Preparatory Mindset
Acute kidney injury (AKI) and chronic kidney disease (CKD) are two sides of the same nephrology core: AKI = abrupt (hours–days) decline in GFR, CKD = progressive, irreversible decline (months–years) (16CM exam tested). The exam skills for AKI: (1) classify the three categories — pre-renal (hypoperfusion), intra-renal (direct damage, ATN most common), post-renal (obstruction) — and use the BUN:Cr ratio + FeNa to separate pre-renal from ATN (the single most-tested AKI point); (2) know the urgent dialysis indications (refractory hyperkalaemia, refractory acidosis, refractory pulmonary oedema, uraemic pericarditis/encephalopathy). For CKD: GFR staging 1–5, the complications ladder (anaemia ↓EPO, renal osteodystrophy ↓vit D/↑PTH, metabolic acidosis, hyperkalaemia, uremia), and SGLT2i + BP <130/80 + renin-angiotensin blockade as modern disease-modifying therapy (17CM exam tested). The HKHA renal-failure section (K 22–24) is LMCHK-critical — it gives the exact fluid/electrolyte/dialysis management.
Core Concepts
AKI — definition & epidemiology
- AKI = abrupt (within 48 h) decline in kidney function: absolute ↑ in serum Cr ≥0.3 mg/dL (26.4 μmol/L) from baseline, OR a ≥50% percentage increase; manifested by ↑Cr and ↑BUN, ↓urine output.
- Normal GFR ~120 mL/min/1.73 m²; only ~20% of nephrons work at a time; ~210 L/day filtered, ~2 L/day urine.
- Epidemiology: ~5–10% of hospitalised patients; ~70% of critically ill; 5–6% of ICU patients require RRT.
- Categories: pre-renal ~85%, intra-renal ~5%, post-renal ~10%; ATN = 85% of intra-renal (intrinsic) AKI.
Classification of AKI
| Category | Mechanism | Causes | Key labs |
|---|---|---|---|
| Pre-renal | ↓ renal perfusion (functional, reversible) | Dehydration, haemorrhage, heart failure, sepsis, cirrhosis, NSAIDs | BUN:Cr >20:1, FeNa <1%, urine osmolality >500 |
| Intra-renal (intrinsic) | Direct kidney damage | ATN (most common — ischaemic or nephrotoxic: aminoglycosides, contrast, rhabdomyolysis), acute interstitial nephritis (drugs), rapidly progressive GN (vasculitis, anti-GBM), acute tubular interstitial disease | BUN:Cr <15:1, FeNa >2%, muddy brown casts (ATN), RBC casts/dysmorphic RBC (GN), eosinophiluria (AIN) |
| Post-renal | Urinary obstruction | Stones, BPH/prostate, tumour, urethral obstruction, blocked catheter | Hydronephrosis on USG, anuria/oliguria |
ATN clinical course: oliguric phase → diuretic phase → recovery phase (weeks–months). Severity staging: RIFLE / AKIN / KDIGO criteria (by Cr rise and urine output).
AKI — clinical & diagnosis
- History (esp. drug history — NSAIDs, aminoglycosides, contrast), volume status, urine output.
- Exclude pre-renal: orthostatic hypotension; exclude post-renal: feel for bladder, bedside USG (hydronephrosis).
- Investigations (HKHA list): CBP, R/LFT, CO₂, Cl, Ca, PO₄, urate, CK, ABG; FeNa / FE urea for pre-renal; urine — MSU microscopy/culture, casts, dysmorphic RBC, eosinophils, spot protein:Cr; autoimmune markers (ANA, anti-dsDNA, ANCA, anti-GBM, C3/4, cryoglobulin), serum/urine electrophoresis + free light chains (myeloma), HBsAg/anti-HCV/HIV; CXR, ECG, KUB, renal USG.
- Classic exam vignette: post-op/contrast/septic patient with K 6.5, urea 24.3, Cr 889 μmol/L, Na 130 → AKI + hyperkalaemia → urgent dialysis assessment.
AKI — treatment
- Hypovolaemia → fluid challenge: NS or balanced crystalloid (Plasma-Lyte) 500–1000 mL over 1–2 h (optimise preload). - Fluid overload → frusemide up to 80 mg IV bolus or 10 mg/hr infusion; add metolazone 5–10 mg PO if refractory. Low-dose dopamine NOT recommended.
- Assess fluid status: fluid intake = 500 mL + urine output (+ ongoing losses).
- Correct electrolytes: hyperkalaemia (calcium gluconate stabilises membrane, insulin+glucose, β-agonist, bicarbonate if acidotic, resonium/sodium zirconium cyclosilicate, dialysis if refractory), hypocalcaemia, hyperphosphataemia, metabolic acidosis.
- Diet: low salt (<100 mmol/day), low K (<20 mmol/day), low phosphate (<800 mg/day); strict I/O chart; daily body weight (<1 kg gain/day).
- Avoid nephrotoxins (NSAIDs, aminoglycosides); consider alternatives to radiocontrast.
- Urgent dialysis indications (memorise): refractory hyperkalaemia; refractory metabolic acidosis (where bicarbonate contraindicated); refractory pulmonary oedema/fluid overload; uraemic pericarditis or encephalopathy (also severe uraemia, drug intoxication).
- Treat underlying disease; relieve obstruction; renal biopsy if cause not apparent.
