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Renal & Urology Topic Index — every topic, tiered: Core · Important · Rare
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Chronic Kidney Disease

CKD: diagnosis & stagingCoretap to open ▾
CKD = eGFR and/or ACR abnormality persisting ≥3 months. Stage by G (eGFR: G1≥90, G2 60–89, G3a 45–59, G3b 30–44, G4 15–29, G5<15) AND A (ACR: A1<3, A2 3–30, A3>30). G1/G2 need markers of damage to diagnose.
Two axes: G (eGFR category) + A (albumin:creatinine ratio) — e.g. G3aA2.
Persistence: Changes must persist ≥3 months (repeat, don’t diagnose on one reading).
G1/G2: Need evidence of kidney damage (e.g. ACR ≥3, haematuria, structural) to call it CKD.
eGFR variables (CAGE): Creatinine, Age, Gender, Ethnicity; affected by pregnancy, muscle mass, recent red meat.
A 76-year-old woman has an eGFR of 45 and an ACR of 87, stable over 3 months. What is her CKD classification?
  • AG2A1
  • BG3aA3
  • CG3bA2
  • DG4A3
  • EG1A2
Correct: B — G3aA3
Why: eGFR 45 is G3a and ACR 87 is A3 (>30), so she is G3aA3.
Options:
  • eGFR too high.
  • (correct)
  • Wrong on both.
  • eGFR too low.
  • Wrong.
  • .
CKD: referral to nephrologyCoretap to open ▾
Refer if: ACR ≥70 (unless known diabetic nephropathy); ACR ≥30 with persistent haematuria; eGFR fall ≥25% + category change, or ≥15 in a year; eGFR <30; resistant hypertension; suspected renal artery stenosis; ADPKD.
ACR-based: ≥70 (unless diabetic nephropathy); ≥30 with persistent haematuria (2/3 dips, UTI excluded).
eGFR-based: Sustained fall ≥25% with category change, or ≥15 mL/min in 12 months; or eGFR <30.
Other: Resistant hypertension (≥4 drugs), suspected renal artery stenosis, ADPKD.
Which finding should prompt referral to a nephrologist?
  • AACR 20 with no other issue
  • BACR ≥70 mg/mmol
  • CStable eGFR 55
  • DIsolated eGFR 62
  • EACR 5 in a non-diabetic
Correct: B — ACR ≥70 mg/mmol
Why: An ACR of 70 mg/mmol or more warrants nephrology referral (unless it is known, managed diabetic nephropathy).
Options:
  • Below threshold.
  • (correct)
  • G3a stable — monitor.
  • Normal-ish, monitor.
  • Not significant.
CKD: management & monitoringCoretap to open ▾
Optimise BP (<140/90; <130/80 if ACR≥70 or diabetic), offer an ACE inhibitor/ARB if ACR≥30+HTN (or ≥70 regardless, or ≥3 + diabetes), a statin for all, SGLT2 inhibitor where indicated; annual U&E/ACR, vaccines, avoid nephrotoxics.
BP/ACEi: ACEi or ARB if ACR ≥70, or ≥30 with hypertension, or ≥3 with diabetes.
Targets: <140/90 generally; <130/80 if ACR ≥70 or diabetic.
Everyone: Statin (document QRISK); SGLT2 inhibitor slows progression in proteinuric/diabetic CKD; vaccines.
Monitor: At least annual eGFR + ACR; more often in advanced/declining CKD.
A diabetic with CKD has an ACR of 10 mg/mmol and normal blood pressure. Should you start an ACE inhibitor?
  • ANo — BP is normal
  • BYes — ACR ≥3 in a diabetic warrants an ACE inhibitor/ARB
  • COnly if ACR ≥30
  • DOnly if hypertensive
  • ENever in CKD
Correct: B — Yes — ACR ≥3 in a diabetic warrants an ACE inhibitor/ARB
Why: In diabetics, an ACR of 3 or more is significant and warrants an ACE inhibitor/ARB for renoprotection regardless of blood pressure.
Options:
  • Renoprotection is the aim.
  • (correct)
  • Threshold is lower in diabetes.
  • Not required.
  • They are indicated.
Anaemia of CKDImportanttap to open ▾
Normocytic normochromic anaemia, mainly from reduced erythropoietin; becomes apparent around eGFR <35. Target Hb 100–120 g/L. Correct iron first, then consider erythropoiesis-stimulating agents.
Mechanism: ↓Erythropoietin; also reduced iron absorption, blood loss, shortened cell survival.
Type: Normocytic, normochromic; appears as eGFR falls below ~35.
Manage: Optimise iron; ESAs to a target Hb 100–120 g/L (not higher — cardiovascular risk).
A patient with stage 4 CKD has a normocytic anaemia. What is the main underlying cause?
  • AIron deficiency
  • BReduced erythropoietin production
  • CB12 deficiency
  • DHaemolysis
  • EMarrow infiltration
Correct: B — Reduced erythropoietin production
Why: Anaemia of CKD is chiefly due to reduced renal erythropoietin, producing a normocytic normochromic picture.
Options:
  • Contributory, not main.
  • (correct)
  • Would be macrocytic.
  • Not the main cause.
  • Not typical.
CKD-mineral bone diseaseRare · recognise
Low active vitamin D and phosphate retention → low calcium, high phosphate, high PTH (secondary hyperparathyroidism) and high ALP. Treat with phosphate binders (e.g. sevelamer) and activated vitamin D.
Polycystic kidney disease (ADPKD)Rare · recognise
Autosomal dominant (PKD1 chr16 85%, PKD2 chr4). Hypertension (ACE inhibitor first-line), berry aneurysms (SAH), liver cysts. Ultrasound screens; tolvaptan may slow progression; refer to nephrology.

