Endocrine disturbances of calcium metabolism in uremia: renal causes and systemic consequences.

Abstract

The genesis of the hormonal disturbances in calcium metabolism of renal failure is complex, but can be understood basically as the consequence of the deranged endocrine function of the kidney, that is, failing biosynthesis of the renal secosterol hormone 1,25 OH2D3. It is of interest to note how our concepts concerning the genesis of these disturbances, and the role of 1,25 OH2D3 therein, have changed with time. We illustrate this using three examples: (i) the signals activating the parathyroid gland in early renal failure; (ii) the genesis of parathyroid hyperplasia; and (iii) the actions of 1,25 OH2D3 in renal failure unrelated to calcium control.