BACKGROUND: The aims of this study were to determine the level of donor-specific antibody (DSA) that allows for successful transplantation after desensitization with IVIG and rituximab and to identify patients at risk for antibody-mediated rejection (AMR). METHODS: Pre- and posttransplant sera from 16 patients with DSA before desensitization were tested. Strength of DSA was determined by single antigen Luminex bead assay and results expressed as standard fluorescence intensity (SFI). T-cell flow crossmatch results were expressed as mean channel shifts (MCS). AMR was determined by biopsy and C4d deposition. RESULTS: Six had negative pretransplant flow crossmatches with a mean DSA of 8,805 SFI. Five had positive flow crossmatches (78-192 MCS) with mean DSA of 55,869 SFI. No patients in either group had AMR. Five had positive flow crossmatches (222-266 MCS) with mean DSA of 118,063 SFI. Three experienced AMR. The MCS and DSA levels for patients with AMR were significantly higher than patients without (P < or = 0.001). For patients without complications (n=7), DSA remained less than 10(5) SFI and usually decreased to approximately 10(4) SFI posttransplant for both class I and II. For patients with AMR (n=3), predominant increases in class II DSA more than 10(5) SFI were observed. All three patients continue to have DSA approximately 10(5) SFI with stable creatinine after treatment for AMR. CONCLUSIONS: Approximately 63% of patients were transplanted with a positive flow crossmatch. The results show that patients with DSA more than 10(5) and FCM more than 200 MCS are at higher risk for AMR. Treatment of AMR improves renal function without significant changes in DSA.
BACKGROUND: The aims of this study were to determine the level of donor-specific antibody (DSA) that allows for successful transplantation after desensitization with IVIG and rituximab and to identify patients at risk for antibody-mediated rejection (AMR). METHODS: Pre- and posttransplant sera from 16 patients with DSA before desensitization were tested. Strength of DSA was determined by single antigen Luminex bead assay and results expressed as standard fluorescence intensity (SFI). T-cell flow crossmatch results were expressed as mean channel shifts (MCS). AMR was determined by biopsy and C4d deposition. RESULTS: Six had negative pretransplant flow crossmatches with a mean DSA of 8,805 SFI. Five had positive flow crossmatches (78-192 MCS) with mean DSA of 55,869 SFI. No patients in either group had AMR. Five had positive flow crossmatches (222-266 MCS) with mean DSA of 118,063 SFI. Three experienced AMR. The MCS and DSA levels for patients with AMR were significantly higher than patients without (P < or = 0.001). For patients without complications (n=7), DSA remained less than 10(5) SFI and usually decreased to approximately 10(4) SFI posttransplant for both class I and II. For patients with AMR (n=3), predominant increases in class II DSA more than 10(5) SFI were observed. All three patients continue to have DSA approximately 10(5) SFI with stable creatinine after treatment for AMR. CONCLUSIONS: Approximately 63% of patients were transplanted with a positive flow crossmatch. The results show that patients with DSA more than 10(5) and FCM more than 200 MCS are at higher risk for AMR. Treatment of AMR improves renal function without significant changes in DSA.
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