Membership of the Royal College of Physicians (MRCP UK) Nephrology Syllabus

Nephrology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Nephrology in Membership of the Royal College of Physicians (MRCP UK), not a summary of it.

1. 1

   Acute Kidney Injury and Critical Care Nephrology

   4 topics

   • Acute kidney injury staging and aetiology
     • Pre-renal, intrinsic and post-renal causes
   • Acute tubular necrosis and acute interstitial nephritis
   • Indications for renal replacement therapy
   • Contrast nephropathy and nephrotoxic drugs
2. 2

   Chronic Kidney Disease and Renal Replacement

   4 topics

   • Chronic kidney disease staging and progression
   • Complications of CKD
     • Renal bone disease and mineral metabolism
     • Anaemia of CKD
   • Haemodialysis and peritoneal dialysis
   • Renal transplantation and immunosuppression
3. 3

   Glomerular and Tubulointerstitial Disease

   4 topics

   • Nephrotic syndrome
     • Minimal change, FSGS, membranous nephropathy
   • Nephritic syndrome and rapidly progressive glomerulonephritis
   • IgA nephropathy and lupus nephritis
   • Diabetic nephropathy and hypertensive nephrosclerosis
4. 4

   Fluid, Electrolyte and Acid-Base Disorders

   5 topics

   • Sodium and water balance disorders
     • Hyponatraemia and hypernatraemia
   • Potassium disorders
     • Hyperkalaemia and hypokalaemia
   • Acid-base disturbances
     • Metabolic acidosis and the anion gap
   • Magnesium and phosphate abnormalities
   • Inherited tubular disorders

Nephrology flashcards for Membership of the Royal College of Physicians (MRCP UK)

24 of 55 cards from the Nephrology deck — real questions with worked answers.

1. What are the KDIGO serum creatinine and urine output criteria for diagnosing Acute Kidney Injury (AKI)?

   AKI is diagnosed by ANY of: (1) rise in serum creatinine $\geq 26.5\ \mu mol/L$ ($\geq 0.3\ mg/dL$) within 48 hours; (2) rise in creatinine $\geq 1.5\times$ baseline known/presumed within 7 days; or (3) urine output $< 0.5\ mL/kg/h$ for $\geq 6$ hours.

2. State the KDIGO staging of AKI (stages 1–3) by serum creatinine and urine output.

   Stage 1: creatinine $1.5–1.9\times$ baseline or $\geq 26.5\ \mu mol/L$ rise; UO $<0.5\ mL/kg/h$ for 6–12 h. Stage 2: creatinine $2.0–2.9\times$ baseline; UO $<0.5\ mL/kg/h$ for $\geq 12$ h. Stage 3: creatinine $\geq 3\times$ baseline or $\geq 353.6\ \mu mol/L$ or RRT initiated; UO $<0.3\ mL/kg/h$ for $\geq 24$ h or anuria $\geq 12$ h.

3. Classify the aetiology of AKI into the three main categories with examples.

   Pre-renal (hypoperfusion: hypovolaemia, sepsis, cardiac/hepatorenal, NSAIDs/ACEi). Intrinsic/renal (ATN, AIN, glomerulonephritis, vasculitis, contrast). Post-renal (obstruction: stones, prostate, tumour, retroperitoneal fibrosis).

4. How do urinary indices (urine osmolality, urine sodium, FENa) distinguish pre-renal AKI from established ATN?

   Pre-renal: urine osmolality $>500\ mOsm/kg$, urine $Na^{+} <20\ mmol/L$, $FE_{Na} <1\%$ (concentrated, sodium avid). ATN: urine osmolality $<350\ mOsm/kg$, urine $Na^{+} >40\ mmol/L$, $FE_{Na} >2\%$ (tubules cannot reabsorb/concentrate).

5. Write the formula for the fractional excretion of sodium ($FE_{Na}$).

   $$FE_{Na} = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100\%$$ where $U$ = urine and $P$ = plasma concentrations of sodium and creatinine.

6. What is acute tubular necrosis (ATN), its two main causes, and the characteristic urinary finding?

   ATN is intrinsic AKI from tubular epithelial cell injury. Two causes: ischaemic (prolonged pre-renal hypoperfusion) and nephrotoxic (drugs, contrast, myoglobin, light chains). Urinary hallmark: muddy brown granular casts and renal tubular epithelial cells.

7. Describe the three clinical phases of recovery in ATN.

   (1) Oliguric phase (days to weeks, risk of fluid overload/hyperkalaemia); (2) Polyuric/diuretic phase (recovering tubules, large urine output, risk of hypokalaemia and dehydration); (3) Recovery phase (gradual return of GFR).

8. What is acute interstitial nephritis (AIN), its classic triad, and the commonest causes?

   AIN is immune-mediated inflammation of the renal interstitium. Classic (but uncommon) triad: fever, rash, eosinophilia. Causes: drugs (penicillins, NSAIDs, PPIs, rifampicin, allopurinol), infections, and autoimmune disease (sarcoid, SLE). Urine may show sterile pyuria and eosinophiluria.

9. Compare ATN and AIN: typical trigger, urinalysis, and treatment.

   ATN: ischaemia/toxins; muddy brown granular casts; supportive care, treat cause. AIN: drug hypersensitivity (NSAIDs/PPIs/antibiotics); sterile pyuria, white cell casts, eosinophiluria, mild proteinuria; stop offending drug, consider corticosteroids.

