Abstract

immunohistocemical staining of MCP and complement after the diagnosis of ATCMR type I and type II. The expression of MCP was then examined for the functional outcome of the graft and clinicopathological correlations. Graft function was determined by serum creatinine measurements, before biopsy, at the time of biopsy, at 2 and 12 months. Graft failure was defined as the resumption of dialysis. ATCMR was generally treated with glucocorticoids and deoxyspergualin. RESULTS: C3b deposition in renal tubular cells was observed in 60 patients (93.8 %), but no C4d deposition was detected in renal tubular cells. No difference in serum creatinine levels were found between the patients with high and low MCP expression before and at the time of biopsy. After the anti-rejection treatment, patients with high MCP expression had lower creatinine levels compared to those with low MCP expression (1.47 0.40 mg/dL v.s. 1.76 0.79 mg/dL at 2 months after biopsy, 1.50 0.40 mg/dL v.s. 1.85 0.66 mg/dL at 12 months after biopsy, Tab. 2). Graft loss was observed in 6 patients (17.6 %) in the low MCP expression graft and 3 patients (10 %) in the high MCP expression group. 5-year graft survival was better in patients with high MCP expression compared to those with low MCP expression, 100 % versus 76.6 % respectively (p 0.042). The age of the donor in the high MCP expression group was significantly lower than that of the low MCP expression group in both univariate and multivariate analyses (p 0.003, p 0.001, respectively, Tab. 3). CONCLUSIONS: We first showed the possibility that MCP expression in renal tubular cells during ATCMR may influence the outcome of treatment and graft survival. Grafts from older donors may be a risk factor for decreased expression of MCP in renal tubular cells. The clinical application of MCP and complement regulatory drugs is considered to have some potential for suppressing ATCMR after transplantation and to improve graft outcome.

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