Programme Hospitalier Recherche Clinique, Institut Pasteur, Inserm, French Public Health Agency.

This series constitutes the largest series of adults with IgAV reported in the literature so far. It provides data on clinical and histologic presentation and therapeutic efficacy, suggesting that CS alone appears to be a reasonable first-line therapy in patients with IgAV, while the benefit of adding CYC to CS remains uncertain.

Background: Acute kidney injury (AKI) with renal tubular obstruction by red blood cell casts (RBCC) has been described in patients treated with warfarin and is known as warfarin-related nephropathy (WRN). Methods: To determine whether other vitamin K antagonists (VKA) cause WRN, we retrospectively collected and analyzed the clinical and histological data of 13 patients treated with different VKA (seven with fluindione, four with warfarin and two with acenocoumarol) in seven French hospitals. Results: They all developed gross hematuria following overanticoagulation complicated by severe AKI (median serum creatinine concentration = 693 μmol/L). Histological analysis of the kidney biopsies highlighted the presence of intratubular RBCC and acute tubular necrosis in all patients and of an underlying kidney disease in 12 patients. WRN was suspected in patients treated with warfarin; however, the initial diagnosis was incorrect in six of the nine patients treated with other VKA. Nine patients progressed to chronic kidney disease, one fully recovered renal function, two died and one still needs dialysis. Conclusions: This is the first report of AKI caused by fluindione. In agreement with the recent publication on AKI in two patients treated with dabigatran, we suggest that the term ‘anticoagulant-related nephropathy’ is more appropriate than WRN. Gross hematuria in patients with an underlying kidney disease and treated with VKA requires rapid control of the international normalized ratio and renal function monitoring.

♦ Background: Transfer to hemodialysis (HD) is a frequent cause of peritoneal dialysis (PD) cessation. In the present study, we set out to describe the transition period between PD and HD.

No abstract

Background Citric acid–based bicarbonate haemodialysis (CIT-HD) has gained more clinical acceptance over the last few years in France and is a substitute for other acidifiers [e.g. acetic acid (CH3COOH) and hydrochloric acid (HCl)]. This trend was justified by several clinical benefits compared with CH3COOH as well as the desire to avoid the consequences of the corrosive action of HCl, but a nationwide clinical report raised concerns about the long-term safety of CIT-HD. The aim of this study was to assess the long-term effects of CIT-HD exposure on patient outcomes in western France. Methods This is a population-based retrospective multicentre observational study performed in 1132 incident end-stage kidney disease patients in five sanitary territories in western France who started their renal replacement therapy after 1 January 2008 and followed up through 15 October 2018. Relevant data, collected prospectively with the same medical software, were anonymously aggregated for the purposes of the study. The primary goal of this study was to investigate the effects of citrate exposure on all-cause mortality. To provide a control group to CIT-HD one, propensity score matching (PSM) at 2:1 was performed in two steps: the first analysis was intended to be exploratory, comparing patients who received citrate ≤80% of the time (CIT-HD ≤80) versus those who received citrate >80% of the time (CIT-HD >80), while the second analysis was intended to be explanatory in comparing patients with 0% (CIT-HD0) versus 100% citrate time exposure (CIT-HD100). Results After PSM, in the exploratory part of the analysis, 432 CIT-HD ≤80 patients were compared with 216 CIT-HD >80 patients and no difference was found for all-cause mortality using the Kaplan–Meier model (log-rank 0.97), univariate Cox regression analysis {hazard ratio [HR] 1.01 [95% confidence interval (CI) 0.71–1.40]} and multivariate Cox regression analysis [HR 1.11 (95% CI 0.76–1.61)] when adjusted for nine variables with clinical pertinence and high statistical relevance in the univariate analysis. In the explanatory part of the analysis, 316 CIT-HD0 patients were then compared with 158 CIT-HD100 patients and no difference was found using the Kaplan–Meier model (log-rank 0.06), univariate Cox regression analysis [HR 0.69 (95% CI 0.47–1.03)] and multivariate Cox regression analysis [HR 0.87 (95% CI 0.57–1.33)] when adjusted for seven variables with clinical pertinence and high statistical relevance in the univariate analysis. Conclusions Findings of this study support the notion that CIT-HD exposure ≤6 years has no significant effect on all-cause mortality in HD patients. This finding remains true for patients receiving high-volume online haemodiafiltration, a modality most frequently prescribed in this cohort.

Fallback is a common event in hemodialysis patients treated in SDUs. Yet, the SDU system operates well since a third of patients treated in these units are still in SDUs at 2 years of follow-up. Factors associated with patient fallback are the center and cardiovascular disease.

We conducted a prospective study to assess the impact of the blood pump flow rate (BFR) on the dialysis dose with a low dialysate flow rate. Seventeen patients were observed for 3 short hemodialysis sessions in which only the BFR was altered (300,350 and 450 mL/min). Kt/V urea increased from 0.54 ± 0.10 to 0.58 ± 0.08 and 0.61 ± 0.09 for BFR of 300, 400 and 450 mL/min. For the same BFR variations, the reduction ratio (RR) of β2microglobulin increased from 0.40 ± 0.07 to 0.45 ± 0.06 and 0.48 ± 0.06 and the RR phosphorus increased from 0.46 ± 0.1 to 0.48 ± 0.08 and 0.49 ± 0.07. In bivariate analysis accounting for repeated observations, an increasing BFR resulted in an increase in spKt/V (0.048 per 100 mL/min increment in BPR [p < 0.05, 95% CI (0.03–0.06)]) and an increase in the RR β2m (5% per 100 mL/min increment in BPR [p < 0.05, 95% CI (0.03–0.07)]). An increasing BFR with low dialysate improves the removal of urea and β2m but with a potentially limited clinical impact.