How do thiazides affect calcium?

By increasing calcium reabsorption from the luminal membrane into the interstitium in exchange for sodium, thiazides reduce urine calcium levels and increase blood calcium.

Why do thiazide diuretics cause hypercalcemia?

Thiazide diuretics can increase renal tubular reabsorption of calcium, resulting in hypercalcemia. However, thiazide-associated hypercalcemia also can represent unmasking of preexisting primary hyperparathyroidism (PHPT) or incidental development of PHPT during thiazide therapy.

Does thiazide waste calcium?

Calcium excretion is increased by loop diuretics and diminished by thiazide-type diuretics and amiloride. How these effects occur is related to the mechanisms of sodium, chloride, and calcium transport in the different diuretic-sensitive segments.

How does hydrochlorothiazide affect calcium?

Hydrochlorothiazide reduced urinary calcium excretion, and it increased serum calcium levels to near the lower limit of normal (Fig. 1).

How do thiazides increase Ca reabsorption?

Thiazides enhance Ca reabsorption in the distal convoluted tubule, by increasing Na/Ca exchange (which makes thiazides useful in treating the calcium-subtype of kidney stones).

Do thiazide diuretics cause hypocalcemia?

Thiazide diuretics can cause hypercalcemia while loop diuretics increase the excretion of calcium which can lead to hypocalcemia. Moreover, loop and thiazide diuretics are sulfonamides and can lead to allergic reactions.

Why do thiazides cause hyperuricemia?

Thiazide diuretics are associated with elevated serum uric acid (SUA) levels. They increase direct urate reabsorption in the proximal renal tubules [3]. Elevated SUA is an independent risk factor for gout [2]. These agents increase the levels of SUA and thus may contribute to the risk of gout.

How does hydrochlorothiazide cause hypercalcemia?

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).

Why are thiazides contraindicated in hypercalcemia?

Hypercalcemia associated with thiazide use is a well-known clinical entity. 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).

How does thiazide cause calcium reabsorption?

Do Thiazides have adverse metabolic effects?

Concerns regarding adverse metabolic effects of thiazides, which are also used to treat hypertension, have reemerged with analysis of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial.

Do thiazides prevent recurrent calcium nephrolithiasis?

Purpose: Thiazide use to prevent recurrent calcium nephrolithiasis is supported by randomized, controlled trials. Concerns regarding adverse metabolic effects of thiazides, which are also used to treat hypertension, have reemerged with analysis of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial.

Does thiazide use affect osteocalcin and parathyroid hormone levels?

Log 25OHD showed a significant inverse relationship to parathyroid hormone (r = .33, P < 0.05). Thiazide users had lower levels of osteocalcin (P < 0.05) and parathyroid hormone levels (P < 0.05) compared with non-thiazide users.

What is the relationship between thiazide and osteoblastic activity?

Parathyroid hormone and testosterone concentration (in men) are correlated with serum osteocalcin, a measure of osteoblastic activity. Long-term thiazide use alters these relationships and produces a biochemical profile suggestive of decreased bone formation. Reduced bioavailable testosterone may also play a role in these biochemical changes.