IM10.4-8 | CKD Foundations — Summary & Reflection

KEY TAKEAWAYS

CKD definition: abnormalities of kidney structure/function persisting >3 months, with health implications. KDIGO staging combines GFR categories G1–G5 (eGFR ≥90 to <15 mL/min/1.73 m²) and albuminuria categories A1–A3 (<30, 30–300, >300 mg/g ACR) — both dimensions are required for risk stratification and management intensity.

Uraemia is multisystem: GI (nausea, gastritis, fetor), cardiovascular (pericarditis — dialysis indication, LVH, vascular calcification), neurological (encephalopathy, asterixis, peripheral neuropathy), haematological (anaemia, platelet dysfunction causing bleeding tendency), skin (pruritus, pallor).

Proteinuria: glomerular (predominantly albumin — ACR based) vs tubular (low-MW proteins) vs overflow (Bence-Jones, myoglobin). Albuminuria drives tubulointerstitial fibrosis. ACE inhibitors/ARBs reduce proteinuria and slow CKD progression.

Anaemia of CKD: EPO deficiency (peritubular fibroblast loss) + functional iron deficiency (hepcidin). Correct iron first (target ferritin >100, TSAT >20%), then add ESA if Hb <10 g/dL; target Hb 10–11.5 g/dL.

CKD-MBD cascade: ↓GFR → phosphate retention → ↑FGF-23 → ↓calcitriol → ↑PTH (secondary hyperparathyroidism) → osteitis fibrosa cystica + vascular calcification. Manage with phosphate binders, calcitriol/analogues, cinacalcet.

Hypertension and CKD: target <130/80 mmHg; ACE inhibitor/ARB first-line with proteinuria; dual RAAS blockade is contraindicated. Diabetes and CKD: metformin hold at eGFR <30; SGLT-2 inhibitors strongly recommended for renoprotection; HbA1c target 7–7.5%, relaxed to 8% in advanced CKD.

REFLECT

Suresh from the opening hook — eGFR 38, ACR in the A2 range, hypertension, rising PTH, low Hb — is at a decision crossroads. Without intervention, he will likely reach dialysis within 5–10 years, and before that he will suffer a major cardiovascular event. With aggressive treatment today — RAAS blockade, an SGLT-2 inhibitor, blood pressure control, phosphate management, and iron repletion — his trajectory can be substantially altered. Think about what information he needs to understand his condition: not the full pathophysiology lecture, but a framing that empowers him. How would you explain why his kidneys are slowly losing function, why the protein in his urine matters, and why taking his medications even when he feels well is the most important thing he can do? The science of CKD management means little if it cannot be translated into a conversation that motivates a patient to engage with his own care.