Acute Kidney Injury & Electrolytes

Acute kidney injuryCoretap to open ▾
Rise in creatinine ≥26 µmol/L in 48 h, or ≥50% in 7 days, or urine output <0.5 mL/kg/h for 6 h. Pre-renal (hypovolaemia), renal (ATN, glomerular), post-renal (obstruction). Stop nephrotoxics; treat cause. Urgent referral if K⁺>7, malignant HTN, nephrotic, or acute renal failure.
Definition: Creatinine ↑≥26 µmol/L in 48 h, or ↑≥50% in 7 days, or oliguria <0.5 mL/kg/h for 6 h.
Causes: Pre-renal (dehydration, sepsis), renal (ATN, glomerulonephritis), post-renal (obstruction — scan the bladder).
Manage: Stop nephrotoxics/‘sick-day’ drugs; assess fluids; treat the cause; monitor potassium.
Urgent referral: K⁺>7, malignant hypertension, suspected intrinsic renal disease, or complications.
A dehydrated patient on ramipril, furosemide and ibuprofen has a rising creatinine. Which immediate action is most important?
  • AIncrease furosemide
  • BStop the nephrotoxic drugs and assess fluid status
  • CStart dialysis
  • DGive potassium
  • ERestrict all fluids
Correct: B — Stop the nephrotoxic drugs and assess fluid status
Why: AKI management starts with stopping nephrotoxics (the ‘triple whammy’ of ACEi + diuretic + NSAID here) and correcting volume status.
Options:
  • Worsens pre-renal AKI.
  • (correct)
  • Rarely first step.
  • Risks hyperkalaemia.
  • May worsen pre-renal AKI.
HyperkalaemiaImportanttap to open ▾
K⁺ ≥6.5 (or ECG changes) is an emergency. ECG: peaked T waves → wide QRS → sine wave. Treat: IV calcium gluconate (cardioprotection), then insulin-dextrose ± salbutamol (shift), then address cause/removal.
Severity: ≥6.5, or any ECG change, is a medical emergency.
ECG: Tall tented T waves → prolonged PR → widened QRS → sine wave → arrest.
Treat: Calcium gluconate first (protects the heart); insulin + dextrose (± nebulised salbutamol) to shift K⁺; treat the cause.
A patient has a potassium of 6.9 with peaked T waves on ECG. What is the first drug to give?
  • AInsulin with dextrose
  • BIV calcium gluconate
  • CSalbutamol nebuliser
  • DCalcium resonium
  • EFurosemide
Correct: B — IV calcium gluconate
Why: IV calcium gluconate is given first to stabilise the myocardium; insulin-dextrose and salbutamol then shift potassium intracellularly.
Options:
  • Second step (shift).
  • (correct)
  • Adjunct shift.
  • Slow, for removal.
  • Not acute treatment.
SIADHImportanttap to open ▾
Euvolaemic hyponatraemia: low serum osmolality (<275), inappropriately high urine osmolality (>100) and high urine sodium (>40). Causes: CNS (stroke/trauma), drugs (carbamazepine, SSRIs), lung (pneumonia, small-cell cancer). Treat fluid restriction; hypertonic saline only if severe.
Biochemistry: Low serum osmolality, urine osmolality >100, urine Na >40, euvolaemic.
Causes: CNS, drugs (SSRIs, carbamazepine), pulmonary (pneumonia, small-cell lung cancer), pain/nausea.
Treat: Fluid restriction ± salt/tolvaptan; hypertonic 3% saline only for severe symptomatic hyponatraemia.
An elderly man on sertraline is confused with a sodium of 121; he is euvolaemic with concentrated urine and high urine sodium. Diagnosis?
  • ADehydration
  • BSIADH
  • CDiabetes insipidus
  • DAddison’s
  • ECerebral salt wasting
Correct: B — SIADH
Why: Euvolaemic hyponatraemia with concentrated urine and high urine sodium is SIADH; SSRIs are a common cause.
Options:
  • Would be hypovolaemic.
  • (correct)
  • Causes hypernatraemia/dilute urine.
  • Hypovolaemic.
  • Hypovolaemic with Na loss.
Diabetes insipidusRare · recognise
Deficient ADH (cranial) or renal resistance (nephrogenic) → large volumes of dilute urine, hypernatraemia. Water-deprivation test; desmopressin for cranial DI.
Cerebral salt wastingRare · recognise
Hyponatraemia with true volume depletion following CNS injury (natriuresis); distinguished from SIADH by hypovolaemia — treat with salt and volume replacement.

