reabsorption of calcium from bone by increased osteoclastic activity, cyst
formation and bone marrow fibrosis (osteitis fibrosa cystica).
complication

3- Skin disease Pruritus (itching) due to retention of nitrogenous waste products of protein catabolism
4-Metabolic abnormalities :hyperkalemia, metabolic acidosis, Gout. Urate retention, Insulin requirements decrease as CKD
progresses. Impaired clearance of triglyceride-rich particles, Hypercholesterolaemia
5- Endocrine abnormalities Hyperprolactinaemia, high LH, abnormal GH, thyroid function
5- Nervous system :Severe uraemia causes depressed cerebral function and decreased seizure threshold (convulsions ) Rapid
correction of severe uraemia by haemodialysis leads to dialysis disequilibrium owing to osmotic cerebral swelling.
6- Cardiovascular disease : Risk factors Hypertension is a frequent complication of CKD. Diabetes mellitus is the commonest
cause of CKD. Dyslipidaemia is universal in uraemic patients, Ventricular hypertrophy is common, as is systolic and diastolic
dysfunction.
7- Pericarditis: indicates severe, pre-terminal uraemia or of underdialysis could associated with Haemorrhagic pericardial
effusion and atrial arrhythmias. usually resolves with intensive dialysis.
! Bushra