Clinical indications for vitamin D

1. Nutritional rickets: Vitamin D deficiency causes a net demineralization of bone, resulting in rickets in children and osteomalacia in adults (Fig. 1). Rickets is characterized by the continued formation of the collagen matrix of bone, but incomplete mineralization results in soft, pliable bones. In osteomalacia, demineralization of preexisting bones increases their susceptibility to fracture. Insufficient exposure to daylight and/or deficiencies in vitamin D consumption occur predominantly in infants and the elderly. Vitamin D deficiency is more common in the northern latitudes, because less vitamin D synthesis occurs in the skin as a result of reduced exposure to ultraviolet light. [Note: Loss-of-function mutations in the vitamin D receptor result in hereditary vitamin D–deficient rickets.]

Figure 1:  Bowed legs of middle-aged man with osteomalacia, a nutritional vitamin D deficiency that results in demineralization of the skeleton.
2. Renal osteodystrophy: Chronic kidney disease causes decreased ability to form active vitamin D as well as increased retention of PO₄³⁻, resulting in hyperphosphatemia and hypocalcemia. The low blood Ca²⁺ causes a rise in PTH and associated bone demineralization with release of Ca²⁺ and PO₄³⁻. Supplementation with vitamin D is an effective therapy.
However, supplementation must be accompanied by PO₄³⁻ reduction therapy to prevent further bone loss and precipitation of calcium phosphate crystals.
3. Hypoparathyroidism: Lack of PTH causes hypocalcemia and hyperphosphatemia. [Note: PTH increases phosphate excretion.] Patients may be treated with vitamin D and calcium supplementation.