Stone formation diuretics

Two renal responses are unique to the thiazide and thiazidehke diuretics. With these compounds, Na+ excretion is increased, while Ca++ excretion is decreased, primarily and directly because of increased distal Ca++ reabsorption, secondarily and indirectly because of a compensatory elevation of proximal solute absorption, making this class of diuretics useful in treating hypercal-ciuria. This effect, which may not be evident upon initial administration of the drug, is particularly benehcial in individuals who are prone to calcium stone formation. 

Calcium and magnesium homeostasis is altered by chronic diuretic therapy. Loop diuretics increase the urinary excretion of Ca2+ and can lead to stone formation. Thiazide administration, on the other hand, has the opposite effect and causes frank hypercalcaemia in some patients. Both thiazide and loop drugs increase the urinary loss of Mg2+ and this has been associated with cardiac arrythmias in the elderly. 

Thiazide diuretics reduce the excretion of calcium and oxalate in the urine and reduce the rate of stone formation. 

Diuretics have been shown to have variable effects in relationship to urinary calcium excretion and supersaturation, most notably including loop diuretic induced hypercalciuria and attenuation of urinary calcium excretion by thiazide diuretics. The factors contributing to nephrotoxicity are most commonly associated with multiple factors that favor calcium salt or uric acid deposition at the tubulo-interstitial level. Management of renal stone formation and nephrocalcinosis therefore presents a unique clinical challenge, balancing factors that increase risk for abnormal calcium salt deposition or crystallization, and factors that reduce this risk. 

Intratubular obstruction due to crystal formation with acetazolamide and stone formation with triamterene has been reported. In addition, uric acid stones, although rare, can result from the administration of those diuretics, which compete with uric acid for secretion, but also from any diuretic that causes severe volume depletion, thus enhancing urate reabsorption and compromising excretion. 

Some individuals with hypercalciuria (an elevated urinary concentration of calcium) are prune In the formation of Ca -enniaining. stnnes within the urinary tract. Becau.se Inng-temi use of thiazide and thiazide-like diuretics de-crea.ses the urinary excretion rate of Ca". they may help prevent Ca" -containing stone fnrmation. "... 

D. Toxicity Drowsiness and paresthesias are commonly reported after oral therapy. Cross allergenicity between these and all other sulfonamide derivatives (other sulfonamide diuretics, hypoglycemic agents, antibacterial sulfonamides) is uncommon but does occur. Alkalinization of the urine by these drugs may cause precipitation of calcium salts and formation of renal stones. Renal potassium wasting may be marked. Patients with hepatic impairment may develop hepatic encephalopathy because of increased ammonia reabsorption. 

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