The etiology of urolithiasis in HIV infected patients

It is commonly thought that urinary lithiasis in HIV infected patients on protease inhibitor therapy is composed primarily of the protease inhibitor itself. Since many HIV infected patients on protease inhibitors presenting to our institution had nonprotease inhibitor stones, we investigated potential underlying metabolic abnormalities that may account for the lithogenesis.

We retrospectively reviewed all HIV infected patients on protease inhibitors with renal colic and evidence of nephrolithiasis who presented to our institution between June 1996 and January 2001. Patients were evaluated for stone composition and metabolic abnormalities of blood and urine when possible.

A total of 24 patients were identified, and all were or had been on protease inhibitors (indinavir 14, ritonavir 3, nelfnavir 2, unspecified 5). Of the 14 patients on indinavir only 4 (28.6%) had indinavir containing stones. The remaining stones in this group and in those not on indinavir contained various amounts of calcium oxalate monohydrate and dihydrate, ammonium acid urate and uric acid. Of 10 patients who underwent 24-hour urine collection for metabolic evaluation 8 (80%) had abnormalities, including hypocitraturia in 5, hyperoxaluria in 4, hypomagnesuria in 4, hypercalciuria in 3, increased supersaturation of calcium oxalate in 3 and hyperuricosuria in 2. Abnormalities in the levels of urinary phosphate and sodium were also observed.

HIV infected patients form many types of stones, which probably are attributable to underlying metabolic abnormalities rather than the use of protease inhibitors. A complete metabolic evaluation is warranted in these patients, as a means of guiding treatment to prevent future stone episodes, while avoiding the need to alter antiretroviral regimens.