MRCP Part 1 → Renal medicine
Renal medicine accounts for roughly 7% of the MRCP Part 1 blueprint. This bank has 165 items tagged to it.
Around 7% of the paper, per MRCP(UK) examination blueprints and regulations. That weighting is why the DocPasser mock builder samples sections in proportion rather than shuffling everything into one pile — practising a flat distribution trains you for a paper that does not exist.
A 24-year-old man notices his urine turned visibly red a day after the onset of a sore throat. This has happened before with colds. Urinalysis shows blood and protein with red-cell casts, and his creatinine is mildly raised. Complement levels are normal. What is the most likely diagnosis?
The point: Glomerulonephritis is a group of conditions in which immune-mediated injury to the glomerulus causes proteinuria, haematuria and often impaired renal function. It is usefully divided into a nephritic pattern (haematuria, red-cell casts, hypertension and a variable fall in renal function) and a nephrotic pattern (heavy proteinuria over 3.5 g per day, hypoalbuminaemia and oedema). Key nephritic causes are IgA nephropathy (visible haematuria a day or two after an upper respiratory infection, the commonest primary glomerulonephritis), post-streptococcal glomerulonephritis (a week or two after a throat or skin infection, with low complement), and the rapidly progressive crescentic pattern of anti-GBM (Goodpasture) disease and ANCA-associated vasculitis. Nephrotic causes include minimal change disease (mostly in children), focal segmental glomerulosclerosis and membranous nephropathy (associated with anti-PLA2R antibodies and, in older patients, malignancy). Investigation includes urinalysis and microscopy for casts, quantification of proteinuria, renal function, complement, and an autoimmune and infection screen, with renal biopsy being the definitive test that guides treatment. Management depends on the cause: blood pressure and proteinuria control with an ACE inhibitor or angiotensin receptor blocker underpins most, immunosuppression is used for aggressive or nephrotic disease, and rapidly progressive glomerulonephritis is a nephrological emergency needing urgent immunosuppression, sometimes with plasma exchange.
Source: UK Kidney Association — clinical practice guidelines UK Kidney Association · tier 2, specialty society or college
A 24-year-old man notices his urine turned visibly red a day after the onset of a sore throat. This has happened before with colds. Urinalysis shows blood and protein with red-cell casts, and his creatinine is mildly raised. Complement levels are normal. What is the most appropriate investigation?
The point: Glomerulonephritis is a group of conditions in which immune-mediated injury to the glomerulus causes proteinuria, haematuria and often impaired renal function. It is usefully divided into a nephritic pattern (haematuria, red-cell casts, hypertension and a variable fall in renal function) and a nephrotic pattern (heavy proteinuria over 3.5 g per day, hypoalbuminaemia and oedema). Key nephritic causes are IgA nephropathy (visible haematuria a day or two after an upper respiratory infection, the commonest primary glomerulonephritis), post-streptococcal glomerulonephritis (a week or two after a throat or skin infection, with low complement), and the rapidly progressive crescentic pattern of anti-GBM (Goodpasture) disease and ANCA-associated vasculitis. Nephrotic causes include minimal change disease (mostly in children), focal segmental glomerulosclerosis and membranous nephropathy (associated with anti-PLA2R antibodies and, in older patients, malignancy). Investigation includes urinalysis and microscopy for casts, quantification of proteinuria, renal function, complement, and an autoimmune and infection screen, with renal biopsy being the definitive test that guides treatment. Management depends on the cause: blood pressure and proteinuria control with an ACE inhibitor or angiotensin receptor blocker underpins most, immunosuppression is used for aggressive or nephrotic disease, and rapidly progressive glomerulonephritis is a nephrological emergency needing urgent immunosuppression, sometimes with plasma exchange.
Source: UK Kidney Association — clinical practice guidelines UK Kidney Association · tier 2, specialty society or college
A 24-year-old man notices his urine turned visibly red a day after the onset of a sore throat. This has happened before with colds. Urinalysis shows blood and protein with red-cell casts, and his creatinine is mildly raised. Complement levels are normal. What is the most appropriate management?
The point: Glomerulonephritis is a group of conditions in which immune-mediated injury to the glomerulus causes proteinuria, haematuria and often impaired renal function. It is usefully divided into a nephritic pattern (haematuria, red-cell casts, hypertension and a variable fall in renal function) and a nephrotic pattern (heavy proteinuria over 3.5 g per day, hypoalbuminaemia and oedema). Key nephritic causes are IgA nephropathy (visible haematuria a day or two after an upper respiratory infection, the commonest primary glomerulonephritis), post-streptococcal glomerulonephritis (a week or two after a throat or skin infection, with low complement), and the rapidly progressive crescentic pattern of anti-GBM (Goodpasture) disease and ANCA-associated vasculitis. Nephrotic causes include minimal change disease (mostly in children), focal segmental glomerulosclerosis and membranous nephropathy (associated with anti-PLA2R antibodies and, in older patients, malignancy). Investigation includes urinalysis and microscopy for casts, quantification of proteinuria, renal function, complement, and an autoimmune and infection screen, with renal biopsy being the definitive test that guides treatment. Management depends on the cause: blood pressure and proteinuria control with an ACE inhibitor or angiotensin receptor blocker underpins most, immunosuppression is used for aggressive or nephrotic disease, and rapidly progressive glomerulonephritis is a nephrological emergency needing urgent immunosuppression, sometimes with plasma exchange.
Source: UK Kidney Association — clinical practice guidelines UK Kidney Association · tier 2, specialty society or college
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