Drug induced nephrolithiaisis

Drug induced nephrolithiaisis - THERAPEUTIC CHALLENGES...

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T HERAPEUTIC C HALLENGES VOL. 5 NO. 4 2003 REVIEWS IN UROLOGY 227 Drug-Induced Urinary Calculi Brian R. Matlaga, MD, MPH, Ojas D. Shah, MD, Dean G. Assimos, MD Department of Urology, Wake Forest University School of Medicine, Winston-Salem, NC Urinary calculi may be induced by a number of medications used to treat a variety of conditions. These medications may lead to metabolic abnormalities that facilitate the formation of stones. Drugs that induce metabolic calculi include loop diuretics; carbonic anhydrase inhibitors; and laxatives, when abused. Correcting the metabolic abnormality may eliminate or dramatically attenuate stone activity. Urinary calculi can also be induced by medications when the drugs crystallize and become the primary component of the stones. In this case, urinary supersaturation of the agent may promote formation of the calculi. Drugs that induce calculi via this process include magnesium trisili- cate; ciprofloxacin; sulfa medications; triamterene; indinavir; and ephedrine, alone or in combination with guaifenesin. When this situation occurs, discon- tinuation of the medication is usually necessary. [Rev Urol. 2003;5(4):227-231 ] © 2003 MedReviews, LLC Key words: Urinary calculi • Nephrolithiasis • Carbonic anhydrase inhibitors • Sulfa medications • Ephedrine • Indinavir A lbeit a rare occurrence, certain medications used to treat a diverse range of disease processes can induce urinary stone disease. Medication-induced calculi can be composed of the drug or one of its metabolites, and their formation may be promoted by the urinary supersaturation of these substances. Alternatively, the drug may induce physiologic changes that facilitate the forma- tion of “metabolic stones.” Composition and radiographic imaging characteristics of drug-induced calculi are listed in Table 1.
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Drug-Induced Metabolic Calculi Loop Diuretics Loop diuretics, such as bumetanide and furosemide, inhibit both sodium and calcium resorption in the thick ascending limb of the loop of Henle. In addition to exerting a diuretic effect, this mechanism of action pro- duces a hypercalciuric state. Renal calculi have been noted in up to 64% of low-birth-weight infants receiving furosemide therapy. 1 Furthermore, the hypercalciuric effect of furosemide in infants is enhanced by a reduced glomerular filtration rate and imma- ture hepatic function, which contribute to significantly prolonging the half- life of this drug. 2 The calculi isolated from these patients are composed exclusively of calcium oxalate. 3 Carbonic Anhydrase Inhibitors Carbonic anhydrase inhibitors, such as acetazolamide, act in the proximal tubule where they block resorption of sodium bicarbonate. Consequently, prolonged use of carbonic anhydrase inhibitors may lead to a hyper- chloremic metabolic acidosis, in which urinary pH is increased and urinary citrate is decreased. Acetazolamide may be used by patients with glau- coma, as it reduces the flow of the aqueous humor, and by mountain
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This note was uploaded on 02/18/2012 for the course PAS 600 - 601 taught by Professor Garrubba during the Fall '10 term at Chatham University.

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Drug induced nephrolithiaisis - THERAPEUTIC CHALLENGES...

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