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Development of Encapsulating Peritoneal Sclerosis in a Renal Transplant Recipient on Sirolimus Immunotherapy

Editor: The causal factors underlying the primary trigger for encapsulating peritoneal sclerosis (EPS) are not completely understood (1). Several centers have reported an increasing incidence of EPS following renal transplantation in peritoneal dialysis (PD) patients (2–5). The reasons for this apparent increase are unclear. Traditional risk factors for EPS, such as an increased duration of PD and recent cessation of PD, may be responsible. Yet, it is tempting to speculate that a history of renal transplantation itself may be evolving as a novel risk factor (2,6). Of concern are the profibrotic effects of calcineurin inhibition (CNI) (7,8), the mainstay of current renal transplant immunosuppression protocols. In contrast, animal data suggest that sirolimus, an alternative to CNI immunotherapy, may attenuate the morphologic profibrotic peritoneal changes induced by EPS (9). Here we report a case of EPS that presented shortly after renal transplantation, in the absence of concurrent CNI and while on sirolimus immunotherapy. In 1999, a 26-year-old woman originally from China developed end-stage renal disease secondary to immunoglobulin A (IgA) nephropathy and was initiated on continuous ambulatory PD. In 2004, PD therapy was complicated by a single episode of PD peritonitis with Lactobacillus species, requiring catheter removal and reinsertion. At that time, the patient was converted to automated PD. In June 2006, after 88 months of PD treatment, she underwent a deceased donor renal transplant. Medications at that time included oral iron, enalapril, and erythropoietin, with no prior exposure to betablockade. Peritoneal equilibration testing performed 2 months prior to transplantation revealed a dialysateto-plasma creatinine ratio of 0.8, which had been stable for the previous 3 years. During that time, she routinely required the use of hypertonic (4.25% glucose) dialysate to maintain adequate peritoneal ultrafiltration. Induction immunotherapy included methylprednisolone and antithymocyte globulin at an initial dose of 5 mg/kg. The posttransplant course was complicated by delayed graft function. A postoperative biopsy revealed nephrocalcinosis without evidence of acute rejection. A subsequent biopsy 1 week later revealed nephrocalcinosis as well as evidence of acute cellular rejection. The rejection was treated with additional antithymocyte globulin to achieve a total dose of 7.5 mg/kg. Initial maintenance immunotherapy included mycophenolate mofetil and tacrolimus, with levels maintained between 5 and 8 μg/L. Enalapril was continued posttransplantation. The patient required supplemental automated PD until January 2007, when her graft was functioning well. In an effort to avoid CNI-mediated nephrotoxicity, her tacrolimus was discontinued at that time and her immunosuppressive regimen consisted of sirolimus 5 mg daily and prednisone 5 mg daily, with sirolimus levels maintained between 4 and 11 μg/L. At 13 months post renal transplantation, the patient developed weight loss, persistent nausea and vomiting, and obstipation. Computed tomography (CT) scan at that time revealed evidence of small bowel obstruction and culture-negative exudative tense ascites, which was drained. She had several admissions over the following 6-month period for recurrent small bowel obstructions. Due to the concern of imminent surgery and the impaired wound healing associated with sirolimus, the patient was switched to CNI tacrolimus, with trough levels between 4 and 6 ng/mL. In February 2008, a CT scan revealed a possible closed-loop obstruction. Emergent laparotomy was performed for lysis of adhesions while confirming the diagnosis of EPS. Despite surgery, progressive recurrent small bowel obstructions and malnutrition persisted. Eventually she was started on total parenteral nutrition. In early 2009, the patient was again admitted to hospital with obstructive symptoms. She also began experiencing a decline in her renal function and hemodialysis was initiated. Tacrolimus was stopped but prednisone 10 mg daily, tapered to 5 mg daily over 3 months, was continued as part of treatment of her EPS. In September 2009, the patient had a second laparotomy for resection of a jejunal segment of small bowel, which appeared to be the major source of her obstructive symptoms. The surgery was successful in that the patient was able to increase