indinavir-sulfate and Acute-Kidney-Injury

In the era of antiretroviral therapy, non-AIDS complications such as kidney disease are important contributors to morbidity and mortality.. To estimate the impact of hepatitis C coinfection on the risk of kidney disease in HIV patients.. Two investigators identified English-language citations in MEDLINE and Web of Science from 1989 through 1 July 2007. References of selected articles were reviewed. Observational studies and clinical trials of HIV-related kidney disease and antiretroviral nephrotoxicity were eligible if they included at least 50 subjects and reported hepatitis C status. Data on study characteristics, population, and kidney disease outcomes were abstracted by two independent reviewers.. After screening 2516 articles, 27 studies were eligible and 24 authors confirmed or provided data. Separate meta-analyses were performed for chronic kidney disease outcomes (n = 10), proteinuria (n = 4), acute renal failure (n = 2), and indinavir toxicity (n = 5). The pooled incidence of chronic kidney disease was higher in patients with hepatitis C coinfection [6.2 versus 4.0%; relative risk 1.49, 95% confidence interval (CI) 1.08-2.06]. In meta-regression, prevalence of black race and the proportion of patients with documented hepatitis C status were independently associated with the risk of chronic kidney disease. The relative risk associated with hepatitis C coinfection was significantly increased for proteinuria (1.15; 95% CI 1.02-1.30) and acute renal failure (1.64; 95% CI 1.21-2.23), with no significant statistical heterogeneity. The relative risk of indinavir toxicity was 1.59 (95% CI 0.99-2.54) with hepatitis C coinfection.. Hepatitis C coinfection is associated with a significant increase in the risk of HIV-related kidney disease.

Topics: Acute Kidney Injury; Black People; Hepacivirus; Hepatitis C; HIV Infections; HIV Protease Inhibitors; HIV-1; Humans; Indinavir; Kidney Failure, Chronic; Proteinuria; Risk

Several medications--notably acyclovir, sulfonamides, methotrexate, indinavir, and triamterene--are associated with the production of crystals that are insoluble in human urine. Intratubular precipitation of these crystals can lead to acute renal insufficiency. Many patients who require treatment with these medications have additional risk factors, such as true or effective intravascular volume depletion and underlying renal insufficiency, that increase the likelihood of drug-induced intrarenal crystal deposition. Acute renal failure in this setting may be preventable if it is anticipated by appropriate drug dosing, volume expansion with high urinary flow, and alkalinization of the urine when appropriate. Renal failure may be reversible if the drug is discontinued, and by volume repletion and alkalinization of the urine when appropriate. Management of established renal insufficiency includes volume repletion, dialytic support if necessary, adjustment of drug doses, and avoidance of further exposure to nephrotoxins.

Topics: Acute Kidney Injury; Acyclovir; Humans; Indinavir; Kidney; Methotrexate; Risk; Sulfonamides; Triamterene

To identify risk factors for acute renal failure (ARF) in HIV-infected patients.. Observational cohort study of HIV-infected patients attending a South London HIV centre between January 1999 and December 2008.. ARF was defined as a transient, more than 40% reduction in renal function as assessed by estimated glomerular filtration rate. Multivariate Poisson regression analysis was used to identify baseline and time-updated factors associated with ARF.. The incidence of ARF was 2.8 (95% confidence interval 2.41-3.24) episodes per 100 person-years. We observed a stepwise increase in ARF incidence with time accrued at lower CD4 cell count and at lower estimated glomerular filtration rate, with adjusted incidence rate ratios of 1 (reference), 1.56 (0.97-2.48), 2.08 (1.11-3.91), 6.38 (3.18-12.78) and 10.29 (5.11-20.98) for CD4 cell counts of more than 350, 201-350, 101-200, 51-100 and of 50/microl or less, and 1 (reference), 1.46 (0.86-2.51), 4.19 (2.37-7.42) and 27.00 (16.13-44.95) for estimated glomerular filtration rate more than 90, 75-89, 60-74 and less than 60 ml/min, respectively. Ethnicity, hepatitis B or C coinfection, exposure to combination antiretroviral therapy with or without indinavir, tenofovir or atazanavir and HIV viraemia were not associated with ARF.. Current levels of immunodeficiency and renal function were independent predictors of HIV-associated ARF.

Topics: Acute Kidney Injury; Adenine; Adult; Atazanavir Sulfate; CD4 Lymphocyte Count; Cohort Studies; Female; Glomerular Filtration Rate; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; London; Male; Oligopeptides; Organophosphonates; Pyridines; Risk Factors; Tenofovir

Indinavir, a protease inhibitor that is commonly used to treat HIV infection, may cause crystal formation within the renal tubules when urine pH is above 3.5. Crystallization in the urine may lead to intrarenal crystal deposition and acute renal failure (ARF).. To establish the beneficial urological management of acute renal failure caused by indinavir treatment of HIV/AIDS patients.. Five HIV positive patients (four men, one woman) with a mean age of 32 years (range 28-36 years) were referred to our Department of Urology from an AIDS outpatient Clinic, because of the development of postrenal acute renal failure with continuously elevated creatinine and urea plasma levels after indinavir therapy. Among the initial therapeutic maneuvers, indinavir administration was interrupted for 1 week while bilateral double-J ureteral stents were inserted in all the HIV/AIDS patients, during the first 24-72 h to secure upper-tract drainage. Concurrently urine has been acidified by oral administration of the amino acid L: -methionine and oral fluid intake was increased.. All the patients responded well to the treatment and their renal function was effortlessly restored to normal within a few days.. HIV-positive patients receiving indinavir therapy might be complicated by acute renal failure, mainly due to intrarenal crystal deposition (tubules) or urolithiasis (postrenal obstruction). This adverse effect may simply manage by the discontinuation of indinavir administration, urine acidification, as well as the possible early insertion of bilateral double-J ureteral stents.

