Chronic Kidney Disease in Children
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Direct answer
Chronic kidney disease in a child is a glomerular filtration rate below 60 mL/min/1.73 m squared persisting beyond three months, and its causes are the mirror image of adult medicine: congenital anomalies of the kidney and urinary tract (CAKUT) — posterior urethral valves being the classic culprit in boys — hereditary nephropathies and glomerular disease, not diabetes and hypertension. The child presents not with uraemia but with falling growth, anaemia unresponsive to iron, rickets-like bone pain, polyuria and nocturia from a kidney that cannot concentrate, and delayed puberty. Conservative care is built on growth nutrition, bicarbonate correction, phosphate control with binders, active vitamin D, erythropoietin and renoprotective ACE inhibition, with renal transplantation as the definitive treatment.
What you must remember
- Cause profile: CAKUT (posterior urethral valves, reflux nephropathy, hypodysplasia) leads in younger children; steroid-resistant nephrotic syndrome/FSGS, Alport syndrome and nephronophthisis rise with age.
- Congenital disease means polyuria, polydipsia, nocturia and salt wasting — these children decompensate with dehydration, and many actually need sodium chloride supplementation rather than restriction.
- Growth failure is the hallmark paediatric complication: anorexia, acidosis, renal osteodystrophy, anaemia and resistance to growth hormone all contribute — monitor height velocity at every visit.
- Renal osteodystrophy: high-turnover bone disease from secondary hyperparathyroidism (raised PTH and alkaline phosphatase, low calcium, high phosphate) plus failed calcitriol synthesis; radiographs show frayed metaphyses in severe disease.
- Normocytic normochromic anaemia from erythropoietin deficiency — correct with erythropoietin and adequate iron, aiming for the age-appropriate haemoglobin.
- Metabolic acidosis accelerates bone loss and catabolism; keep bicarbonate at or above 22 mEq/L with oral alkali.
- Phosphate strategy: dietary restriction plus calcium-based binders such as calcium carbonate taken with meals; calcitriol or analogues for the failed vitamin D activation.
- Estimate GFR with the Schwartz formula; stage CKD 1 to 5, with stage 5 (below 15 mL/min/1.73 m squared) meaning renal replacement therapy.
- ACE inhibitors reduce proteinuria and slow progression in glomerular disease — with monitoring of potassium and creatinine after initiation.
- Dialysis in children: peritoneal dialysis is the modality of choice, especially in infants; transplantation is the best long-term option, and pre-emptive transplant before dialysis is the ideal.
A typical exam case
A four-year-old boy, operated in infancy for posterior urethral valves, follows up with height below the third centile, haemoglobin 8.9 g/dL, bicarbonate 16 mEq/L, phosphate 6.8 mg/dL, calcium 8.2 mg/dL, PTH three times the upper limit and an eGFR of 28 mL/min/1.73 m squared — stage 4 CKD. The management list is the exam: correct the acidosis with sodium bicarbonate, start a phosphate binder with meals, begin calcitriol, give erythropoietin with iron, ensure calorie-rich (not protein-restricted) nutrition, plot growth each visit, screen for left ventricular hypertrophy on echocardiography, and start ACE inhibition for proteinuria while watching potassium.
Six months later his weight has stalled and PTH keeps climbing despite optimisation: add recombinant growth hormone — a specifically paediatric intervention with no adult equivalent. When eGFR drifts toward the teens with fluid overload or uncontrolled phosphate, plan renal replacement — peritoneal dialysis via a Tenckhoff catheter in a child — and activate the transplant work-up including family donor evaluation. The recurring thread: in children you treat growth, bone and neurodevelopment alongside the kidney, and adult-style "restrict fluids and protein" reflexes are often wrong for a salt-wasting, polyuric child.
Where students slip
Two import errors dominate. First, treating every CKD child as salt- and fluid-retentive: the congenital CAKUT child is typically a salt waster who needs liberal salt and water, and blanket restriction dehydrates him. Second, reaching for erythropoietin without iron, or for vitamin D without measuring PTH, phosphate and calcium — renal osteodystrophy is a chemistry-managed disease, and a calcium-containing binder taken with meals is an entirely different intervention from calcium supplementation between meals. Candidates also forget the uraemic bleeding tendency from platelet dysfunction, the need for immunisation before transplantation (especially varicella and hepatitis B), and that peritoneal dialysis, not haemodialysis, is the paediatric default. Finally, the poster mistake: defining CKD by a single creatinine value rather than eGFR criteria sustained over three months.
Frequently asked questions
Which causes of CKD dominate in children compared with adults?
Congenital anomalies of the kidney and urinary tract — posterior urethral valves, reflux nephropathy, renal hypodysplasia — plus hereditary and glomerular diseases, unlike the diabetic and hypertensive vasculopathy of adults.
Why do many children with CKD need sodium and water supplementation rather than restriction?
Congenital and tubulointerstitial disease impairs concentrating ability and salt conservation, producing polyuria and salt wasting; restricting these children precipitates dehydration and further loss of kidney function.
What laboratory pattern defines renal osteodystrophy?
High phosphate, low-to-normal calcium, markedly raised parathyroid hormone and alkaline phosphatase with failed calcitriol synthesis — managed with phosphate binders, dietary phosphate control and active vitamin D.
Which dialysis modality is preferred in young children?
Peritoneal dialysis via a Tenckhoff catheter — better tolerated haemodynamically, avoids difficult vascular access in small children, and can be delivered at home by trained parents.