How are bone complications managed in children with chronic kidney disease (CKD)?

Updated: Jul 21, 2020
  • Author: Sanjeev Gulati, MD, MBBS, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada); Chief Editor: Craig B Langman, MD  more...
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Children with stage II chronic kidney disease usually have no signs or symptoms of bone abnormalities. However, these children may have evidence of abnormalities on laboratory testing (eg, decreased serum calcitriol [1,25 dihydroxyvitamin D] and elevated serum parathyroid hormone [PTH]). Counsel the child and family about chronic kidney disease and its impact on bone metabolism. The importance of laboratory monitoring should be emphasized, and future interventions to prevent renal osteodystrophy should be discussed. Subtle signs of renal osteodystrophy begin to be observed when the glomerular filtration rate (GFR) decreases to 50% of the reference range (stage III disease).

The 2 major types of bone disease commonly encountered in patients with chronic kidney disease before maintenance dialysis include enhanced bone resorption (osteitis fibrosa) and osteomalacia/rickets. As chronic kidney disease advances to end-stage renal disease (ESRD), adynamic bone disease may also be found. Mild forms of these derangements in bone metabolism may be observed in the early stages (eg, stage II) and may become more severe as kidney function deteriorates.

Serum concentrations of calcium, phosphate, and PTH should be measured on an ongoing basis in all children with chronic kidney disease, even those with mild disease who often have evidence of abnormalities in bone metabolism. Vitamin D insufficiency and deficiency are very prevalent in pediatric patients across all stages of chronic kidney disease, particularly in nonwhite and obese patients, and may contribute to growth deficits during the earliest stages of chronic kidney disease. [21]

For calcium and phosphorus measurements, the Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines recommend monthly measurements in stage V disease, whereas PTH measurements should be obtained at least every 3 months. [4, 15] Early detection of bone metabolic abnormalities ensures that therapeutic interventions can be initiated, thereby preventing or minimizing renal osteodystrophy.

According to the KDOQI clinical practice guidelines for pediatric osteodystrophy, phosphate binders are recommended if phosphorus or intact PTH levels cannot be controlled within the target range despite dietary phosphorus restriction. [4, 15] Calcium-based phosphate binders are effective in lowering serum phosphorus levels and may be used as the initial binder therapy, but total calcium uptake should be rechecked. [22] The serum levels of corrected total calcium should be maintained within the reference range for the laboratory used. The serum calcium-phosphorus product should be maintained at less than 55 mg2/dL in adolescents.

Serum PTH concentration is inversely correlated with renal function and is almost always elevated when the GFR falls below 60 mL/min per 1.73 m2. Although the optimal serum PTH values in children with chronic kidney disease are uncertain, the KDOQI guidelines recommend targeted levels of serum intact PTH in stage V disease to be 200-300 pg/mL. [4, 15]

Patients with serum levels of intact PTH of more than 300 pg/mL may be treated with active vitamin D sterols to maintain PTH levels at about 2-4 times the reference range.

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