CKD_in_Pediatrics_Elaborated by Dr Vinod

CKD in children, etiology, evaluation and management

1. Chronic Kidney Disease in Pediatrics Dr. Himanshu Dave Department of Pediatrics NRCH, New Delhi

2. Definition (NKF KDOQI) Chronic Kidney Disease (CKD) in children is defined by: 1. Kidney damage ≥3 months: - Structural/functional abnormalities - Abnormal urine/blood composition - Abnormal imaging or biopsy findings 2. GFR <60 mL/min/1.73m² for ≥3 months: - With or without evidence of kidney damage.

3. Stages of CKD Stage 1: Kidney damage, normal/increased GFR ≥90 Stage 2: Kidney damage, mild ↓ GFR (60–89) Stage 3: Moderate ↓ GFR (30–59) Stage 4: Severe ↓ GFR (15–29) Stage 5: Kidney failure <15 or dialysis 👉 Staging helps in prognosis, management, and transplantation planning.

4. Epidemiology • Prevalence: 18 per 1 million children. • ESRD carries 30-fold ↑ mortality vs peers. • Cardiovascular & infections → leading causes of death. • CKD children have growth, neurocognitive & psychosocial impact.

5. Etiology by Age < 5 years: - Congenital anomalies of kidney & urinary tract (CAKUT) - Hypoplasia, dysplasia, obstructive uropathy > 5 years: - Acquired/inherited GN - Immune-mediated diseases

6. Nonglomerular Causes • Renal dysplasia, hypoplasia, aplasia • Obstructive uropathy (PUV, neurogenic bladder) • Cystinosis, Nephronophthisis • ARPKD, ADPKD • Reflux nephropathy • Eagle-Barrett syndrome • Tumors (Wilms)

7. Glomerular Causes • Chronic GN, FSGS • Congenital nephrotic syndrome • HUS, HSP nephritis • IgA nephropathy, MPGN, Membranous nephropathy • Alport syndrome, SLE, Wegener • Sickle cell nephropathy

8. Pathogenesis A) Hyperfiltration injury: Compensatory ↑ GFR in remaining nephrons → sclerosis. B) Proteinuria: Tubular toxicity, macrophage recruitment, fibrosis. C) Hypertension: Arteriolar nephrosclerosis + worsens hyperfiltration. D) Hyperphosphatemia: Ca-P deposition in kidney/vessels. E) Hyperlipidemia: Oxidative injury to glomeruli. ➡ Final common pathway: Tubulointerstitial fibrosis.

9. Pathophysiology 1) Nitrogenous waste accumulation → Uremia. 2) Acidosis: ↓ NH3, ↓ HCO3 reabsorption, ↓ acid excretion. 3) Sodium wasting + concentrating defect. 4) Hyperkalemia. 5) Renal osteodystrophy (Vit D deficiency, hyperPTH). 6) Growth retardation (nutrition, acidosis, anemia, GH resistance). 7) Anemia (↓ EPO, nutritional). 8) Immunodeficiency, infections. 9) GI symptoms, hypertension, cardiomyopathy.

10. Clinical Features General: • Pallor (anemia), Growth failure, Fatigue. CV: • Hypertension, LVH, Cardiomyopathy. Renal: • Polyuria, Oliguria, Frothy urine (proteinuria). • Hematuria. Other: • Edema, Itching, Muscle cramps. • GI: Anorexia, vomiting, uremic fetor. • CNS: Cognitive impairment, poor school performance. • Skeletal: Bone pain, deformities.

11. Laboratory Findings • ↑ BUN, Creatinine • Hyperkalemia, Acidosis • Dysnatremias (hypo/hyper) • Hypocalcemia, Hyperphosphatemia • Anemia (normocytic normochromic) • Dyslipidemia • Urine: - GN: Hematuria, Proteinuria - Dysplasia: Low specific gravity, minimal proteinuria

12. Assessment of Renal Function • Gold standard: Inulin clearance (rare). • Other: Iohexol, radioisotopes (DTPA, EDTA, Iothalamate). • Clinical: Serum creatinine, cystatin C. • Schwartz formula (eGFR): eGFR = (0.43 × Height in cm) / Serum creatinine • K values: Infant LBW 0.33, Term 0.45, Child 0.55, Adolescent boy 0.70.

13. Management Principles Goals: • Slow progression • Treat complications • Maintain growth & nutrition • Prepare for dialysis/transplant Approach: • Monitor blood/urine, proteinuria, BP. • Nutrition: Adequate calories, vitamins. • Manage anemia, CKD-MBD, acidosis. • BP control (ACEi/ARB). • Immunization.

14. CKD-Mineral & Bone Disorder Pathophysiology: • Early FGF23 rise (Stage 2). • ↓ Vit D (1,25), Hypocalcemia, Hyperphosphatemia. • Secondary hyperparathyroidism. Clinical forms: • Osteitis fibrosa cystica (high turnover). • Adynamic bone disease (low turnover). Complications: • Rickets, fractures, deformities. • Vascular & soft tissue calcification.

15. CKD-MBD Treatment • Low phosphorus diet (special formula in infants). • Phosphate binders (Ca-based, Sevelamer, Ferric citrate). • Avoid Aluminum binders. • Correct Vit D insufficiency (25OH Vit D ≥30). • Active Vit D sterols (Calcitriol, Alfacalcidiol) if PTH ↑. • Goal: Normalize Ca, P, PTH; prevent bone disease & calcification.

16. Growth & Anemia Growth retardation: • GH resistance • Correct nutrition, acidosis, bone disease. • rHuGH if height <-2SD despite optimal care. Anemia: • Appears when GFR <40. • Causes: ↓ EPO, Iron/B12/Folate deficiency. • Iron therapy if TSAT ≤20%, Ferritin ≤100. • ESA (Erythropoietin, Darbepoetin). • Hb target 11–12 g/dL.

17. Hypertension & Proteinuria • Causes: Volume overload, ↑ Renin. • Both accelerate CKD progression. Management: • Sodium restriction (<2 g/day). • Lifestyle changes. • Pharmacologic: - ACEi (Enalapril), ARB (Losartan) - Target BP <50th percentile for age/sex/height. • Diuretics if edema/volume overload.

18. Other Aspects of Management • Fluid & electrolytes: Restrict K, treat acidosis (Bicitra, NaHCO3). • Immunization: All vaccines; avoid live vaccines if immunosuppressed. • Drug dosing: Adjust for renal excretion. • Prevent infections: Catheter care, avoid nephrotoxins. • Psychosocial support for family & child.

19. Progression & Prognosis • GFR decline: - Nonglomerular: 1.5 mL/min/yr - Glomerular: 4.3 mL/min/yr Risk factors: • Nonmodifiable: Age, puberty, severity, etiology. • Modifiable: HTN, proteinuria, anemia, dyslipidemia. Prevention: • Control BP & proteinuria. • Correct anemia, dyslipidemia. • Avoid nephrotoxins, dehydration. • Encourage healthy lifestyle, avoid tobacco.