We describe 7 cases of renal tubular injury in HIV-infected patients receiving an antiretroviral regimen containing tenofovir. Our patients (5 women and 2 men) developed renal tubular dysfunction, with hypophosphatemia, normoglycemic glycosuria, proteinuria, and decrease of creatinine clearance. The first biologic signs of renal toxicity were observed after duration of tenofovir treatment from 5 weeks to 16 months, and they resolved less than 4 months after discontinuation of tenofovir. Six patients had a low body weight (<60 kg). Five patients received low doses of ritonavir, and 1 received didanosine. In 5 patients, the signs resolved with the discontinuation of only the tenofovir. A renal biopsy performed in 1 patient was consistent with tubulointerstitial injury. Proximal tubulopathy appears to be a rare adverse effect of long-term tenofovir therapy. In patients with low weight or mild preexisting renal impairment, regular monitoring of tubulopathy markers could lead to early detection of this dysfunction.

we prospectively evaluated the prevalence of resistance to penicillins, cephalosporins, carbapenem, quinolones, aminoglycosides, and trimethoprim-sulfamethoxazole (SXT) in 320 Escherichia coli isolates isolated from hospitalized patients with acute urinary tract infections (UTIs). We also studied for these strains risk factors for resistance to amoxicillin-clavulanic acid (AMC), fluoroquinolones (FQs), and SXT. Resistance rates were consistent with those from major recent studies reported in the literature. Multivariate analyses selected the following factors as being significantly associated with E. coli resistance: (i) for resistance to AMC, prior (1 year) UTI (odds ratio [OR] ‫؍‬ 2.71, P ‫؍‬ 0.006), prior (1 year) urinary catheter (OR ‫؍‬ 2.98, P ‫؍‬ 0.0025), and prior (6 months) antibiotic exposure (OR ‫؍‬ 2.68, P ‫؍‬ 0.005); (ii) for resistance to FQs male sex (OR ‫؍‬ 3.87, P ‫؍‬ 0.03), with a trend toward significance for age >65 years (OR ‫؍‬ 7.67, P ‫؍‬ 0.06) and prior (1 year) UTI (OR ‫؍‬ 2.98, P ‫؍‬ 0.07); and (iii) for resistance to SXT, male sex (OR ‫؍‬ 1.91, P ‫؍‬ 0.046), hospitalization in an intermediate-term-care unit (OR ‫؍‬ 2.18, P ‫؍‬ 0.008), and prior (1 year) UTI (OR ‫؍‬ 2.03, P ‫؍‬ 0.03). Ours results suggest that prior UTI is a common risk factor for resistance to the different antibiotics tested. Although few studies on risk factors for E. coli resistance to antibiotics have been published, careful interpretation of their findings, taking into consideration the population, infection site, and period studied, should contribute to the formulation of a better strategy that can be used to overcome antibiotic resistance.Escherichia coli, the most common member of the family Enterobacteriaceae implicated in human infectious diseases, has not been spared acquisition of antibiotic resistance, a complex therapeutic problem (7,15,38). The evolution of this microorganism's antibiotic resistance patterns identified from clinical isolates has been reported in many studies on amoxicillin (AMZ), amoxicillin-clavulanic acid (AMC), fluoroquinolones (FQs), and trimethoprim-sulfamethoxazole (SXT). Also, the intimate mechanisms of E. coli antibiotic resistance have been studied and explained in numerous publications (23,24,26,35,39). Unfortunately, few analyses of the demographic, epidemiological, and clinical data for patients with E. coli infection for determination of risk factors for resistance to antimicrobial agents have been reported (1,10,13,17,27,31).To evaluate the prevalence of resistance to a panel of antibiotics, including penicillins, cephalosporins, carbapenem, quinolones, aminoglycosides, and SXT, of E. coli strains isolated from hospitalized patients with acute urinary tract infections (UTIs) and to identify the risk factors for E. coli resistance to AMC, FQs, and SXT, which are routinely used to treat these infections, we conducted a prospective study in our hospital over a 3-month period. We discuss our observations, taking into consideration the most recent major studies on E. coli resist...

The mitochondrial toxicity of antiretrovirals, such as didanosine, seems to play a major role in worsening of fibrosis during HCV therapy. Therefore, anti-HCV therapy should ideally be administered before antiretroviral treatment initiation. If anti-HCV and anti-HIV treatments have to be administered concomitantly, then nucleoside reverse-transcriptase inhibitors with the lowest mitochondrial toxicity should be preferred.

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