[Fragility Fractures in Hemodialysis Patients. Loss of kidney function and system for calcium homeostasis.]

Abstract

Extracellular calcium concentrations are tightly regulated within a narrow range through the coordinated participation of the parathyroid glands, kidneys, and bone. In patients with chronic kidney disease, the production of 1,25-dihydroxyvitamin D and urinary calcium excretion decrease as kidney function declines. When patients reach end-stage renal disease and start dialysis, calcium metabolism is further complicated by loss of kidney function, calcium flux during dialysis, and pronounced impact of bone metabolism on extracellular calcium concentrations. In this article, I outline the alterations in calcium metabolism during the progression of chronic kidney disease and after initiation of dialysis, review data on the effects of secondary hyperparathyroidism and osteoporosis medications on calcium metabolism, and discuss the characteristic aspects of altered calcium homeostasis in end-stage renal disease.