CKD — definition, stages & complications
- Anaemia: ↓ erythropoietin → fatigue; treat with EPO-stimulating agent (darbepoetin, Mircera) + iron repletion + transfusion if symptomatic. - Renal osteodystrophy: ↓vitamin D activation → hypocalcaemia → ↑PTH → bone disease; treat — low-PO₄ diet, phosphate binders with meals, activated vitamin D (Rocaltrol/alfacalcidol 0.25–2 μg/day, paricalcitol), calcimimetics (cinacalcet), correct calcium. - Metabolic acidosis: correct with NaHCO₃. - Hyperkalaemia: diet + resonium/sodium zirconium cyclosilicate. - Hypertension: target <130/80 mmHg — long-acting CCB, ACEi/ARB, diuretic, β-blocker, MRA (monitor K⁺ with ACEi/ARB/MRA). - Uremia: nausea, pruritus, pericarditis, encephalopathy → dialysis. - Cardiovascular: CAD/LVH (leading cause of death), dyslipidaemia, fluid overload.
- CKD = progressive, irreversible decline in GFR over months–years; leading causes: diabetes (No. 1), hypertension, glomerulonephritis (also polycystic kidney disease, obstructive nephropathy).
- GFR staging (KDIGO): Stage 1 ≥90 (normal, with kidney damage), 2 = 60–89 (mild), 3 = 30–59 (moderate), 4 = 15–29 (severe), 5 <15 = ESRD (dialysis/transplant).
- Complications ladder:
- Disease-modifying therapy (HKHA/KDIGO 2022): SGLT2i in CKD (continue once started unless intolerant or RRT commenced); ACEi/ARB for proteinuric CKD; glycaemic and BP control; smoking cessation.
- ESRD management: consult nephrologist for RRT (haemodialysis, CAPD, transplant); avoid blood-taking/BP measurement from AV fistula arm; monitor fistula/exit site daily; renal diet (low PO₄, high biological-value protein); fluid restriction; manage Ca/phosphate; dialysis indications — uraemia, refractory hyperkalaemia/acidosis/fluid overload.
HKHA Handbook (LMCHK) — Key Points
- Causes checklists (K 22): pre-renal — hypotension/effective volume depletion (dehydration, cirrhosis, CHF, sepsis, third-spacing); post-renal — obstruction (stones, urethral obstruction, BPH); renal — RPGN, vasculitis, ATN, tubulointerstitial nephritis. Careful drug history; exclude pre-renal with orthostatic BP, post-renal with bladder exam + bedside USG.
- AKI treatment (K 23): fluid = 500 mL + urine output; hypovolaemia → NS/Plasma-Lyte 500–1000 mL over 1–2 h; overload → frusemide up to 80 mg IV bolus or 10 mg/h infusion (add metolazone if refractory); no low-dose dopamine; low salt/K/phosphate diet; avoid nephrotoxins; urgent dialysis: refractory hyperkalaemia, refractory metabolic acidosis (bicarbonate contraindicated), refractory pulmonary oedema, uraemic pericarditis/encephalopathy; renal biopsy if cause unclear.
- CKD/ESKD (K 23–24): nephrology consult for RRT feasibility; protect AV fistula; renal diet; BP <130/80 (CCB, ACEi/ARB, diuretic, β-blocker, MRA — monitor K⁺); correct acidosis with NaHCO₃; SGLT2i per KDIGO 2022; phosphate binders + activated vitamin D + calcimimetics; anaemia → ESA + iron; hyperkalaemia → resonium/SZC.
- UTI (In 9): uncomplicated cystitis — analgesics + fluids, empirical 7-day therapy (amoxicillin-clavulanate or nitrofurantoin — avoid nitrofurantoin if CrCl <30; FDA warns against fluoroquinolones for uncomplicated cystitis); pyelonephritis — prompt effective IV antibiotics (amoxicillin-clavulanate, piperacillin-tazobactam if Pseudomonas, meropenem for severe/deteriorating), complete 14-day course; do not treat asymptomatic bacteriuria except in pregnancy and pre-invasive urological procedures.
High-Yield Points
- AKI: Cr ↑ ≥0.3 mg/dL (26.4 μmol/L) within 48 h, or ≥50% rise.
- Pre-renal: BUN:Cr >20, FeNa <1%; ATN: BUN:Cr <15, FeNa >2%, muddy brown casts; post-renal: hydronephrosis.
- ATN = 85% of intrinsic AKI; phases: oliguric → diuretic → recovery.
- Urgent dialysis: refractory hyperkalaemia / acidosis / pulmonary oedema / uraemic pericarditis or encephalopathy.
- CKD stages: 1 ≥90 … 5 <15 (ESRD); diabetes + hypertension = leading causes.
- Complications: anaemia (EPO), osteodystrophy (↓vit D → ↑PTH), acidosis, hyperkalaemia, uraemia.
- SGLT2i + ACEi/ARB + BP <130/80 = modern CKD therapy; K⁺ monitoring with RAAS blockade.
- Treat asymptomatic bacteriuria only in pregnancy / pre-urological procedure.
Topic Summary
AKI is an abrupt decline in GFR classified pre-renal (85% — BUN:Cr >20, FeNa <1%), intra-renal (ATN most common — BUN:Cr <15, FeNa >2%, muddy brown casts) and post-renal (obstruction — hydronephrosis). Management is fluid-status-driven (challenge with crystalloid for hypovolaemia, frusemide for overload), electrolyte correction (hyperkalaemia first), nephrotoxin avoidance, and urgent dialysis for refractory hyperkalaemia/acidosis/pulmonary oedema/uraemia. CKD is progressive, staged by GFR, driven by diabetes and hypertension, and managed with RAAS blockade + SGLT2i, BP <130/80, and the complication ladder (anaemia, osteodystrophy, acidosis, hyperkalaemia), culminating in RRT — the HKHA renal-failure guidance being LMCHK-critical.