PE20.6 | Chronic Renal Failure — Summary & Reflection

KEY TAKEAWAYS

Chronic Kidney Disease in children — key takehome points:

• Paediatric CKD differs from adult CKD: ~50% is CAKUT (structural/congenital, esp. PUV + reflux nephropathy); glomerular causes (FSGS, lupus, Alport) and hereditary metabolic causes make up the rest; diabetes/hypertension are rare causes in children.
• KDIGO staging: G1–G5 by eGFR (Bedside Schwartz formula), plus A1–A3 albuminuria. CKD defined as eGFR <60 or kidney damage marker for ≥3 months. RRT typically at eGFR <10–15.
• Major complications: anaemia (EPO deficiency) → ESA + iron; renal osteodystrophy (low 1,25(OH)2D3 + phosphate retention) → phosphate binders + active vitamin D (alfacalcidol); growth failure → optimise nutrition + correct acidosis + rhGH; hypertension/proteinuria → ACE inhibitor/ARB (first-line, slows progression).
• ESA target Hb: 10–12 g/dL; correct iron stores FIRST before starting ESA.
• Active vitamin D, NOT native cholecalciferol: the failing kidney cannot 1α-hydroxylate — prescribe alfacalcidol or calcitriol.
• Transplantation = treatment of choice: pre-emptive preferred; start planning by G4; living related donor optimal.
• Alport syndrome trap: X-linked, boys more severe, haematuria + proteinuria + sensorineural hearing loss — genetic testing + audiogram.

REFLECT

Reflect on the hook scenario: a 9-year-old with short stature and pallor who turns out to have advanced CKD from a structural cause. What systems and conditions allowed this child to reach this stage undetected? Consider: what screening opportunities exist in India (school health checks, antenatal ultrasound for CAKUT, routine urinalysis in children with recurrent UTIs) and how might earlier detection have changed her trajectory? As a future clinician, what practice change would you implement based on this case?