Renal Medicine MCQs: MRCP Part 2
Ten original single-best-answer renal questions with detailed explanations, spanning AKI, glomerulonephritis and electrolyte emergencies.
Structured the way you revise — mechanism, discriminators, first-line management, and the details that separate the right answer from the plausible one.
30 notes
Ten original single-best-answer renal questions with detailed explanations, spanning AKI, glomerulonephritis and electrolyte emergencies.
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.
A rapid-recall table of the glomerular diseases — each with its signature test and the pearl examiners love.
The commonest cause of nephrotic syndrome in older Caucasian adults — with a signature anti-PLA2R antibody and subepithelial deposits.