Biochemical markers of renal osteodystrophy in pediatric patients undergoing CAPD/CCPD (original) (raw)

1994, Kidney International

Biochemical markers of renal osteodystrophy in pediatric patients undergoing CAPD/CCPD. Serum intact PTH [1-84] levels were evaluated as a potential non-invasive method for the diagnosis of renal osteodystrophy in children treated with CAPD/CCPD. Sixty-eight bone biopsy samples were obtained from 55 patients, aged 13 5 (X SD) years, undergoing CAPD/CCPD for 29 13 months; osteitis fibrosa was present in 34 cases, mild lesions of secondary hyperparathyroidism in six, 15 had adynamic lesions, and 13 were classified as normal histology. Serum calcium levels were higher in patients with adynamic bone or normal bone histology than in those with secondary hyperparathyroidism, whereas serum phosphorus, alkaline phosphatase and PTH levels were greater in patients with osteitis fibrosa. The combination of a serum PTH level >200 pg/ml and a serum calcium value <10 mgldl was 85% sensitive and 100% specific for identifying patients with high-turnover lesions of bone. Serum PTH values <200 pg/ml were 100% sensitive but only 79% specific for patients with adynamic bone; specificity increased to 92%, however, using the combined criteria of a PTH level <150 pglml and a serum calcium level >10 mgldl. Higher serum calcium levels and serum PTH values within or below the normal range characterize patients with the adynamic lesion of renal osteodystrophy. Serum PTH levels of approximately 200 pg/mI are useful for distinguishing patients with low-turnover lesions of renal osteodystrophy from those with secondary hyperparathyroidism. Secondary hyperparathyroidism develops in most patients with chronic renal failure. Accordingly, osteitis fibrosa has been the most common histologic lesion of bone both in adults and in children undergoing hemodialysis or peritoneal dialysis [1-4]. Recent reports suggest, however, that the prevalence of lowturnover skeletal disorders, in particular the adynamic or aplastic lesion of renal osteodystrophy, has increased substantially. Thus, as many as 66% of adult patients receiving peritoneal dialysis have evidence of adynamic bone on histologic evaluation [5], and a substantial proportion of these do not have diabetes or evidence of bone aluminum deposition, factors previously recognized as causes of the adynamic lesion in patients with chronic renal failure .