Peritoneal transport status and first episode of peritonitis: a large cohort study

Abstract

Background: Peritonitis is one of the most serious complications of peritoneal dialysis (PD). This study aimed to explore the relationship between peritoneal transport status and the first episode of peritonitis, as well as the prognosis of patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Method: A retrospective cohort study was conducted, analyzing data of CAPD patients from 1st January 2009, to 31st December 2017. Baseline data within 3 months after PD catheter placement was recorded. Cox multivariate regression analysis was performed to determine the risk factors for the first episode of peritonitis, technique failure and overall mortality. Results: A total of 591 patients were included in our analysis, with a mean follow-up visit of 49 months (range: 27-75months). There were 174 (29.4%) patients who had experienced at least one episode of peritonitis. Multivariate Cox regression analysis revealed that a higher peritoneal transport status (high and high-average) (HR 1.872, 95%CI 1.349-2.599, p ¼ 0.006) and hypoalbuminemia (HR 0.932,95% CI 0.896, 0.969, p ¼ 0.004) were independent risk factors for the occurrence of the first episode of peritonitis. In addition, factors including gender (male) (HR 1.409, 95%CI 1.103, 1.800, p ¼ 0.010), low serum albumin (HR 0.965, 95%CI 0.938, 0.993, p ¼ 0.015) and the place of residence (rural) (HR 1.324, 95%CI 1.037, 1.691, p ¼ 0.024) were independent predictors of technique failure. Furthermore, low serum albumin levels (HR 0.938, 95%CI 0.895, 0.984, p ¼ 0.008) and age (>65years) (HR 1.059, 95%CI 1.042, 1.076, p < 0.001) were significantly associated with the risk of overall mortality of PD patients. Conclusions: Baseline hypoalbuminemia and a higher peritoneal transport status are risk factors for the first episode of peritonitis. Factors including male gender, hypoalbuminemia, and residing in rural areas are associated with technique failure, while hypoalbuminemia and age (>65years) are predictors of the overall mortality in PD patients. Nevertheless, the peritoneal transport status does not predict technique failure or overall mortality of PD patients.

Glycoprotein 96 in Peritoneal Dialysis Effluent-Derived Extracellular Vesicles: A Tool for Evaluating Peritoneal Transport Properties and Inflammatory Status

“…Previous reports indicate that peritoneal injury triggers the activation of inflammatory cells, such as neutrophils, macrophages, and mesothelial cells, which recognize bacterial pathogens via Toll-like receptors (TLRs), activate relative inflammatory signaling pathways, and ultimately release a large number of pro-inflammatory cytokines ( 27 – 29 ). It is also suggested that higher PSTR may predispose patients to more inflammation than lower PSTR ( 30 ). Among the differentially expressed proteins between the groups, we identified three proteins (ITGB2, S100A8, and GP96) with a fold change ≥1.9 for their possible participation in the immune inflammatory response according to GO and KEGG analysis.…”

Association between serum total indoxyl sulfate, intraperitoneal inflammation, and peritoneal dialysis technique failure: a 3-year prospective cohort study

“…Conversely, high peritoneal transport status is a well-known PD-related peritonitis risk factor [40,41].…”

Albumin-to-alkaline phosphatase ratio as a novel prognostic indicator in patients undergoing peritoneal dialysis: a propensity score matching analysis

“…However, hypoalbuminemia was recently reported to correlate with poor prognosis in PD patients and was attributed more to inflammation than malnutrition ( 19 ). A sufficient amount of albumin is likely to improve intravascular volume and bind inflammatory cytokine, all of which are risk factors for the incidence of PD related peritonitis, resulting in technique failure of PD and increased hophitalization rate and mortality ( 20 , 21 ). Second, with regard to ALP, it is evidently related to nutritional status and inflammation in CKD ( 22 , 23 ) and may be further involved in the progression of vascular calcification.…”