Stones, UTI & Haematuria

Renal & ureteric stonesCoretap to open ▾
Loin-to-groin colicky pain + haematuria. First-line analgesia: an NSAID by any route (IM diclofenac / oral naproxen); IV paracetamol second-line. Imaging: low-dose non-contrast CT-KUB within 24 hours (ultrasound in pregnancy). <5 mm usually pass; MET (tamsulosin) for distal stones <10 mm.
Pain: NSAID first-line by any route; IV paracetamol second-line; opioids only if these fail.
Imaging: Low-dose non-contrast CT-KUB within 24 hours; ultrasound in pregnancy/children.
Manage: <5 mm usually pass spontaneously; MET with an alpha-blocker for distal ureteric stones <10 mm.
Intervention: Shock-wave lithotripsy or ureteroscopy; PCNL for large/staghorn stones; admit if obstructed+infected (emergency).
A 36-year-old has acute loin-to-groin pain with microscopic haematuria. What is first-line analgesia?
  • AIV morphine
  • BAn NSAID (e.g. IM diclofenac or oral naproxen)
  • CParacetamol
  • DCodeine
  • EBuscopan
Correct: B — An NSAID (e.g. IM diclofenac or oral naproxen)
Why: NICE recommends an NSAID by any route as first-line analgesia for renal colic; IV paracetamol is second-line and opioids are reserved.
Options:
  • Opioids are reserved.
  • (correct)
  • Second-line.
  • Opioid, not first.
  • Antispasmodics not advised.
Urinary tract infectionCoretap to open ▾
Dipstick: nitrites + leucocytes → treat and send MSU if needed. First-line: nitrofurantoin (avoid if eGFR<45) or trimethoprim; men treated 7 days (consider prostatitis). Send MSU in men, pregnancy, treatment failure, recurrent or systemic features.
Dipstick: Nitrites are the more specific marker; leucocytes support infection.
First-line: Nitrofurantoin (avoid eGFR<45; not at all <30) or trimethoprim.
Men: Treat for 7 days; consider prostatitis; send MSU.
Always MSU: Men, pregnancy, recurrent, treatment failure, systemic illness.
A man has dysuria with positive nitrites and leucocytes. How long should he be treated and what else should you do?
  • A3 days, no MSU
  • B7 days and send an MSU
  • CSingle dose
  • DNo antibiotic
  • E5 days topical
Correct: B — 7 days and send an MSU
Why: Male UTIs are treated for 7 days (consider prostatitis) and an MSU is sent, as infection in men is regarded as complicated.
Options:
  • Too short; MSU needed.
  • (correct)
  • Insufficient in men.
  • Symptomatic — treat.
  • Not a topical condition.
Haematuria: referral rulesCoretap to open ▾
Visible haematuria ≥45 → 2-week-wait (bladder/renal cancer). Non-visible ≥60 with dysuria or raised WCC → 2-week-wait. Confirm persistence (2 of 3 dips), exclude transient causes and UTI. Nephrology if haematuria + proteinuria/declining eGFR; urology for isolated visible haematuria.
Urology 2WW: Visible haematuria ≥45; non-visible ≥60 with dysuria or raised white cells.
Confirm: Exclude UTI, menstruation, exercise, beetroot/rifampicin; persistent = 2 of 3 dips positive.
Nephrology vs urology: Haematuria + proteinuria/declining eGFR → nephrology; isolated visible haematuria → urology.
A 50-year-old man has painless visible haematuria and no infection. Appropriate referral?
  • ARoutine urology
  • BUrgent 2-week-wait urology referral
  • CNephrology routine
  • DReassure
  • ERepeat in 6 months
Correct: B — Urgent 2-week-wait urology referral
Why: Unexplained visible haematuria at 45 or over triggers an urgent suspected-cancer (2-week-wait) urology referral.
Options:
  • Too slow.
  • (correct)
  • Urology for visible haematuria.
  • Needs investigation.
  • Delays diagnosis.
Bladder cancerRare · recognise
Painless visible haematuria is classic; risk factors smoking and aromatic amines. Refer per haematuria rules; flexible cystoscopy is diagnostic; most are transitional-cell carcinoma.
Catheter problemsRare · recognise
Bypassing usually = bladder spasm (re-catheterise/reassess size, not antibiotics). Blocked catheter → flush/replace. Avoid treating asymptomatic bacteriuria in catheterised patients.

