Abstract
Background and Aims
Type I membrane failure (T1MF), increased transport status with ultrafiltration, and solute removal inadequacy are among the most challenging issues in peritoneal dialysis (PD) continuity. Although quite common, the causes of T1MF are not fully understood. This study aims to identify risk factors associated with T1MF.
Method
This is a retrospective, single site, cohort study of incident adult peritoneal dialysis patients sampled between January 2000 and January 2020. Patients were classified as “increased transporters” who had two or more categories of a rise in peritoneal equilibration test (PET), and “stable transporters” who had had a rise of 1 or no categories from their baseline during follow-up. The four-hour dialysate/plasma creatinine ratio was used to classify PET categories. The study endpoint was five years for stable transporters, and at the time of two category rise in the PET test for increased transporters.
Results
Baseline demographics, diabetes frequency, residual renal function (RRF), non-phosphate baseline laboratory, parathormone levels, and PD modalities were similar between the increased transporters (n=48) and the stable transporters (n=93). Significantly more patients were using renin-angiotensin-aldosterone system (RAAS) blockers in stable transporters and high-glucose dialysates in increased transporters (p=0.03 and p<0.01). Icodextrin, calcitriol, calcium-based phosphate binder use, and the number of peritonitis episodes were similar between the groups. Increased transporters reached the endpoint in 3.9(±0.7) years. Increased transporters had a higher baseline phosphate than stable transporters (p=0.02). The frequency of patients with an RRF and groups’ mean RRF in ml were similar at the endpoint (p=0.37, p=0.13). Increased transporters had a significantly higher baseline and endpoint CaXP than stable transporters (p<0.01 and p=0.02). Baseline weekly peritoneal Kt/V and peritoneal creatinine clearance (PCrCl) were similar at baseline. Increased transporters had significantly lower endpoint peritoneal Kt/V and insignificantly lower endpoint PCrCl than stable transporters (p<0.01 and p=0.05). ΔUF was negative for increased transporters and positive for stable transporters. Age, diabetes, peritonitis episodes, RAAS blocker use, and PD modality were insignificant in Cox regression analysis. A CaXP of >55 was related to 2.51-fold, and high-glucose dialysates were associated with a 2.93-fold increased risk for a rise in transport status (p=0.01 and p<0.01). Mean follow-up was 7.0 (±3.9) years for stable transporters and 5.6 (±2.0) years for increased transporters. Technical survival was significantly higher in stable transporters (p=0.03).
Conclusion
Our study revealed a CaXP of >55 is a risk factor for a significant increase in transport status, presumably due to peritoneal calcification. The peritoneal Kt/V, PCrCl, and UF rates declined accordingly. The high-glucose dialysates are associated with a high risk in analyses. However, it is not possible to determine whether these solutions are the cause or the result of Type I membrane failure.
Methods to Analyze Time-to-Event Data: The Cox Regression Analysis