Topics: Acquired Immunodeficiency Syndrome; Acute Kidney Injury; Adult; Comorbidity; Female; HIV Protease Inhibitors; HIV Seropositivity; Humans; Indinavir; Male; Stents

A 60-year-old male had tested in 1986, at age 46, positive for human immunodeficiency virus (HIV). In mid-1996 he was started on a protease inhibitor regimen, which included indinavir, lamivudine and stavudine, and remained on this therapy until his death. In April 1999 he was hospitalized after a fainting episode. Although examination focusing on cardiac disease did not disclose any remarkable findings, he died suddenly one week after being discharged from hospital. At autopsy the kidneys were enlarged, with a total weight of 500 g, patchy pale gray and pinkish. Microscopy showed leukocytic cell casts in many of the tubules and collecting ducts. In many of these casts there were clefts left by crystals. In the interstitium, both in the cortex and the medulla, there was focal inflammation and fibrosis. Death was attributed to sudden cardiac dysfunction, probably ventricular fibrillation as a consequence of severe nephropathy with electrolyte disturbances. It is likely that kidney damage developed secondary to the indinavir treatment as indinavir can cause not only nephrolithiasis but also crystal-induced acute renal failure.

Topics: Acute Kidney Injury; AIDS Dementia Complex; Antiretroviral Therapy, Highly Active; Crystallization; Death, Sudden, Cardiac; Diagnosis, Differential; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Lamivudine; Male; Middle Aged; Solubility; Stavudine; Syncope; Ventricular Fibrillation; Water-Electrolyte Imbalance

Topics: Acute Kidney Injury; Adult; AIDS-Related Opportunistic Infections; Anti-HIV Agents; Drug Therapy, Combination; Humans; Indinavir; Male; Urinary Calculi

Topics: Acquired Immunodeficiency Syndrome; Acute Kidney Injury; Adult; Alcoholism; Chemical and Drug Induced Liver Injury; Hepatitis C, Chronic; HIV Protease Inhibitors; Humans; Indinavir; Male; Rhabdomyolysis; Ritonavir

Topics: Acute Kidney Injury; Anti-HIV Agents; Child; Female; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Kidney

Topics: Acute Kidney Injury; Anuria; HIV Protease Inhibitors; Humans; Indinavir; Kidney Calculi; Male; Middle Aged

Evaluate the frequency and assess curative and preventive measures against urinary lithiasis in patients treated with indinavir.. Fourteen HIV seropositive patients who developed severe and acute flank pain were included. Four of the patients receiving 800 mg indinavir t.i.d. had fever (38.5 degrees C) or delayed secretion (> 2 h). Delay from indinavir treatment onset was 1 to 321 days. During the same period, 155 patients had been treated with indinavir. Clinical features, radiology and laboratory results were recorded in addition to an analysis of the lithiasis if possible.. Transient moderate renal failure occurred in 8 patients. Mean urine pH was 6. Serum phosphorus, calcium, and uric acid, liver tests and urinalysis were normal. A JJ ureteral stent was inserted in 4 cases due to complications. In all cases, fluids, analgesics and antispasmodics provided favorable outcome. Inversely, nonsteroid antiinflammatory drugs given in 2 patients had a deleterious effect on renal function. The lithiasis was eliminated in 3 cases and infrared spectrophotometry demonstrated a structure compatible with indinavir monohydrate.. The formation of urinary lithiasis is a frequent complication of indinavir therapy (9%). Hyperhydration and urine acidification are usually successful but emergency drainage is required in approximately 3% of cases. Nonsteroidal antiinflammatory drugs should be avoided due to the risk of renal toxicity. A precise evaluation of fluid intake and diet, drug associations and personal history is needed to recognize patients at risk of recurrent lithiasis formation.

Topics: Acute Kidney Injury; Adult; Aged; Analgesics; Anti-HIV Agents; Anti-Inflammatory Agents, Non-Steroidal; Calcium; Colic; Evaluation Studies as Topic; Female; Fluid Therapy; HIV Protease Inhibitors; Humans; Hydrogen-Ion Concentration; Indinavir; Kidney Calculi; Kidney Diseases; Male; Middle Aged; Parasympatholytics; Phosphorus; Spectrophotometry, Infrared; Uric Acid; Urine

Two patients with oliguric acute renal failure (ARF) attributed to crystalluria and nephrolithiasis with obstructive uropathy caused by the human immunodeficiency virus protease inhibitor indinavir are described. In both patients, ARF resolved with administration of intravenous fluids. One patient required urologic intervention to relieve bilateral ureteral obstruction.

Topics: Acute Kidney Injury; Adult; Crystallization; Fluid Therapy; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Kidney Calculi; Male