Endogenous calcitonin does not protect against hyperparathyroid bone disease in renal failure

The paper challenges the widely held notion that calcitonin antagonizes effects of the parathyroid hormone (PTH) on bone and inhibits the development of hyperparathyroid bone disease in uremic patients. This was done by studying 16 patients on chronic maintenance dialysis with various levels of PTH and endogenous calcitonin. In addition, 2 patients with normal kidney function and high calcitonin levels due to medullary carcinoma of the thyroid were evaluated, one of them with an excessive, the other with a low-normal PTH level. Undecalcified bone histology was done in all patients and quantitative static and dynamic parameters of bone structure, bone formation, mineralization and resorption were correlated with serum calcitonin and PTH levels using Dunn's multiple comparison procedure. Covariables such as bone aluminum accumulation, immobilization or other diseases were taken into consideration or avoided. In contrast to the literature, no correlations were found between calcitonin and PTH or between calcitonin and bone histology, whereas PTH correlated with parameters of bone resorption and formation. One uremic patient with no circulating calcitonin and high PTH did not show excessive signs of PTH activity on bone. In addition, bone histology in the nonuremic patient with high PTH and high calcitonin did reveal signs of a PTH overactivity on bone which were not seen in the other nonuremic patient with high calcitonin only. These findings indicate that endogenous calcitonin is not protective against hyperparathyroid bone disease.