Intermittent oral calcitriol and intravenous pamidronate in renal allograft recipients: Divergent effects on bone metabolism and parathyroid function.
ASN 30th Annual Meeting, San Antonio
J Am Soc Nephrol (Sep) 8:575A 1997
Persistent hyperparathyroidism is a common and clinically important finding which may lead to hypercalcemia and contribute to bone loss in the months following renal transplant. While most cases resolve spontaneously in the first year, as many as 10% of patients may require intervention to prevent ongoing bone resorption and symptomatic hypercalcemia (see Massari, Kidney International 52:1412, 1997 and Julian et al., Am J of Kidney Diseases, 19:99, 1992). Parathyroidectomy has been the mainstay of treatment, however the availability of bisphosphonates, which are inhibitors of osteoclast activity and an effective treatment for hypercalcemia, may provide a non-surgical alternative.
Ittel et al. studied six patients with hypercalcemia persisting more than 6 months after renal transplant. All had excellent graft function, with GFR > 60 ml/min. They were treated with intravenous pamidronate 30 mg every 2-6 weeks until the calcium normalized, and then with oral calcitriol 2.5-3 µg twice weekly to suppress parathyroid hormone secretion. Pamidronate successfully reduced calcium levels and prevented symptomatic hypercalcemic events. Chemical markers of bone turnover, including serum osteocalcin and deoxypyridinoline excretion, also fell during the 24 month study period. Bone biopsies revealed normalization of histomorphometric measures and bone density increased despite steroid treatment. Parathyroid hormone levels fell soon after the onset of calcitriol treatment but gradually rose over the course of the study. After the termination of the study, hypercalcemia recurred in all patients and they underwent subtotal parathyroidectomy. Histologic examination of the tissue revealed nodular hyperplasia, a paucity of vitamin D receptors and no apoptotic cells.
Comment: In summary, hypercalcemia was successfully treated with pamidronate, and bone loss was prevented. In contrast, hypersecretion of parathyroid hormone persisted despite vitamin D treatment. It is unclear if surgical intervention would have been necessary if the treatment had continued. In addition, it would have been helpful to know values for bone histologic parameters and bone density in non-hyperparathyroid transplant recipients. However, the effect of pamidronate and calcitriol on bone density is encouraging as studies in transplant patients have shown significant early bone loss even in the absence of hyperparathyroidism, and bone disease continues to be major cause of morbidity in these patients. While this bone disease is multifactorial, this abstract suggests that at least one cause may be effectively treated. (Judith Benstein, M.D., NYU University Hospital, New York City)
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ASN 30th Annual Meeting, San Antonio
Transplant : Transplantation