Glomerular Disease

Nephrotic vs nephritic syndromeCoretap to open ▾
Nephrotic: heavy proteinuria (>3 g), hypoalbuminaemia, oedema (normal BP/eGFR often) — e.g. minimal change, membranous. Nephritic: haematuria, hypertension, oliguria, some proteinuria — e.g. post-strep, IgA. Quantify with protein:creatinine ratio (or 24-h protein).
Nephrotic: Proteinuria >3 g, low albumin, oedema; complications from urinary protein loss (VTE, infection).
Nephritic: Haematuria, hypertension, reduced eGFR, mild–moderate proteinuria.
Quantify: 24-hour protein or protein:creatinine ratio (heavy proteinuria under-represented by ACR).
A man has periorbital and leg oedema, a very low albumin and heavy proteinuria with a normal blood pressure. Which syndrome?
  • ANephritic syndrome
  • BNephrotic syndrome
  • CAcute tubular necrosis
  • DPrerenal AKI
  • EUTI
Correct: B — Nephrotic syndrome
Why: Heavy proteinuria with hypoalbuminaemia and oedema is nephrotic syndrome; normal BP/eGFR is common early.
Options:
  • Nephritic has haematuria/HTN.
  • (correct)
  • Different picture.
  • Different.
  • Different.
IgA nephropathy vs post-streptococcal GNImportanttap to open ▾
IgA nephropathy: visible haematuria 1–2 DAYS after an URTI (synpharyngitic), normal complement. Post-streptococcal GN: haematuria/oedema 1–2 WEEKS after a sore throat/skin infection, low complement.
IgA nephropathy: Haematuria within 1–2 days of an URTI; normal complement; commonest GN worldwide.
Post-strep GN: Haematuria, oedema, hypertension 1–2 weeks after streptococcal infection; low C3.
Key discriminator: Timing (days vs weeks) and complement (normal vs low).
A young man has visible haematuria appearing one day into a sore throat, with normal complement levels. Most likely diagnosis?
  • APost-streptococcal glomerulonephritis
  • BIgA nephropathy
  • CMinimal change disease
  • DMembranous nephropathy
  • EGoodpasture’s
Correct: B — IgA nephropathy
Why: Haematuria synchronous with (1–2 days into) an URTI with normal complement is IgA nephropathy; post-strep GN occurs 1–2 weeks later with low complement.
Options:
  • That’s 1–2 weeks later, low C3.
  • (correct)
  • Nephrotic, no haematuria link.
  • Nephrotic.
  • Pulmonary-renal.
Minimal change diseaseRare · recognise
Commonest nephrotic syndrome in children; normal BP; responds to steroids (cyclophosphamide if relapsing).
Membranous nephropathyRare · recognise
Common adult nephrotic cause; associations malignancy, hepatitis B, SLE, NSAIDs/penicillamine; anti-PLA2R antibodies.
Henoch-Schönlein purpuraRare · recognise
IgA vasculitis: purpuric rash (buttocks/legs), abdominal pain, arthralgia, haematuria; usually post-viral in children; supportive/analgesia; monitor renal function.
Rapidly progressive (crescentic) GNRare · recognise
Goodpasture’s (anti-GBM, haemoptysis+haematuria), granulomatosis with polyangiitis (c-ANCA, sinusitis+haemoptysis+renal). Urgent nephrology; immunosuppression.
Alport syndromeRare · recognise
Hereditary nephritis with sensorineural deafness (and eye signs); X-linked; progresses to renal failure.
Haemolytic uraemic syndromeRare · recognise
Triad: microangiopathic haemolytic anaemia, AKI, thrombocytopenia; child with bloody diarrhoea (E. coli O157). Supportive; avoid antibiotics.
Nephroblastoma (Wilms tumour)Rare · recognise
Commonest childhood renal tumour; presents as an abdominal mass in a young child; associated with Beckwith-Wiedemann (macroglossia, omphalocele — check glucose).

