PE20.5 | Acute Renal Failure — Summary & Reflection

KEY TAKEAWAYS

Acute Kidney Injury (AKI) in children — key takehome points:

• Three categories: prerenal (commonest in India — dehydration/sepsis), intrinsic renal (HUS, APSGN, ATN, interstitial nephritis), postrenal (obstruction — PUV in boys).
• HUS critical trap: MAHA + thrombocytopenia + AKI triad following EHEC O157:H7 (Shiga toxin) — antibiotics CONTRAINDICATED as they increase toxin release and worsen renal outcome.
• Staging: KDIGO Stages 1–3 by creatinine rise (×1.5/×2/×3 baseline) and urine output (<0.5 mL/kg/h × 6h / 12h / 24h); pRIFLE is the paediatric eGFR-based staging tool.
• Urine indices: prerenal = urine Na <20, FENa <1%, osmolality >500; intrinsic (ATN) = urine Na >40, FENa >2%, osmolality <350.
• Management: fluid challenge for prerenal (10–20 mL/kg isotonic); fluid restriction once intrinsic established; hyperkalaemia sequence — Ca-gluconate first (cardioprotect) → bicarbonate/salbutamol/glucose-insulin (shift) → resonium/dialysis (remove).
• Dialysis indications (AEIOU): Acidosis, Electrolytes, Intoxication, Overload, Uraemia.
• Prognosis: D+HUS 80% full recovery; APSGN excellent; bilateral cortical necrosis → CKD risk; long-term renal follow-up mandatory for all significant AKI.

REFLECT

Reflect on the hook scenario — the junior resident reaching for an antibiotic in a child with the HUS triad. What knowledge gap created this instinct, and how would you have corrected it in the moment? Consider: when is a seemingly logical action (treat infection with antibiotics) actually harmful, and how does understanding pathophysiology protect against well-intentioned but dangerous management errors? How will you apply this principle of 'mechanism-based contra-intuitive traps' to other paediatric conditions you will encounter in your clinical postings?