ICU · Renal and metabolic

Acute kidney injury: KDIGO staging, prevention, biomarkers, and RRT timing

Also known as AKI · Acute kidney injury · KDIGO · Acute renal failure

Acute kidney injury (AKI) = abrupt reduction in kidney function (hours-days) → accumulation of nitrogenous waste (urea, creatinine) + inability to regulate fluid/electrolyte/acid-base. KDIGO STAGING (2012): Stage 1 (creatinine ≥26.5 μmol/L in 48h OR 1.5-1.9x baseline; urine <0.5 mL/kg/hr for 6-12h). Stage 2 (creatinine 2-2.9x baseline; urine <0.5 for ≥12h). Stage 3 (creatinine ≥3x OR ≥354 μmol/L OR RRT; urine <0.3 for ≥24h OR anuria ≥12h). CAUSES: PRE-renal (hypovolaemia, shock — most common — reduced perfusion), INTRA-renal (ATN from ischaemia/toxins — most common intrinsic; AIN from drugs; GN; interstitial nephritis), POST-renal (obstruction — catheter to exclude). PREVENTION (the mainstay — NO proven TREATMENT for established AKI): (1) AVOID nephrotoxins (NSAIDs, aminoglycosides, contrast, ACEi/ARB if hypoperfused). (2) OPTIMISE PERFUSION (fluids if hypovolaemic — goal-directed; vasopressors if vasodilated). (3) MONITOR (creatinine + urine output daily in ICU). BIOMARKERS: NGAL, TIMP-2•IGFBP7 (NephroCheck — predict AKI within 12-24h — before creatinine rises — emerging). RRT TIMING: AKIKI + STARRT-AKI — NO mortality benefit of EARLY RRT (wait for clinical indications: AEIOU). MORTALITY: Stage 1 10%, Stage 2 20%, Stage 3 40-50%. AKI → CKD in 10-30% of severe AKI survivors.

Checked against its sources on 14 Oct 2026