4). We postulate, that

the lack of further peritoneal thickening and encapsulation over the last 24 months reflects a positive therapeutic response to ongoing medical therapy with everolimus, tamoxifen and low dose corticosteroids. Graft function remains SP600125 stable with a creatinine of 90 μmol/L. He has developed moderate proteinuria, 700 mg/day, since commencing everolimus, though this has remained stable with time. EPS is a rare, but devastating complication of PD therapy.[1] It is characterised by marked sclerotic thickening of the peritoneal membrane that causes bowel loops to become adherent and encapsulated resulting in intermittent bowel obstruction. The clinical presentation is with ultrafiltration failure and altered gastrointestinal transit in a patient who has been on peritoneal dialysis for many years. Fludarabine Symptoms of altered gastrointestinal transit include abdominal fullness, bloating, anorexia, nausea and vomiting initially, and complete intestinal obstruction in the most severe stage. It is commonly associated with malnutrition as a result of reduced oral intake, and a recurrent bloody effluent that collects in pockets created within the peritoneal cavity.

The aetiology of EPS is unclear. Traditional risk factors include increased risk proportional to duration of PD, recent cessation of PD, use of dialysis solutions with lower biocompatibility and peritonitis episodes. The ‘two hit theory’ suggests that long term deterioration of the peritoneum combined with intraperitoneal inflammation is needed in the pathogenesis of EPS.[2] This case is consistent with that theory. Long term PD induced peritoneal

damage is an inevitable consequence of the use of dialysis solutions that are inherently bio-incompatible. This damage to the membrane is histologically seen as mesothelial denudation, submesothelial interstitial fibrosis and vascular sclerosis. The vascular changes result in chronic plasma exudation from the peritoneal vasculature to the peritoneal surface and eventual fibrin deposition.[2] The deposition and organisation of fibrin results in formation of a peritoneal capsule, and combined Staurosporine clinical trial with peritoneal fibroblast activation and proliferation, they are major features in the pathogenesis of EPS.[2] Honda et al. have proposed that the presence of fibrin deposition, fibroblast swelling, capillary angiogenesis and a mononuclear cell infiltrate on peritoneal biopsy be required for a histological diagnosis of EPS.[2] Recent studies have reported an increase in the incidence of EPS following renal transplantation.[3] One proposed factor is that following transplantation, fibrin can accumulate on a reactive peritoneum as PD fluid-related peritoneal lavage has stopped.