MRCP Part 1 Nephrology: 50 Rapid-Review Facts
- Crack Medicine
- 2 days ago
- 6 min read
TL;DR
If you’re preparing for mrcp part 1 nephrology: 50 rapid-review facts, this article distils the essential renal medicine topics you must know for MRCP Part 1. It covers glomerular diseases, tubular disorders, electrolyte imbalances, AKI/CKD, study-tips and exam traps — ideal for efficient revision. Use this guide alongside question banks and mock tests to maximise recall.
Why this matters
Nephrology is a discipline that blends detailed physiology, pathophysiology and clinical reasoning. In the MRCP(UK) Part 1 you will face questions requiring not just factual recall but swift pattern recognition — for example, linking electrolyte derangements, renal biopsy findings or acute kidney injury (AKI) phenotypes. As part of your revision for the primary hub of MRCP Part 1, you need a compact, high-yield nephrology summary you can dip into in the final weeks. This article provides 50 rapid-review facts, integrates practical revision advice and links to further resources such as our Free MRCP MCQs and a chance to Start a mock test.
Scope of nephrology in MRCP Part 1
The syllabus of MRCP Part 1 covers medicine broadly, including renal disorders. According to official guidance, the exam has two papers, each of three hours, 100 “best of five” questions per paper. thefederation.uk+2studymrcp.com+2 Nephrology may appear under internal medicine, physiology, electrolytes, acute and chronic disease themes. Familiarity with UK-based guideline frameworks (such as those from National Institute for Health and Care Excellence – NICE) is beneficial. NICE+1In this article I highlight five most tested nephrology sub-topics and five classic traps you should avoid, then present 50 rapid facts for ready recall.
Five most-tested nephrology sub-topics
1. Glomerular disease (nephrotic & nephritic syndromes)
Understanding glomerular pathology (e.g., minimal change, FSGS, membranous, IgA) and recognising syndromic patterns is frequently tested.
2. Electrolytes & acid-base disturbances
Questions on hyponatraemia, hyperkalaemia, metabolic acidosis/alkalosis are common and involve renal physiology.
3. Acute kidney injury (AKI) and acute tubular/obstructive injury
Differentiating pre-renal, intrinsic and post-renal AKI, knowing FeNa criteria, and management implications.
4. Chronic kidney disease (CKD) and complications
Recognising staging, complications (anaemia, bone disease), and guideline-based management (NICE CKD NG203). NICE+1
5. Tubular/interstitial renal disorders
Including renal tubular acidosis, nephrogenic diabetes insipidus, acute interstitial nephritis (AIN), drug-induced tubular injury — frequently under-revised but high-yield.
Five classic nephrology traps
Mistaking IgA nephropathy (haematuria concurrent with infection) for post-streptococcal GN (latent onset + low complement).
Assuming all AKI in ACE-I use is “benign” – missing bilateral renal artery stenosis.
Overlooking hyperkalaemia risk in type 4 RTA or in CKD with aldosterone deficiency.
Confusing nephrotic vs nephritic syndrome definitions (proteinuria vs haematuria predominance).
Ignoring guideline-based CKD risk stratification: e.g., using eGFR alone rather than the newer Kidney Failure Risk Equation (KFRE) as recommended in UK guidance. UK Kidney Association
50 Rapid-Review Facts for Nephrology
Minimal change disease is most common nephrotic syndrome in children; steroid responsive.
Focal segmental glomerulosclerosis (FSGS) often presents with nephrotic syndrome and is associated with obesity, HIV, heroin.
Membranous nephropathy is the commonest cause of adult primary nephrotic syndrome in white adults and shows “spike and dome” appearance on EM.
IgA nephropathy: episodic visible haematuria post-upper respiratory tract infection, normal complement.
Post-streptococcal glomerulonephritis: low C3 complement, latent 2–3 weeks after throat infection.
Acute interstitial nephritis: classically due to drugs (NSAIDs, PPIs, penicillins) with fever, rash, eosinophilia.
Renal tubular acidosis (RTA) type 1 (distal): high urine pH >5.5, hypokalaemia, risk of calcium stones.
RTA type 2 (proximal): defective bicarbonate reabsorption; Fanconi-type features.
RTA type 4: hyperkalaemia due to reduced aldosterone action/resistance.
Hyponatraemia: check osmolality and volume status; SIADH common in in-patient setting.
Hypernatraemia: often due to water loss > sodium loss; consider diabetes insipidus.
Hyperkalaemia: peaked T waves on ECG, may require IV calcium, insulin-glucose, and urgent management.
Hypokalaemia: may manifest with U-waves on ECG; often due to diuretics or GI loss.
AKI pre-renal: FeNa <1%, often volume depletion or hypotension.
AKI intrinsic (ATN): FeNa >2%, muddy brown casts, often after ischaemia or toxins.
AKI post-renal: obstruction, hydronephrosis on imaging.
CKD definition: eGFR <60 mL/min/1.73 m² for >3 months or markers of kidney damage.
CKD complications: anaemia (↓ EPO), secondary hyper-parathyroidism, metabolic acidosis.
Nephrotic syndrome: proteinuria >3.5 g/day, hypoalbuminaemia, oedema, hyperlipidaemia.
