Exogenous calcitonin protects against renal bone disease in rats with early renal failure.

Chronic renal failure was induced in four groups of male Sprague-Dawley rats by unilateral nephrectomy followed by removal of the outer poles and cautery of the remnant kidney. The four groups of animals received isocaloric diets with normal (groups 1 and 4) or low (groups 2 and 3) phosphate contents and variable amounts of calcium. In addition, rats in group 4 were given salmon calcitonin. After 90-160 days the 4 groups of rats had developed comparable levels of chronic renal failure. The serum phosphate values were significantly lower in rats on low phosphate intake than in those on normal phosphate diet. Bone histology was evaluated on tibiae, lumbar vertebrae and ribs. The rats kept on low phosphate diet (groups 2 and 3) had significantly lower frequency of osteomalacia and bone resorption than those fed a normal phosphate diet. Rats treated with calcitonin (group 4) had the lowest frequency of osteomalacia and virtually no association with bone resorption, despite normal phosphate intake. The serum levels of parathyroid hormone were not significantly different in rats in groups 1 and 4 as compared to controls. Serum 1,25-dihydroxycholecalciferol levels were significantly lower in group 1 than in controls and were significantly higher in group 4 than in group 1. These data show that calcitonin effectively prevents bone lesions in rats with early chronic renal failure.