Direct Comparison of the Thickness Of The Parietal Peritoneum Using Peritoneal Biopsy and Ultrasonography of the Abdominal Wall in Patients Treated with Peritoneal Dialysis.

Background:Long-term treatment with peritoneal dialysis (PD) results in peritoneal fibrosis. Peritoneal biopsies have been used to determine the severity of fibrosis. Ultrasonography (US) of the abdominal wall has been used to measure peritoneal thickness non-invasively. However, direct comparison of both methods in the same patient has never been done. Furthermore, the validity of US to measure peritoneal thickness has not been investigated.Methods:We performed 3 studies: 1) a human biopsy study to compare US measurement of peritoneal thickness with histological examination; 2) a human cadaver study to investigate the effect of removing the peritoneum on US results; and 3) a phantom study in which we used US to measure the thickness of membrane-like structures with a known thickness to investigate the influence of different US settings.Results:The median thickness in biopsies of the peritoneum was 113 µm (interquartile range [IQR] 72 -129 µm), while this was 370 µm (IQR 324 - 458 µm) when measured by US (p < 0.0001). The mean difference between the 2 measures was -257 µm (limits of agreement -4.6 and -511 µm). In the cadaver study, removal of the peritoneum did not have an effect on the presence or thickness of the hyperechoic line reported to represent the peritoneum. In the phantom study, results were highly dependent on frequency of the transducer, scan depth, and gain settings.Conclusions:Ultrasonography results differ markedly from histological measurement using peritoneal biopsies. However, the hyperechoic line generated by US represents the interface between 2 neighboring tissues and not a separate morphological structure. Moreover, its thickness is greatly influenced by user-defined US settings.

Absence of Post-Transplantation Encapsulating Peritoneal Sclerosis after Relatively Short Exposure to Peritoneal Dialysis: Prospective Analysis Using Repeated Abdominal CT Scanning.

BACKGROUND: Encapsulating peritoneal sclerosis (EPS) is the most severe complication of peritoneal dialysis (PD). Several retrospective reports published between 2007 and 2009 have suggested an increasing incidence of EPS occurring after kidney transplantation. We conducted a prospective observational study to determine the incidence of post-transplantation EPS and identify possible risk factors. METHODS: Consecutive PD patients undergoing kidney transplantation between 2009 and 2013 were included. Encapsulating peritoneal sclerosis was defined as gastrointestinal obstruction combined with radiological evidence of EPS. Gastrointestinal symptoms were assessed using a self-administered Gastrointestinal Symptom Rating Scale (GSRS) questionnaire. Abdominal computed tomography (CT) was performed prospectively at 6 and 18 months post-transplantation. The primary end point was EPS during follow-up. RESULTS: Fifty-three PD patients were included (age 51 ± 14 years). Mean PD duration was 31.3 months. Peritoneal dialysis solutions low in glucose degradation products and icodextrin were used by 86.8% of patients. A fast or average-fast transport status was documented in 83.0%. After a median follow-up of 19 months, complete data of 47 patients were available for analysis. None of the patients developed clinical or radiological signs of EPS. The GSRS score improved from 1.87 to 1.55 (p = 0.024) and body weight increased from 75.9 to 78.3 kg (p = 0.003). Only 1 patient had new onset localized (< 20%) peritoneal thickening on CT 22 months post-transplantation. CONCLUSION: Post-transplantation EPS did not develop in this cohort of patients with a relatively short time of PD exposure. This suggests that these patients can be transplanted safely without concern for the development of EPS, at least within the follow-up period of 19 months.

Impact of Intraoperative Hypotension During Cardiopulmonary Bypass on Acute Kidney Injury After Coronary Artery Bypass Grafting.

OBJECTIVE: The aim of this study was to investigate whether acute kidney injury (AKI) after coronary artery bypass grafting can be attributed to intraoperative hypotension during cardiopulmonary bypass (IOH-CPB). DESIGN: Retrospective analysis. SETTING: Tertiary-care hospital. PARTICIPANTS: Patients undergoing on-pump coronary artery bypass grafting from June 2011 to January 2014. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: IOH-CPB was defined as blood pressure below several absolute and relative mean arterial pressure (MAP) thresholds and as the area under the curve for absolute MAP thresholds. AKI was defined as an absolute increase in serum creatinine of≥26 µmol/L within 48 hours or an increase to 150% or more within 7 days of surgery. Poisson regression with robust standard errors both before and after adjustment for confounders was used. Of the 1,891 patients included, 386 (20%) developed AKI. In univariable analysis, all IOH-CPB thresholds defined as a MAP of 50 mmHg or less and as a decrease in MAP of 60% from baseline were associated with a 1.07-to-1.11 times increased risk of AKI per 10 minutes of IOH-CPB (p<0.01). After adjustment for potential confounders, IOH-CPB, irrespective of the definition chosen, was not associated with an increased risk of AKI. CONCLUSIONS: In the authors' study population, univariable analysis showed an association of IOH-CPB with AKI in patients undergoing isolated CABG, but this relationship disappeared after correction for well-known risk factors for AKI.

Patients with encapsulating peritoneal sclerosis have increased peritoneal expression of connective tissue growth factor (CCN2), transforming growth factor-ß1, and vascular endothelial growth factor.

INTRODUCTION: Encapsulating peritoneal sclerosis (EPS) is a devastating complication of peritoneal dialysis (PD). The pathogenesis is not exactly known and no preventive strategy or targeted medical therapy is available. CCN2 has both pro-fibrotic and pro-angiogenic actions and appears an attractive target. Therefore, we studied peritoneal expression of CCN2, as well as TGFß1 and VEGF, in different stages of peritoneal fibrosis. MATERIALS AND METHODS: Sixteen PD patients were investigated and compared to 12 hemodialysis patients and four pre-emptively transplanted patients. Furthermore, expression was investigated in 12 EPS patients in comparison with 13 PD and 12 non-PD patients without EPS. Peritoneal tissue was taken during kidney transplantation procedure or during EPS surgery. In a subset of patients, CCN2 protein levels in peritoneal effluent and plasma were determined. Samples were examined by qPCR, histology, immunohistochemistry, and ELISA. RESULTS: Peritoneal CCN2 expression was 5-fold higher in PD patients compared to pre-emptively transplanted patients (P < 0.05), but did not differ from hemodialysis patients. Peritoneal expression of TGFß1 and VEGF were not different between the three groups; neither was peritoneal thickness. Peritoneum of EPS patients exhibited increased expression of CCN2 (35-fold, P < 0.001), TGFß1 (24-fold, P < 0.05), and VEGF (77-fold, P < 0.001) compared to PD patients without EPS. In EPS patients, CCN2 protein was mainly localized in peritoneal endothelial cells and fibroblasts. CCN2 protein levels were significantly higher in peritoneal effluent of EPS patients compared to levels in dialysate of PD patients (12.0 ± 4.5 vs. 0.91 ± 0.92 ng/ml, P < 0.01), while plasma CCN2 levels were not increased. CONCLUSIONS: Peritoneal expression of CCN2, TGFß1, and VEGF are significantly increased in EPS patients. In early stages of peritoneal fibrosis, only CCN2 expression is slightly increased. Peritoneal CCN2 overexpression in EPS patients is a locally driven response. The potential of CCN2 as biomarker and target for CCN2-inhibiting agents to prevent or treat EPS warrants further study.