Nephrotic syndrome complications include thrombosis (renal vein thrombosis) and infection.
Diabetes mellitus is the leading cause of CKD in the developed world.
ADPKD (autosomal dominant polycystic kidney disease) may present with haematuria, hypertension, and intracranial aneurysm risk.
ACE-inhibitors/ARBs are renal-protective in proteinuric CKD but may cause rises in creatinine (especially bilateral renal artery stenosis).
In CKD, BP target is usually <130/80 mmHg (if tolerated) to slow progression.
Dialysis initiation is considered when eGFR <10 mL/min/1.73 m² or symptomatic uraemia.
Haemodialysis corrects uraemia rapidly; peritoneal dialysis is gradual and home-based.
For acid-base disorders: metabolic acidosis shows ↓HCO₃⁻ and ↓pH; metabolic alkalosis shows ↑HCO₃⁻.
Urgent management of hyperkalaemia includes calcium gluconate (to stabilise myocardium), insulin and glucose (to shift K+).
Urate nephropathy (tumour lysis syndrome) causes crystal-induced AKI.
Myeloma kidney: light chain cast nephropathy – look for Bence-Jones proteinuria.
Goodpasture syndrome: anti-GBM antibodies cause lung + kidney involvement (RPGN).
Alport’s syndrome: hereditary nephritis + sensorineural hearing loss.
Nephrogenic diabetes insipidus: resistance to ADH; may be lithium-induced or congenital.
Drug-induced kidney injury: NSAIDs (reduce prostaglandins), aminoglycosides (ATN), ACE-I (reduced filtration in bilateral RAS).
In CKD, phosphate binders may be needed due to hyperphosphataemia and bone disease.
The UK guideline for CKD (NICE NG203) recommends referral when 5-year risk of kidney failure >5% using the KFRE. UK Kidney Association+1
In nephritic syndrome look for red cell casts, haematuria, usually moderate proteinuria.
In nephrotic syndrome look for heavy proteinuria, hypoalbuminaemia, oedema.
Minimal change disease: podocyte foot-process effacement on EM.
Membranous nephropathy: associated with PLA2R antibodies in primary form.
IgA nephropathy: sometimes progresses to CKD over years — monitor.
Chronic NSAID use may cause analgesic nephropathy leading to CKD.
Renal biopsy is often required to distinguish glomerular pathology when presentation is atypical.
In metabolic acidosis, expect compensatory hyperventilation (low PaCO₂).
In respiratory acidosis (e.g., COPD exacerbation) expect elevated PaCO₂ and compensatory ↑HCO₃⁻ over time.
In respiratory alkalosis (e.g., PE or anxiety) PaCO₂ ↓ and HCO₃⁻ falls.
Urinalysis remains a vital initial test: dipstick for protein/haematuria, microscopy for casts.
For CKD, lifestyle measures (smoking cessation, salt restriction, exercise) are essential alongside medical therapy. nhs.uk
Always review drug doses in renal impairment (e.g., metformin, gentamicin).
In suspected AKI always exclude obstruction (via ultrasound) before labelling intrinsic renal failure.
Practical example: mini-MCQ
Question: A 52-year-old male presents with oedema and frothy urine. Laboratory studies show albumin 22 g/L, cholesterol 8.5 mmol/L and proteinuria 4 g/day. He has no diabetes and is hepatitis B-negative. What is the most likely diagnosis?
Answer: Idiopathic membranous nephropathy. Explanation: This presentation (adult, heavy proteinuria, low albumin, hypercholesterolaemia) fits a nephrotic syndrome in an adult. Membranous nephropathy is the commonest cause of primary adult nephrotic syndrome in white adults; secondary causes (malignancy, HBV/HCV, SLE) should always be considered and excluded as part of your management plan.
Practical study-tip checklist
✅ Use a spaced-repetition system (flashcards) to memorise the 50 rapid-review facts.
✅ After each QBank session, review why each nephrology answer was correct/incorrect (error-review).
✅ Run subject-specific QBank blocks for nephrology (e.g., electrolyte, AKI, glomerular disease).
✅ On weekends, devote a “focused topic” slot to one of the five sub-topics (e.g., one weekend = glomerular disease, next = acid-base).
✅ At the end of each week, simulate a timed 60-minute block of nephrology-related MCQs to improve time management.
✅ In the final two weeks, do full mock papers under exam conditions via Start a mock test.
✅ Use the anchor link “MRCP Part 1 overview” (/mrcp-part-1/) to revisit the overarching syllabus and ensure you’re not neglecting renal alongside other specialties.
Ready to start?
Precision in nephrology matters — it’s not just the facts but applying them under exam pressure that counts in MRCP Part 1. Use this rapid-review sheet alongside targeted QBank practice and mock tests to embed your knowledge. Visit our Free MRCP MCQs and consider scheduling your next mock test now. Your revision strategy backed by high-yield facts means fewer surprises on exam day. Good luck!
Sources
“Examinations – Part 1 – MRCP UK” thefederation.uk
“Format – MRCP UK Part 1” thefederation.uk
“Chronic kidney disease: assessment and management – NICE NG203” NICE+1
“UK eCKD Guide – UK Kidney Association” UK Kidney Association
“Chronic kidney disease – Treatment – NHS” nhs.uk
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