Protective effect of mycophenolate mofetil on residual renal function in peritoneal dialysis patients: An open label feasibility study

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Peritoneal dialysis (PD) has become an established form of renal replacement therapy for patients with end‐stage renal disease (ESRD).1 According to the Chinese Renal Data Registration System, as of the end of 2013, the number of patients in mainland China receiving PD was 46 000.2 As a renal replacement therapy, PD offers several advantages over haemodialysis (HD). The modality is characterized by comparatively slow loss of residual renal function (RRF), which is an important prognostic indicator in PD patients.3
The original cause of kidney disease has an impact on the loss of RRF in PD patients. An annual rate of decline in RRF of 3.8 ± 2.5, 2.5 ± 4.8 and 1.9 ± 3.6 mL/min per 1.73m2 has been reported for patients with cystic kidney disease, diabetic kidney disease and glomerulonephritis, respectively.4 Another study reported that patients with proteinuric renal diseases were more likely to have a rapid loss of RRF.5 Few studies have evaluated therapeutic approaches for preserving RRF after the initiation of PD. One study reported that the angiotensin‐converting enzyme inhibitors (ACEIs) may decrease the loss of RRF in PD patients.6 A small single centre trial reported that low protein diets along with keto acid supplementation have been shown to better maintain RRF in incident PD patients.7 Effects of icodextrin, volume status, biocompatible peritoneal fluid on RRF needs to be confirmed.8 However, strategies that can help preserve RRF in PD patients are not well established.
Mycophenolate mofetil (MMF), a reversible DNA synthesis inhibitor, has found extensive application ranging from renal transplantation to the treatment of glomerulonephritis. Recent studies have revealed that MMF is also associated with an anti‐fibrosis effect. It has been reported that MMF can ameliorate transplant fibrosis in an experimental animal chronic allograft nephropathy (CAN) model, thus efficiently retarding the progression of CAN.9 It has been shown that MMF treatment effectively prevented the deterioration of renal function and interstitial fibrosis in ischaemia‐reperfusion injury rats, which may be associated with decreased transforming growth factor β1 (TGF‐β1), monocyte chemotactic protein 1 (MCP‐1) and macrophages.10 In murine lupus nephritis model, MMF was highly effective in suppressing fibrotic mediators, histological fibrosis score, and expression of TGF‐β1 in the kidney.11 Renal fibrosis is considered the common pathway of progressive kidney disease and strongly correlates with the deterioration of kidney function.12 Based on these findings, we reasoned that PD patients might benefit from the administration of MMF through its anti‐fibrosis effect, which may positively affect the RRF. We conducted a randomized clinical study to investigate the effect of MMF dosing during PD on the loss of RRF.
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