Acute Kidney Injury: MCCQE Notes
Pre-renal, renal, post-renal — and an ultrasound plus a urinalysis will usually tell you which.
Structured the way you revise — mechanism, discriminators, first-line management, and the details that separate the right answer from the plausible one.
30 notes
Pre-renal, renal, post-renal — and an ultrasound plus a urinalysis will usually tell you which.
Volume status plus urine sodium and osmolality gets you to the cause, and the rate of correction is what keeps the patient safe.
Large urine volumes with a short differential — sort them into osmotic, water diuresis and drug causes.
Removing pathogenic antibodies and immune complexes from plasma — key in anti-GBM disease, TTP and severe vasculitis.
Home dialysis using the peritoneum as a membrane — with peritonitis as its defining complication.
Ischaemic death of the renal papillae — think analgesic nephropathy, diabetes and sickle cell disease.
An acute kidney injury a few days after iodinated contrast — largely preventable with hydration and risk-factor control.
Heavy urinary protein loss brings predictable complications — thrombosis, infection and hyperlipidaemia chief among them.
A mixed nephritic-nephrotic glomerulonephritis with 'tram-track' basement membranes and low complement — think hepatitis C and complement dysregulation.
The physiology of clearance — inulin for GFR, PAH for renal plasma flow, and why creatinine clearance overestimates GFR.
The world's commonest glomerulonephritis — visible haematuria a day or two after an upper respiratory infection.
Low potassium sorted by whether it comes with alkalosis or acidosis — plus the classic U-wave ECG and safe replacement.
Dilatation of the renal pelvis and calyces from obstruction — with useful mnemonics for the unilateral and bilateral causes.
A collapsing FSGS of advanced HIV — heavy proteinuria, large echogenic kidneys and rapid progression, best treated with antiretrovirals.
A thrombotic microangiopathy with a classic triad — usually following Shiga-toxin E. coli, occasionally from complement dysregulation.
A framework for the glomerular diseases — splitting them along the nephritic-to-nephrotic spectrum.
The NICE framework for prescribing IV fluids — resuscitation, routine maintenance, replacement, redistribution and reassessment.
Generalised proximal tubular failure — leaking glucose, amino acids, phosphate and bicarbonate into the urine.
Often the first warning sign of cardiovascular disease — with a useful organic-versus-psychogenic split guiding assessment.
Polyuria from ADH deficiency (cranial) or ADH resistance (nephrogenic) — distinguished by the water deprivation test.
An inherited defect in dibasic amino-acid reabsorption causing recurrent, poorly soluble cystine stones from a young age.
Persistent pelvic pain and urinary symptoms — most cases are non-bacterial chronic pelvic pain syndrome rather than infection.
A normochromic normocytic anaemia driven by erythropoietin deficiency — correct iron first, then use ESAs to a modest haemoglobin target.
The childhood form of polycystic kidney disease — presenting antenatally or in infancy, with congenital hepatic fibrosis.
A pulmonary-renal syndrome from antibodies against type IV collagen — rapidly progressive glomerulonephritis with lung haemorrhage.
A simple calculation that splits metabolic acidosis into raised-gap and normal-gap causes — and points you to the diagnosis.
Extracellular deposition of misfolded protein causing nephrotic syndrome, cardiac and multi-system disease — diagnosed by Congo red staining.
A rare syndrome combining acute interstitial nephritis with anterior uveitis, classically in young women.
An immune-mediated cause of acute kidney injury — usually drug-induced — with eosinophilia, sterile pyuria and white cell casts.
The commonest cause of nephrotic syndrome in older Caucasian adults — with a signature anti-PLA2R antibody and subepithelial deposits.