Despite advances in the management of patients with
chronic renal failure, histologic features associated with
secondary hyperparathyroidism remain the predominant skeletal findings; however, over the last decade the prevalence of adynamic bone has increased in both adult and pediatric patients with
chronic renal failure. The management of children with
secondary hyperparathyroidism and mild to moderate
chronic renal failure should be started early, and should include correction of
hypocalcemia and
metabolic acidosis, maintenance of age-appropriate serum
phosphorus levels, and institution of
vitamin D therapy when serum intact
parathyroid hormone (PTH) measurements are elevated to maintain the blood levels within normal limits; however, in children undergoing chronic dialysis
therapy, the current recommendation is to maintain the serum intact PTH levels at least 2-4 times the upper limits of normal to prevent the development of low bone turnover disease. Serum
calcium,
phosphorus,
alkaline phosphatase, and PTH levels should be monitored frequently, especially in infants and very young children. Discontinuation or reduction of
vitamin D should be considered when there is a rapid decline in PTH levels, persistent elevation in serum
calcium and serum
phosphorus levels, and a significant diminution in
alkaline phosphatase levels. In addition, a reduction in the
calcium concentration of the dialysis fluid, and judicious use of
calcium-containing
salts as
phosphate binding agents should also be performed in these patients. Although not yet extensively used in pediatric patients with
secondary hyperparathyroidism, several therapeutic alternatives, such as the less calcemic
vitamin D analogs, including
paricalcitol [19-nor-
1,25-(OH)(2)D(2)] and
doxercalciferol [1-alpha-(
OH)(2)D(2)], calcimimetics, and the availability of a
calcium-free,
aluminum-free
phosphate binder such as
sevelamer hydrochloride and
lanthanum carbonate, may play significant roles in the future management of children with
secondary hyperparathyroidism to promote linear growth, prevent parathyroid gland
hyperplasia, avoid
calciphylaxis and, in the long run, avert
vascular calcifications.