Control of Serum Phosphorus in Uremia

Abstract

Phosphate retention and hyperphosphatemia play a pivotal part in producing and aggravating the secondary hyperparathyroidism that develops in nearly all patients with chronic renal failure and in creating extraskeletal calcifications in such patients. The principal pathway through which phosphate retention leads to secondary hyperparathyroidism remains elusive.¹ Hyperphosphatemia, however, can indirectly stimulate the release of parathyroid hormone by lowering the serum calcium level. Phosphate loading also reduces the renal synthesis of calcitriol, which enhances the release of parathyroid hormone.² With progressive renal insufficiency, phosphate is retained, although hyperphosphatemia rarely develops before renal function has declined to about 25 percent of normal. . . .