Abstract

Background: Acute antibody-mediated rejection (AMR) is the leading cause of early and late renal allograft dysfunction. The purpose of this study was to compare the clinico-pathological features between early and late acute AMR in Thai kidney transplant patients. Method: We examined our kidney transplant recipients for acute AMR demonstrated on biopsy between January 2005 and December 2013. Patients who had glomerulitis and/or peritubular capillaritis were enrolled and stratified by early (≤ 3 months) and late acute AMR (> 3 months after transplantation). Results: Of 64 patients with biopsy-proven acute AMR, 27 cases of early acute AMR were analyzed for associated factors compared with 37 cases of late acute AMR. Early acute AMR was more common in older patients (46.5 ± 10.0 vs. 34.9 ± 9.8; p < 0.001), female recipients (66.7% vs. 32.4%; p = 0.007), deceased donor allografts (70.4% vs. 37.8%; p = 0.01), and highly sensitized patients (74.1% vs. 13.5%; p = 0.01). Non-adherence was observed in 9 cases (24.3%) with late acute AMR whereas none with early acute AMR (p = 0.01). Endothelialitis was more prevalent in early acute AMR (77.8% vs. 10.8%; p < 0.001). Transplant glomerulopathy and interstitial fibrosis/tubular atrophy, the pathological features of chronic changes, were already demonstrated in late acute AMR (70.3% and 13.5%, respectively) but none in early acute AMR (p < 0.001 and 0.05, respectively). Peritubular capillary C4d deposition were commonly revealed in late acute (70.3% vs. 25.9%; p <0.001, respectively). Donor specific antibodies (DSA) were significantly evidenced in late acute AMR (67.6% vs 37%; p = 0.01). Anti-HLA class II (mostly anti-HLA DQ) was more common than class I (62.2% vs 21.6%; p = 0.003) in late acute AMR while anti-HLA class I (mostly anti-HLA A) was more prevalent than class II (29.6% vs 11.1%; p = 0.09) in early acute AMR. The patients with stable graft function at one year after anti-humoral treatment were observed in 21 cases (77.8%) with early acute AMR but only 13 cases (35.1%) with late acute AMR (p = 0.001). Conclusion: Despite similar pathological findings, early and late acute AMR are distinct clinical syndromes. Late acute AMR has worse prognosis than early acute AMR.

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