8.3 Chronic Kidney Disease, Dialysis & Transplant

Staging and Nutrition Goals in Pediatric CKD

Chronic kidney disease (CKD) in children is staged by glomerular filtration rate (GFR) using the KDIGO classification: G1 (>=90), G2 (60-89), G3a (45-59), G3b (30-44), G4 (15-29), and G5 (<15 mL/min/1.73 m2), with G5 subdivided into G5D when on dialysis. Unlike adults, in whom slowing progression dominates, pediatric nutrition has a dual mandate: preserve linear growth and neurodevelopment while preventing CKD-mineral and bone disorder (CKD-MBD), cardiovascular calcification, and uremic toxicity.

Protein and Energy

The guiding rule: avoid protein excess but never restrict protein below the Dietary Reference Intake (DRI) for age — inadequate protein costs growth, and growth is the non-negotiable outcome in children. Very high protein intakes are discouraged because they increase solute load and phosphorus intake. Energy must be adequate (generally at the estimated requirement for age, individualized to growth velocity) so that dietary protein is used for synthesis rather than catabolized for fuel; in infants, feeds are concentrated and tube feeding is used freely to hit energy targets.

Potassium, Sodium, and Fluid

Potassium restriction is introduced as GFR falls and hyperkalemia appears — typically in CKD G4-G5 or with oliguria. Strategies include choosing lower-potassium fruits and vegetables, leaching techniques, and low-potassium infant formulas when needed. Sodium and fluid management is disease-specific: children with salt-wasting tubular disorders (e.g., obstructive uropathy, renal dysplasia) need sodium supplementation and liberal fluid to grow, whereas children with hypertension, edema, or oliguria need sodium and fluid restriction — a classic exam contrast.

CKD-Mineral and Bone Disorder

CKD-MBD is the triad of biochemical abnormalities (rising parathyroid hormone (PTH) and phosphorus, falling calcium and activated vitamin D), bone disease, and vascular calcification. Management pillars:

• Phosphorus restriction: limit dairy-heavy and processed foods, with particular attention to phosphate additives in processed meats, colas, and convenience foods, which are nearly 100% absorbed.
• Phosphate binders (calcium acetate, sevelamer) must be given with meals and snacks to bind dietary phosphorus in the gut; given between meals they do nothing.
• Active vitamin D sterols (calcitriol or analogs) suppress PTH; nutritional vitamin D deficiency is repleted first.
• Monitor PTH, calcium, and phosphorus regularly against age-specific targets; both under- and over-suppression of PTH harm bone.

Renal Formulas and Dialysis Nutrition

Specialized products simplify renal diets. For infants, Similac PM 60/40 is a low-renal-solute, reduced-mineral formula - a 60:40 whey-to-casein blend with markedly lower phosphorus, calcium, and potassium than standard term formula - used when serum phosphorus or potassium must be controlled; concentrated renal enteral products (the pediatric use of Suplena/Nepro-type formulas, and pediatric-specific renal products) deliver calorie-dense, electrolyte-restricted nutrition for fluid-limited children on dialysis.

Hemodialysis (HD) removes amino acids and small peptides into the dialysate, so protein needs rise above the DRI (classically the DRI plus an increment of roughly 0.1 g/kg/day, per KDOQI-style guidance). HD is intermittent, so management centers on interdialytic fluid gains (sodium control to limit thirst), potassium and phosphorus control between sessions, and adequacy monitoring via Kt/V.

Peritoneal dialysis (PD) is the most common home modality for infants and small children because it is continuous and gentle. Two nutrition signatures: glucose is absorbed from the dialysate — these calories count toward the energy budget, may blunt appetite, and can drive excessive weight gain — and protein is lost into the effluent, losses that increase markedly during peritonitis, raising protein requirements (classically DRI plus roughly 0.15-0.3 g/kg/day).

Infant CKD and Transplant

Growth failure is a near-universal concern in infant CKD: anorexia, vomiting, and fluid and electrolyte burdens make oral intake inadequate, so NG or gastrostomy-tube feeding — often with overnight continuous feeds — is the norm, and intensive (frequent) dialysis regimens enable growth by controlling uremia and fluid. Kidney transplant is the goal therapy; children typically become surgical candidates at about 10 kg body weight, which frames early nutrition as the bridge to transplant.

Post-transplant, corticosteroids stimulate appetite and weight gain, cause hyperglycemia and bone loss, and suppress growth; tacrolimus adds hyperglycemia, hyperkalemia, and hypomagnesemia and — like in heart transplant — has a strict grapefruit interaction via CYP3A4. Food safety counseling (no unpasteurized products, thoroughly cooked meats, careful produce washing) is mandatory while immunosuppressed.

Nephrotic Syndrome and Acute Kidney Injury

In nephrotic syndrome, heavy proteinuria drives hypoalbuminemia and edema, but the prescription is adequate — not high — protein (excess protein increases proteinuria without raising serum albumin), paired with sodium restriction to control edema; diuretics and corticosteroids bring their own electrolyte and appetite effects. In acute kidney injury (AKI), provide adequate energy to limit catabolism with protein adapted to the clinical course — restriction is minimized once dialysis (especially continuous renal replacement therapy (CRRT), which causes substantial amino acid and micronutrient losses) is in place, when protein needs actually increase.

Micronutrients, Growth Hormone, and Monitoring

Dialysis removes water-soluble vitamins (B-complex, folate, vitamin C), so children on maintenance HD or PD receive a renal multivitamin formulated without fat-soluble vitamin excess; fat-soluble vitamins (especially vitamin A) accumulate in CKD and are not routinely supplemented. When growth failure persists despite adequate calories, controlled electrolytes, and correction of CKD-MBD and acidosis, recombinant human growth hormone is an approved and effective therapy that improves height velocity in children with CKD. Routine monitoring includes weight, length/height, and head circumference on growth charts; mid-upper arm circumference as a fluid-status-independent measure of lean mass; and serial labs — bicarbonate (acidosis impairs growth and is treated with alkali), albumin, potassium, phosphorus, calcium, PTH, and 25-hydroxyvitamin D — with the prescription adjusted at every stage transition.