IM10.1-3 | AKI Foundations — Summary & Reflection

KEY TAKEAWAYS

Acute kidney injury is defined by the KDIGO 2012 criteria: creatinine rise ≥0.3 mg/dL within 48 h, ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 h. Three KDIGO stages (1–3) stratify severity and predict need for RRT.

The three-category framework is the cornerstone of AKI management:
- Pre-renal (50–70%): inadequate perfusion (volume depletion, low CO, drugs); urine concentrated (FENa <1%, osmolality >500 mOsm/kg); reversible with fluid correction.
- Intrinsic renal: ATN (ischaemic or nephrotoxic — the most common), glomerular (GN, HUS/TTP), interstitial (drug-AIN, infection), vascular; hallmark casts on urinalysis; tubular injury = granular/epithelial cell casts.
- Post-renal (obstructive): hydronephrosis on ultrasound; relieve obstruction promptly; post-obstructive diuresis requires careful fluid replacement.

ATN natural history: initiation → extension → maintenance (oliguric plateau, 1–2 weeks) → recovery (diuretic phase — do not abandon monitoring).

Management priorities: identify and correct cause; stop nephrotoxins; manage hyperkalaemia (calcium gluconate first for membrane stabilisation → insulin+dextrose → remove from body); strict volume balance; dose-adjust renally cleared drugs; nutritional support.

AEIOU indications for dialysis: Acidosis (pH <7.1), Electrolytes (K⁺ refractory), Intoxication (dialysable), Overload (pulmonary oedema), Uraemia (pericarditis, encephalopathy, bleeding).

REFLECT

Consider the two patients from the opening hook — Rajesh (pre-renal AKI from gastroenteritis-dehydration) and Kavitha (nephrotoxic ATN from gentamicin). Both had KDIGO Stage 2–3 AKI, but Rajesh's kidneys had no intrinsic injury and would fully recover within hours of volume restoration, while Kavitha's proximal tubules were damaged and would take weeks to regenerate. Think about how you would explain this difference to a worried family: 'The kidneys are not permanently damaged, but the plumbing that works them needs time to repair.' Now reflect on a preventable harm: every time a patient receives gentamicin without having baseline creatinine checked, or every time a hypotensive patient's creatinine is not monitored daily, the window to prevent ATN closes. What systems or habits would you build into your clinical practice to catch AKI before it becomes established?