Treatment for human immunodeficiency virus with indinavir may cause relevant urological side‐effects, effectively treatable by rehydration

Abstract

Objective To explore the occurrence of, and diagnostic and therapeutic procedures for urological side‐effects (e.g. micro‐ and macrohaematuria, and kidney stone formation) in individuals treated with indinavir for the human immunodeficiency virus (HIV). Patients and methods The study comprised a retrospective follow‐up of 74 individuals infected with HIV‐1 and who were treated with indinavir orally at a daily dose of 2.4 g. Data were collected at the outpatient department of our institution between March 1996 and November 1997. Results Of the 74 individuals treated with indinavir, 15 (20%) had indinavir‐related urological side‐effects (19 episodes), most commonly dull flank pain and dysuria. Microhaematuria occurred in 16 of the 19 episodes. Four patients showed urinary tract distension ultrasonographically as a possible indirect sign of urolithiasis and one patient passed a kidney stone. In four patients treatment had to be stopped permanently, but in the remaining 11 patients treatment was continued. Some patients required dose reduction and/or interruption of treatment; only conservative therapeutic measures were required, consisting of rehydration (fluid intake >1.5 L/day) and analgesics. Conclusions Urological side‐effects of indinavir may be apparent in 20% of patients so treated; some (5%) may require permanent withdrawal. In addition to a history and clinical examination, urine analysis and ultrasonography were the only diagnostic procedures required. Therapy is mainly conservative, using rehydration, analgesics and a brief discontinuation of therapy, according to the severity of the symptoms.

Occurrence of adverse, often preventable, events in community hospitals involving nephrotoxic drugs or those excreted by the kidney

“…Chertow et al found that an inexpensive decision support system added to CPOE significantly improved drug dosing in patients with renal insufficiency, although there was still substantial room for improvement. 13 The same study showed a reduction of the LOS of 0.5 days for patients with renal insufficiency. In another study of psychotropic medication use in a geriatric population, when clinical decision support was delivered, agreement with recommended dosing guide-lines improved by 34% and the fall rate fell significantly.…”

“…The list of drugs potentially causing acute renal insufficiency is long: affecting renal hemodynamics (e.g., non-steroidal anti-inflammatory drugs, nonsteroidal anti-inflammatory drugs), direct tubular toxicity (e.g., aminoglycosides), intratubular obstruction-like sulfonamides and certain human immunodeficiency virus drugs (e.g., indinavir), as well as allergic interstitial nephritis (e.g., penicillins, cephalosporins, diuretics). 12,13 Classen et al 17 found a similar array of culprit drugs, namely, analgesics (morphine and derivates, acetaminophen), antiarrhythmic drugs (digoxin), antibiotics (imipenem, cefazolin, vancomycin), as well as meperidine and warfarin. Gandhi et al 18 found in their analysis of 181 ADEs in an ambulatory setting that 10% were caused by selective serotonin reuptake-inhibitors, 9% by b-blockers, 8% each by angiotensin-converting enzyme inhibitors and nonsteroidal anti-inflammatory drugs.…”