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The epidemiology of thiazide-associated hypercalcemia is poorly understood. Conversely, loop diuretics induce natriuresis by inhibiting the Na-K-2Cl transporter in the thick ascending limb of the loop of Henle, causing increased urinary calcium losses and increased PTH ( 5, 8).
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Serum calcium concentrations are increased independently of PTH levels ( 8). Thiazides have several metabolic effects contributing to higher serum calcium levels, but increased renal tubular reabsorption of calcium resulting in reduced urine calcium excretion is the most likely cause ( 5– 7). Thiazides exert their antihypertensive effect through an increase in sodium excretion by blocking the thiazide-sensitive NaCl transporter in the distal convoluted tubule, which is closely linked to calcium transport ( 5). Hypercalcemia associated with thiazide use is a well-known clinical entity. In 2008, there were nearly 135 million prescriptions in the United States when combination products with hydrochlorothiazide, which comprise approximately two-thirds of total prescriptions, were included ( 2, 4). Hydrochlorothiazide is the most commonly prescribed antihypertensive medication worldwide, with over 50 million dispensed prescriptions for monotherapy in the United States alone in 2013 ( 2). Thiazides are first-line treatment in essential hypertension and reduce mortality and cardiovascular events ( 1, 3). Over 65 million persons in the United States are affected by hypertension ( 1), with approximately 45.7 million patients utilizing antihypertensive therapy in 2013, almost twice the number in the next closest medication category ( 2).