The effects of diuretics on water and electrolyte metabolism are well-established, but less known to the clinician are their effects on bone and mineral metabolism, and in particular on that of calcium homeostasis. In general, and clinically most relevant, diuretics acting at the thick ascending limb of the loop of Henle cause loss of calcium into the urine, thus making them a useful tool in treating hypercalcemia. However the hypercalciuria caused by loop diuretics may lead to the development of urolithiasis and nephrocalcinosis, as well as secondary hyperparathyroidism and bone disease. On the other hand, thiazide diuretics that act more distally, increase tubular calcium reabsorption, thus providing protection against hypercalciuria, and with that may raise serum calcium, suppress PTH secretion and improve bone metabolism. Additional hypocalciuric effect may be observed with the use of potassium-sparing diuretics. This review will address the effects of diuretics on mineral metabolism in the kidney and consequently on systemic mineral and bone metabolism.
Keywords: Amiloride; Bone; Loop diuretics; Parathyroid hormone; Thiazides.
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