Drugs & the Kidney

Nephrotoxic & renally-cleared drugsCoretap to open ▾
Avoid/adjust in renal impairment: NSAIDs (avoid if eGFR falling), metformin (stop <30, review <45; hold around IV contrast), nitrofurantoin (avoid <45, not at all <30), lithium (avoid <30), dabigatran (<30), doxycycline avoid in renal failure. Hold ‘sick-day’ drugs in dehydration.
Metformin: Stop if creatinine >150 or eGFR <30; review if creatinine >130 / eGFR <45; hold for IV contrast, restart after 48 h.
Nitrofurantoin: Avoid/short-course if eGFR <45; do not use if <30.
Others: Lithium and dabigatran avoid if eGFR<30; avoid NSAIDs when eGFR falling.
Sick-day rules: Hold ACEi/ARB, diuretics, metformin, NSAIDs during acute dehydrating illness.
A patient with an eGFR of 38 needs treatment for a lower UTI. Which antibiotic should be avoided?
  • ATrimethoprim
  • BNitrofurantoin
  • CAmoxicillin
  • DPivmecillinam
  • ECefalexin
Correct: B — Nitrofurantoin
Why: Nitrofurantoin should be avoided (or only short-course) when eGFR is below 45, and not used at all below 30, as it becomes ineffective and more toxic.
Options:
  • Usable with monitoring.
  • (correct)
  • Usable.
  • Usable.
  • Usable.
ACE inhibitors & the kidneyImportanttap to open ▾
Check U&E before and 1–2 weeks after starting/uptitration. A creatinine rise up to 30% (or eGFR fall up to 25%) is acceptable; beyond that, or K⁺ ≥6, stop. A big early rise suggests bilateral renal artery stenosis.
Monitor: U&E before and 1–2 weeks after starting or dose change.
Acceptable: Creatinine ↑ up to 30% / eGFR ↓ up to 25% is tolerated.
Stop: Creatinine ↑>30%, eGFR ↓>25%, or K⁺ ≥6.
Big rise: Marked early deterioration → suspect bilateral renal artery stenosis.
Two weeks after starting ramipril, creatinine has risen 20% and potassium is 5.1. What should you do?
  • AStop the ramipril
  • BContinue and recheck as this is acceptable
  • CHalve the dose urgently
  • DAdd spironolactone
  • ERefer urgently
Correct: B — Continue and recheck as this is acceptable
Why: A creatinine rise up to 30% and potassium below 5.5 are acceptable after starting an ACE inhibitor — continue and monitor.
Options:
  • Not yet indicated.
  • (correct)
  • Not needed.
  • Raises potassium.
  • Not yet.