10. List the emergency indications for renal replacement therapy in AKI (the 'AEIOU' mnemonic).

    A – Acidosis (severe metabolic, $pH <7.1$ refractory). E – Electrolytes (refractory hyperkalaemia $K^{+} >6.5\ mmol/L$ or with ECG changes). I – Intoxication (dialysable poisons: lithium, salicylates, methanol, ethylene glycol). O – Overload (refractory pulmonary oedema). U – Uraemia (encephalopathy, pericarditis, $urea >40\ mmol/L$).

11. What is contrast-induced nephropathy (CIN): definition, timing, and main risk factors?

    CIN is a rise in creatinine $\geq 25\%$ or $\geq 44\ \mu mol/L$ within 48–72 h of iodinated contrast. Peaks at 3–5 days, usually recovers by 7–10 days. Risk factors: pre-existing CKD, diabetes, dehydration, high contrast volume, age, heart failure, nephrotoxic drugs.

12. What is the main proven prophylaxis against contrast-induced nephropathy?

    Volume expansion with intravenous isotonic saline (or sodium bicarbonate) before and after contrast. Use lowest volume of iso-/low-osmolar contrast, withhold nephrotoxins, and stop metformin around the procedure. N-acetylcysteine is not reliably effective.

13. Name common nephrotoxic drug classes and their mechanism of kidney injury.

    NSAIDs (reduce afferent arteriolar prostaglandins → pre-renal/AIN); ACEi/ARB (efferent vasodilation → reduced GFR); aminoglycosides (proximal tubular ATN); amphotericin B (tubular toxicity, tubular wasting); ciclosporin/tacrolimus (vasoconstriction); contrast (ATN/vasoconstriction); vancomycin (ATN/AIN).

14. State the staging of CKD by eGFR (G stages, KDIGO).

    G1: $\geq 90$ (normal, with kidney damage); G2: $60–89$ (mild); G3a: $45–59$; G3b: $30–44$; G4: $15–29$ (severe); G5: $<15\ mL/min/1.73\,m^{2}$ (kidney failure). All in $mL/min/1.73\,m^{2}$. CKD requires abnormality persisting $\geq 3$ months.

15. How is albuminuria categorised in CKD (KDIGO A stages)?

    A1: ACR $<3\ mg/mmol$ (normal–mildly increased); A2: ACR $3–30\ mg/mmol$ (moderately increased, 'microalbuminuria'); A3: ACR $>30\ mg/mmol$ (severely increased). Higher albuminuria predicts faster progression and cardiovascular risk.

16. What interventions slow progression of CKD?

    Blood pressure control (target $<130/80$); ACE inhibitor/ARB especially with proteinuria; SGLT2 inhibitors (renoprotective in diabetic and proteinuric CKD); glycaemic control; treat acidosis; avoid nephrotoxins; smoking cessation; lipid lowering.

17. List the major systemic complications of CKD.

    Anaemia (reduced erythropoietin); CKD–mineral bone disorder (renal osteodystrophy); secondary/tertiary hyperparathyroidism; metabolic acidosis; hyperkalaemia; fluid overload/hypertension; accelerated cardiovascular disease; uraemia.

18. Explain the biochemical sequence producing secondary hyperparathyroidism in CKD.

    Reduced GFR → phosphate retention (hyperphosphataemia) and reduced $1\alpha$-hydroxylation of vitamin D (low calcitriol) → hypocalcaemia. High phosphate, low calcium and low calcitriol all stimulate PTH → secondary hyperparathyroidism and renal osteodystrophy. FGF-23 also rises early.

19. How is anaemia of CKD managed, and what must be optimised before starting an ESA?

    Anaemia is normochromic normocytic from EPO deficiency. Optimise/replace iron stores first (target transferrin saturation $>20\%$, ferritin $>100\ \mu g/L$), then use erythropoiesis-stimulating agents (e.g. epoetin/darbepoetin) targeting Hb $100–120\ g/L$ (avoid overcorrection → stroke/thrombosis risk).

20. What is the principle of haemodialysis and what gradient drives solute clearance?

    Blood and dialysate flow countercurrent across a semipermeable membrane. Small solutes (urea, $K^{+}$) move by diffusion down their concentration gradient; fluid is removed by ultrafiltration driven by a transmembrane pressure gradient (convection).

21. What is the principle of peritoneal dialysis (PD) and what acts as the membrane?

    The patient's own peritoneal membrane is the dialysing surface. Hypertonic (glucose-based) dialysate is instilled into the peritoneal cavity; solutes diffuse from blood across the peritoneum and water is removed by osmotic ultrafiltration. Modes: CAPD (manual exchanges) and APD (overnight machine).

22. Compare key complications of haemodialysis versus peritoneal dialysis.

    Haemodialysis: access problems (fistula thrombosis/stenosis, line infection), intradialytic hypotension, disequilibrium syndrome, bleeding. Peritoneal dialysis: PD peritonitis (turbid effluent, abdominal pain), exit-site infection, catheter malfunction, hernias, encapsulating peritoneal sclerosis, hyperglycaemia/weight gain.

23. What organism most commonly causes PD-associated peritonitis and how is the diagnosis made?

    Coagulase-negative staphylococci (e.g. Staphylococcus epidermidis), often skin contamination. Diagnosis: cloudy PD effluent with WCC $>100\ cells/\mu L$ and $>50\%$ neutrophils. Treat with intraperitoneal antibiotics.

24. What HLA loci are matched in renal transplantation, and which donor type gives best graft survival?

    HLA-A, HLA-B and HLA-DR are matched (DR most important). Living-donor (especially HLA-identical) transplants give the best graft survival; pre-transplant crossmatch must exclude preformed donor-specific antibodies.

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