The role of steroid treatment in drug-induced acute interstitial nephritis (DI-AIN) is controversial. We performed a multicenter retrospective study to determine the influence of steroids in 61 patients with biopsy-proven DI-AIN, 52 of whom were treated with steroids. The responsible drugs were antibiotics (56%), non-steroidal anti-inflammatory drugs (37%) or other drugs. The final serum creatinine was significantly lower in treated patients while almost half of untreated patients remained on chronic dialysis. Among treated patients, over half showed a complete recovery of baseline renal function, whereas the rest remained in renal failure. There were no significant initial differences between these two subgroups in terms of duration or dosage of steroids. After withdrawal of the presumed causative drug, we found that when steroid treatment was delayed (by an average of 34 days) renal function did not return to baseline levels compared to those who received steroid treatment within the first 2 weeks after withdrawal of the offending agent. We found a significant correlation between the delay in steroid treatment and the final serum creatinine. Renal biopsies, including three patients who underwent a second biopsy, showed a progression of interstitial fibrosis related to the delay in steroid treatment. Our study shows that steroids should be started promptly after diagnosis of DI-AIN to avoid subsequent interstitial fibrosis and an incomplete recovery of renal function.
Background Patients with advanced chronic kidney disease (CKD) exhibit higher prevalence of coronary artery calcification (CaC) than general population. CaC has been proposed as a risk factor for mortality in end-stage CKD, but most studies in the field are based on short-term follow-up. Methods We conducted a cohort, 10-year prospective longitudinal study of consecutive cases referred to the renal unit. A non-enhanced multislice coronary computed tomography was performed at baseline. CaC was assessed by Agatston method. Patients were stratified according to their CaC score: severe calcification group (CaCs< 400 HU) and mild-moderate calcification group (CaCs≥400 HU). The overall and cardiovascular (CV) mortality, CV events, and factors potentially associated with CaC development were recorded. Results 137 patients with advanced CKD were enrolled and provided consent. Overall mortality rate was 58%; 40% due to CV events. The rate of overall mortality in the severe calcification group was 75%, and 30% in the low calcification group, whereas the rate of CV mortality was 35% vs. 6%, respectively ( p < 0.001). The severe calcification group was older, had higher prevalence of type 2 diabetes mellitus, former cardiologic events, and lower albumin serum levels than the mild-moderate calcification group. In a multivariate Cox model, severe CaC was a significant predictor of CV mortality (HR 5.01; 95%CI 1.28 to 19.6, p = 0.02). Conclusions Among advanced CKD, there was a significantly increase of CV mortality in patients with severe CaCs during a 10-year follow-up period. CaCs could be a useful prognostic tool to predict CV mortality risk in CKD patients. Electronic supplementary material The online version of this article (10.1186/s12882-019-1367-1) contains supplementary material, which is available to authorized users.
Little is known about raltegravir removal by hemodialysis in patients with end-stage renal disease (ESRD). We therefore measured raltegravir concentrations in plasma in pre-and postdialyzer blood samples from 2 ESRD HIV-infected patients. The hemodialysis extraction ratio and raltegravir hemodialysis clearance were 5.5% and 9.1 ml/min in patient 1 and 9.5% and 19.1 ml/min in patient 2, respectively. Our results suggest minimal raltegravir removal by hemodialysis with no specific raltegravir dosage adjustments required in HIV-infected patients undergoing hemodialysis.The prevalence of chronic renal disease in HIV-infected patients has been estimated to be 5% to 40% (1, 6), depending on the definition applied in each study, and on the racial composition and comorbidity of the population studied. In any case, the progressive aging of the HIV-infected population together with the presence of some comorbid diseases (such as diabetes or hypertension), as well as direct toxicity derived from the antiretroviral drugs, provides a basis for growing concern that the prevalence of chronic renal disease and endstage renal disease (ESRD) may increase in the future (8). This means that an increasing number of HIV-infected patients will need renal replacement therapy.Raltegravir is an integrase inhibitor of HIV with demonstrated efficacy in naïve and treatment-experienced HIV-infected patients (5, 9). It is mainly metabolized by glucuronidation through UGT1A1 in the liver, with only 9% of the raltegravir dose excreted unchanged in the urine. Raltegravir is approximately 83% bound to plasma proteins, has a low molecular weight, and presents a relatively high solubility in water (blood-to-plasma partition coefficient, 0.6) (4). These characteristics make it possible for hemodialysis to remove raltegravir from plasma in patients with ESRD. As a result, subtherapeutic concentrations of raltegravir after the dialysis sessions might be possible.Here we report two cases of ESRD HIV-infected patients undergoing routine hemodialysis who were receiving antiretroviral therapy with raltegravir. To evaluate the effect of hemodialysis on raltegravir clearance, predialyzer and postdialyzer blood samples were collected at the beginning and end of a single dialysis session. Both patients gave their oral informed consent before sampling.Blood samples for raltegravir determinations were collected into potassium and EDTA-containing 10-ml tubes. Plasma was isolated by centrifugation (3,200 ϫ g for 15 min) and stored at Ϫ20°C until analysis. Raltegravir concentrations in plasma were determined by high-performance liquid chromatography with a fluorescence detector (HPLC multifluorescence detector 2475; Waters) according to a validated method (7). Chromatographic separation was performed on a Sunfire C 18 column (5 m; 4.6 by 150 mm) (Waters). The mobile phase was phosphate buffer-acetonitrile (25 mM, pH 3). The fluorescence detector was set at 299 and 396 nm for excitation and emission wavelengths, respectively. The drug was extracted from plasma by l...
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