Summary Among factors determining long‐term kidney allograft outcome, pretransplant renal replacement therapy (RRT) is the most easily modifiable. Previous studies analysing RRT modality impact on patient and graft survival are conflicting. Studies on allograft function are scarce, lack sufficient size and follow‐up. We retrospectively studied patient and allograft survival together with allograft function and its decline in 2277 allograft recipients during 2000–2014. Pretransplant RRT modality ≥60 days as grouped into “no RRT” (n = 136), “haemodialysis (HD)” (n = 1847), “peritoneal dialysis (PD)” (n = 159), and “HD + PD” (n = 135) was evaluated. Kaplan–Meier analysis demonstrated superior 5‐/10‐/15‐year patient (93.0/81.8/73.1% vs. 86.2/71.6/49.8%), death‐censored graft (90.8/85.4/71.5% vs. 84.4/75.2/63.2%), and 1‐year rejection‐free graft survival (73.8% vs. 63.8%) in PD versus HD patients. Adjusted Cox regression revealed 34.5% [1.5–56.5%] lower hazards of death, whereas death‐censored graft loss was similar [HR = 0.707 (0.469–1.064)], and rejection was less frequent [HR = 0.700 (0.508–0.965)]. Allografts showed higher 1‐/3‐/5‐year estimated glomerular filtration rate (eGFR) in “PD” versus “HD” groups. Living donation benefit for allograft function was most pronounced in groups “no RRT” and “PD”. Functional allograft decline (eGFR slope) was lowest for “PD”. Allograft recipients on pretransplant PD versus HD demonstrated superior all‐cause patient and rejection‐free graft survival along with better allograft function (eGFR).
Background Dialysis patients are at increased risk of HF. However, diagnostic utility of NT-proBNP as a biomarker is decreased in patients on dialysis. GDF-15 and cNEP are biomarkers of distinct mechanisms that may contribute to HF pathophysiology in such cohorts. The aim of this study was to determine whether growth differentiation factor-15 (GDF-15) and circulating neprilysin (cNEP) improve the diagnosis of congestive heart failure (HF) in patients on dialysis. Methods and results We compared circulating concentrations of NT-proBNP, GDF-15, and cNEP along with cNEP activity in patients on chronic dialysis without ( n = 80) and with HF ( n = 73), as diagnosed by clinical parameters and post-dialysis echocardiography. We used correlation, linear and logistic regression as well as receiver operating characteristic (ROC) analyses. Compared to controls, patients with HF had higher median values of NT-proBNP (16,216 [interquartile range, IQR = 27739] vs. 2883 [5866] pg/mL, p < 0.001), GDF-15 (7512 [7084] vs. 6005 [4892] pg/mL, p = 0.014), but not cNEP (315 [107] vs. 318 [124] pg/mL, p = 0.818). Median cNEP activity was significantly lower in HF vs. controls (0.189 [0.223] vs. 0.257 [0.166] nmol/mL/min, p < 0.001). In ROC analyses, a multi-marker model combining clinical covariates, NT-proBNP, GDF-15, and cNEP activity demonstrated best discrimination of HF from controls (AUC = 0.902, 95% CI 0.857–0.947, p < 0.001 vs. base model AUC = 0.785). Conclusion We present novel comparative data on physiologically distinct circulating biomarkers for HF in patients on dialysis. cNEP activity but not concentration and GDF-15 provided incremental diagnostic information over clinical covariates and NT-proBNP and may aid in diagnosing HF in dialysis patients. Graphic abstract Electronic supplementary material The online version of this article (10.1007/s00392-020-01597-x) contains supplementary material, which is available to authorized users.
Background Peritoneal dialysis (PD)-associated peritonitis remains by far the most important complication requiring patients to transfer to hemodialysis and has a major impact on patient morbidity and mortality. Current International Society for Peritoneal Dialysis (ISPD) guidelines on peritonitis recommend analysis of peritonitis episodes only in trained patients. In a large tertiary care center, we analyzed peritonitis episodes accounting for different groups of untrained patients and compared these with episodes in the trained patient population. Methods We analyzed data collected prospectively over a 15-year time span regarding differences between peritonitis episodes in trained patients and episodes in untrained patients post-catheter insertion but prior to training completion as well as on in-center intermittent PD with respect to incidence rates, pathogenic organisms, outcome, and peritonitis predictors. Results In 275 patients, a total of 160 peritonitis episodes in trained patients were counted. A total of 27 additional episodes in untrained patients were recorded. When accounting for these episodes, the peritonitis incidence significantly increased and the percentage of peritonitis-free patients decreased. Peritonitis episodes in untrained patients were most often culture-negative and the pathogen spectrum differed significantly compared with episodes counted as per ISPD recommendations, while outcome of peritonitis episodes did not differ. Predictors of peritonitis after multivariate logistic regression analysis included glomerulonephritis as primary kidney disease, being on home PD rather than being on in-center intermittent PD, and higher dialysis vintage. Conclusions Depending on local practice patterns, we argue that centers should additionally monitor peritonitis episodes in untrained patients because computation of statistics as per ISPD recommendations could underestimate peritonitis incidence and may depict a distorted pathogen spectrum.
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