Peritoneal dialysis (PD), as one of the main renal replacement modalities for end-stage renal disease, gets the advantages of better protection of residual renal function and better quality of survival. However, ultrafiltration failure after peritoneal injury is an important reason for patients to withdraw from PD treatment. Peritonitis is a major complication of peritoneal dialysis, which results in an accelerated process of peritoneal injury due to direct damage from acute inflammation and local release of cytokine TGF-β. In this paper, the application of ultrasound to examine the peritoneum revealed a positive correlation between peritoneal thickness and the development of peritonitis. The results of this study also further confirmed the effect of peritonitis on peritoneal thickening. A multifactorial regression analysis also revealed that peritonitis and its severity were independent risk factors for peritoneal thickening and omental structural abnormalities. This paper reported a correlation between mural peritoneal thickness and peritoneal transit function. In this study, patients with high peritoneal transit and high mean transit were found to be more prone to omental structural abnormalities than patients with low mean and low transit and a higher proportion of patients with mural peritoneal thickening, but this did not reach statistical significance, which may be related to the still small number of cases.

No abstract

No abstract

Background Accumulating evidence from observational studies has shown that circulating C-reactive protein (CRP) levels are correlated with Type 1 diabetes (T1D) appearing a potential predictive marker of intervention, yet are of unknown causality. To clarify, we introduce a bidirectional two-sample Mendelian randomization (MR) framework to investigate the causality between circulating CRP levels and T1D. Methods Based on aggregated statistics from large-scale genome-wide association studies (GWAS), we evaluated the pooled impact of CRP on the risk of developing T1D. We obtained 6 single nucleotide polymorphisms (SNPs) for CRP selected as instrumental variables from a recent GWAS (n = 204,402). The T1D related SNPs were from a large-scale T1D GWAS (n = 6,808 T1D cases; n = 12,173 controls). Subsequent inverse-variance weighted (IVW) method, simple median method, weighted median method were conducted to acquire the genetic correlation between CRP levels and T1D. In sensitivity analyses, MR-Egger, MR-PRESSO, and leave-one-out analysis were applied to exclude the potentially pleiotropic variants in this study. Results The results of IVW provided no causal evidence that genetically predicted circulating CRP levels on the risk of T1D, with OR of 0.922 (95% CI: 0.662–1.285, P = 0.631). Furthermore, we denoted 14 T1D-related SNPs as an instrumental variable in MR analyses and yielded no significant associations of T1D on CRP levels according to the IVW result (OR: 1.000, 95% CI: 0.990–1.010, P = 0.930). MR-Egger, MR-PRESSO, and leave-one-out analysis indicated no indication for potential directional pleiotropy effects. Conclusion Our findings failed to provide evidence to support the causal relationship between CRP levels and T1D.