Vitamin D in kidney disease
Vitamin D is obtained from sunlight and dietary intake. After conversion in the liver to 25-hydroxyvitamin D, it is further converted to the active form of 1,25-dihydroxyvitamin D in the kidney. 1,25-Dihydroxyvitamin D is a hormone that interacts with vitamin D receptor complexes to impact a broad range of cellular functions. Classic functions include augmentation of calcium and phosphorus absorption in the gastrointestinal tract, calcium reabsorption in the kidney, and stimulation of bone osteoclasts, each of which maintains calcium homeostasis to prevent osteomalacia and rickets. Peripheral conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D is increasingly recognized and could play a role in additional impacts on immunity, cell survival, and insulin resistance among other effects. Although supplementation to treat vitamin D deficiency is justified, a large and growing body of clinical trials in cardiovascular disease, cancer, and skeletal health currently do not support unselected supplementation. However, in kidney disease, distinct abnormalities in vitamin D pathways occur. As kidney disease advances, deficient conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D leads to the development of secondary hyperparathyroidism. Treatment with active 1,25-dihydroxyvitamin D or its analogs can treat this condition in advanced or end-stage kidney disease. Few trials are available that define optimal treatment doses, biochemical targets, and long-term health impacts.
