Nephrolithiasis and its interrelationship with vitamin d, parathyroid hormone, and calcium

Calcium is a major component of 85 % of renal stones. The incidence of renal stone diseases is increasing, possibly consequent to the widespread use of calcium supplementation. A genetic contribution with defects in the regulation of renal calcium excretion has been suggested as a cause of renal stone disease. The parathyroid hormone (PTH) and vitamin D axis plays a key role in the calcium and phosphate homeostasis. The parathyroid gland responds with rapid changes of PTH in response to fl uctuations in the extracellular calcium concentration, thereby regulating minute-to-minute normalization of serum ionized calcium, through stimulation of renal tubular calcium reabsorption and bone resorption. On a more chronic basis, PTH also stimulates the con ersion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol) in the proximal renal tubular cells, thereby stimulating intestinal calcium absorption. Hypersecretion of parathyroid hormone results in hypercalcemia thus predisposing the individual to development of nephrolithiasis. Vitamin D is recognized as an important hormone in health and disease. There has been an increasing appreciation of the complexity and importance of its regulation, functions, and supplementation. The use of calcium and vitamin D supplementation, though safe, has been shown to be associated with an increase in the incidence of renal lithiasis. Abnormalities related to vitamin D de fi ciency and parathyroid hormone disorders in the general population are reported globally with an increased incidence of cardiovascular disease, diabetes, metabolic syndrome, and cancer rates, which is linked to protracted exposure to abnormal internal milieu such as occurs with vitamin D de fi ciency. This chapter reviews the recent advances and interrelationship in the understanding of calcium, vitamin D, and PTH axis as they affect the process of stone formation in the kidney in health and diseases.