Symptom burden can be explained to a limited extent by demographic and clinical variables and not by dialysis characteristics. Addition of symptom burden to the other variables makes it possible to explain one-third of perceived QL. This underlines the importance of symptom reduction in order to improve patient's QL.

Objective To analyze clinical features of peritoneal sclerosis (PS) in a group of peritoneal dialysis (PD) patients, and to compare potential risk factors and peritoneal transport characteristics with a control group matched for duration of PD. Design Study 1: Retrospective study of 16 PD patients with PS. Study 2: Case-control study comparing 10 patients with evident PS to 30 control patients who were matched for duration of PD. Setting Continuous Ambulatory Peritoneal Dialysis unit in the Academic Medical Centre in Amsterdam. Results The incidence of PS was 3.5 per 1000 patient years. PS was diagnosed either during PD (n = 10), in patients on hemodialysis (n = 2), or after successful transplantation (n = 4). Presenting symptoms were bowel obstruction, ascites, blood-stained effluent, and impaired net ultrafiltration. Macroscopic confirmation of the diagnosis was possible in 13 patients. Sclerotic encapsulation was present in 8 of them. Patients with PS were divided into three groups based on clinical symptoms and typical macroscopical findings. In category I the diagnosis PS was obvious (10 patients), in category II the diagnosis was highly suggestive (3 patients), and in category III it was doubtful (3 patients). Treatment was conservative in most patients. Surgical treatment was only possible in four and immunosuppressive therapy was given in 5 patients. Peritoneal sclerosis was the direct cause of death in 1 patient. Five patients died during follow-up due to other causes. At present, 7 patients are well and 3 patients (all from category I) still have recurrent bowel obstruction. Compared to matched controls, no difference existed in peritonitis incidence, or in the percentage of patients with former renal transplantations. The number of patients treated with β-blocking agents and the number of previous abdominal surgeries were not different. The number of catheter-related surgical procedures was higher in the PS patients than in the control group. The mass transfer area coefficient (MTAC) of creatinine was higher in PS patients and net ultrafiltration with 1.36% glucose was lower. The estimated cumulative glucose exposure until the diagnosis of PS was made was larger in PS patients than in their controls. This difference was already present in the first year of PD treatment in 8 of 10 patients. The initial values for the MTAC creatinine were similar in both groups. Conclusions The presenting symptoms of PS were bowel obstruction, ascites, and blood-stained effluent, often in combination with loss of net ultrafiltration. Peritoneal sclerosis is a complication of long-duration PD and could also become manifest after a successful renal transplant. Treatment should be conservative unless complications require surgical intervention. Patients with PS had lower net ultrafiltration and higher transport rates compared to controls who were matched for duration of PD. Although peritonitis incidence was similar, a relation of PS with severe peritonitis may be present in some patients. Glucose exposure is likely to be an important risk factor for PS.

Peritoneal permeability to proteins was measured in diabetic and non-diabetic continuous ambulatory peritoneal dialysis patients during peritonitis and control periods. Clearances of albumin, transferrin, IgG, C3 and α₂-macroglobulin appeared to decrease as molecular weight increased. This relationship could be described by a power curve fit. The decrease was more than could be explained by differences in free diffusion only, indicating a size-selective barrier in the peritoneum. For all measured proteins clearances were higher in the diabetic patients. This may reflect a generally increased permeability due to their microangiopathy. The largest increase in protein loss and protein clearances was found during peritonitis. Our results do not suggest increased local production of any of the investigated proteins during the inflammation. Therefore, an increase in either peritoneal permeability or effective surface area or both is the most likely explanation. It is concluded in this study that peritoneal protein clearances are dependent on their molecular weight and that they are proportionally increased in patients with diabetes and during peritonitis.

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The efficacy of peritoneal transport was assessed in 13 permeability studies in 11 continuous ambulatory peritoneal dialysis (CAPD) patients. During each study the in situ intraperitoneal volume was measured as well as the dialysate and plasma concentrations of various solutes with a molecular weight range from 60 to 5,500. As clearance estimations are unsuitable for the purpose of permeability studies, mass transfer area coefficients were used. By applying a simple mathematical model assuming first-order kinetics, these coefficients were calculated for urea, lactate, creatinine, glucose, kanamycin, and inulin. The accuracy of the calculations is indicated by their r values. After pooling these correlation coefficients, the mean approached 1.00 for all solutes with high confidence limits, indicating the usefulness of the model. A further simplification was tested using only an initial- and end-dialysate sample and two blood samples, without the measurement of the in situ intraperitoneal volume. Except for inulin the results of this simplification correlated well with the results described above. The reproducibility of the simplified mass transfer area coefficient calculations was investigated on 15 occasions in 3 other CAPD patients. The coefficients of variation of low molecular weight solutes varied between 15 and 20%. It is concluded that mass transfer area coefficient estimations using the latter method can be performed in any CAPD patient and probably yield sufficient information to establish the efficacy of the membrane transport mechanism during clinical follow-up.