Drug-induced renal stones

Abstract

Drug-induced stones represent about 1% of all renal stones. They involve two main mechanisms. The first one includes stones made of the drug and/or its metabolites identified by X-ray diffraction or infrared spectroscopy on the basis of their specific diagrams. Nowadays, the most commonly observed ones are antiproteases (such as indinavir) used in HIV-infected patients, high-dose sulfadiazine used for the treatment of cerebral toxoplasmosis, and abuse of ephedrine/guaifenesin-containing preparations, whereas triamterene, formerly the most often involved drug, is less frequently observed. The second one includes stones of common composition, induced by the metabolic effects of the drug on urinary pH and excretion of calcium, oxalate, phosphate, citrate, uric acid, or other purines. The most frequent causes are unsupervised calcium/vitamin D supplementation and carbonic anhydrase inhibitors, including anticonvulsants (such as topiramate). Incidence of metabolically induced stones is probably underestimated, because they are of apparently usual composition and may reveal long after drug withdrawal. Formation of iatrogenic calculi is favored by high-dose or long-lasting treatments, high renal excretion and low solubility of the drug or its metabolites, low urine output or inadequate urine pH, and is especially frequent in patients with a history of stones. Better awareness of potentially lithogenic drugs may allow more efficient prevention and reduce the incidence of drug-induced nephrolithiasis. © 2011 Springer-Verlag London Limited.