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Introduction: Uterus transplantation (UTx) is a novel treatment for absolute uterine infertility. Acute T cell–mediated rejection (TCMR) can be monitored only through serial cervical biopsies. Methods: This study, the first of its kind in human transplantation, evaluated clinical, serological, and pathophysiological manifestations of allograft rejection from immunosuppression withdrawal (ISW) to graft hysterectomy (Hx). Results: Following live birth, immunosuppression was abruptly withdrawn from six living‐donor UTx recipients. ISW occurred at a median of 7.4 weeks before graft Hx. Post‐ISW signs of rejection included: (1) discoloration of the cervix; (2) increased uterine size compared to day of ISW; (3) serological evidence of eosinophilia and progressive development of donor‐specific antibodies (DSA) or child‐specific antibodies (CSA); (4) histopathological evidence of TCMR in cervical biopsies preceding the development of antibodies in serum; and (5) C4d deposition in tissue before formation of DSA or CSA in all but two recipients. At graft Hx, endometrial glands were preferentially targeted for destruction over stroma while parametrial arteries displayed variable arteritis and fibrointimal hyperplasia. Conclusion: Recognition of the progression of uterine allograft rejection may be important for other human organ recipients and drive research on modulation of immunosuppression and the paradoxical relationship between adaptive cellular and humoral immunity in natural pregnancies. Trial Registration: ClinicalTrials.gov identifier: NCT02656550 [ABSTRACT FROM AUTHOR]

Introduction: This study investigated the impact of immunosuppressive drug concentrations on microvascular inflammation (MVI) in kidney transplant recipients with negative donor-specific antibodies (DSA) against human leukocyte antigen (HLA) and negative C4d deposition in peritubular capillaries., Methods: We analyzed data from 268 living kidney transplant recipients at the Department of Urology, University of Osaka, Japan. Patients received immunosuppressive therapy comprising extended-release tacrolimus, mycophenolate mofetil (MMF), and/or everolimus, with or without steroids. Graft biopsies were routinely performed at 3, 12, 36 and 60 months post-surgery., Results: No significant differences were observed between the MVI+DSA-C4d- and MVI-DSAC4d groups regarding graft survival rates (95.5% vs. 96.6%, p = 0.772) or patient survival rates (95.7% vs. 95.9%, p = 0.735). Lower tacrolimus and everolimus concentrations were significantly associated with an increased risk of MVI+DSA-C4d- (tacrolimus: OR, 0.169; 95% CI, 0.055-0.515; p = 0.002; everolimus: OR, 0.386; 95% CI, 0.171-0.874; p = 0.022). In contrast, MPA concentration was not significantly associated with MVI+DSA-C4d- (OR, 0.994; 95% CI, 0.554-1.780; p = 0.984). Steroid discontinuation did not significantly impact the risk of MVI+DSA-C4d- (OR, 1.980; 95% CI, 0.318-12.000; p = 0.470)., Conclusion: Lower trough levels of tacrolimus and everolimus correlated with a higher incidence of antibody-independent MVI, supporting the need for tailored immunosuppressive regimens in kidney transplantation., (© 2025 The Author(s). Clinical Transplantation published by Wiley Periodicals LLC.)

The development of donor‐specific antibodies (DSA) has a significant impact on graft outcome in solid organ transplantation. Mismatched HLAs are recognized directly and indirectly by the recipient immune system. Both pathways occur in parallel and result in the generation of plasma cells, DSA, cytotoxic and T helper lymphocytes. Here, we present the results of an analysis of the epitope load of mismatched HLAs in a cohort of 220 lung transplant recipients using two in silico algorithms, HLAMatchmaker and PIRCHE‐II (Predicted Indirectly ReCognizable HLA Epitopes). De novo DSA (dnDSA) were detected by single antigen bead assays. The percentage of recipients who developed dnDSA was significantly higher in the group of patients who received lung transplants with a mismatching score above the detected threshold than in the group of patients who received lung transplants with a mismatching score below the threshold. In a multivariate Cox proportional hazard analysis, the PIRCHE‐II score appeared to be a superior predictor of dnDSA formation. In addition, PIRCHE‐II technology was shown to be useful in predicting separate dnDSA1 and dnDSA2 formation. We conclude that both algorithms can be used for the evaluation of the epitope load of mismatched HLAs and the prediction of DSA development in lung transplant recipients. [ABSTRACT FROM AUTHOR]

Introduction: Chronic active antibody‐mediated rejection (cAMR) is a major determinant of late allograft failure. Rituximab/immunoglobulins (IVIg) + plasma exchange (PLEX) showed controversial results in cAMR treatment. Tocilizumab (TCZ), a humanized anti‐interleukin 6 receptor antibody, has been recently used as rescue therapy in patients non‐responsive to rituximab/IVIg/PLEX with favorable outcomes. Whether TCZ acts "per se" or requires a priming effect from previous treatments is currently unknown. Methods: Fifteen patients with cAMR were treated with TCZ as a first‐line therapy and followed for a median time of 20.7 months. Results: Despite the majority of patients experiencing advanced transplant glomerulopathy (TG) at diagnosis (60% with cg3), glomerular filtration rate and proteinuria stabilized during the follow‐up, with a significant reduction in donor‐specific antibodies. Protocol biopsies after 6 months demonstrated significant amelioration of microvascular inflammation and no TG, C4d deposition, or IF/TA progression. Gene‐expression and immunofluorescence analysis showed upregulation of three genes (TJP‐1, AKR1C3, and CASK) involved in podocyte, mesangial, and tubular restoration. Conclusion: Tocilizumab adopted as a first‐line approach in cAMR was associated with early serological and histological improvements and functional stabilization even in advanced TG, suggesting a role for the use of TCZ alone with the avoidance of unnecessary previous immunosuppressants. [ABSTRACT FROM AUTHOR]

Abstract: Background: Although the presence of donor‐specific antibodies (DSA) is known to impact lung allograft, limited data exist regarding DSA management. Methods: We did a retrospective study at our center evaluating DSA management in adult lung transplant recipients undergoing lung transplantation between January 1, 2010 and June 30, 2014. Study follow‐up was completed through October 2017. All recipients were stratified into 2 groups based on the presence or absence of DSA. Those with DSA were evaluated for the impact of treatment of DSA. The primary outcomes were postlung transplant survival and freedom from bronchiolitis obliterans syndrome (BOS), subset of chronic lung allograft dysfunction (CLAD). Simon‐Makuch method was used to estimate overall survival and BOS‐free survival to account for DSA as time‐dependent covariate. Survival differences between the groups were analyzed using time‐dependent Cox proportional hazards model. Results: Sixty‐four percent of 194 total subjects developed post‐lung transplant DSA. Overall survival was different with worse survival in the DSA positive group that never cleared DSA (P = .002). BOS‐free survival was lower, but did not reach significance in this group. Response to treatment was poor, with only 12 of 47 (25.5%) who received treatment demonstrating clearance of DSA. Conclusions: Donor‐specific antibodies prevalence is high after lung transplantation. Clearance of DSA correlated with improved outcomes. Current therapeutic strategies against DSA are relatively ineffective. Multicenter collaborative studies will be required to evaluate current treatment strategies and other innovative modalities. [ABSTRACT FROM AUTHOR]

Abstract: The effect of preformed donor‐specific antibodies (DSAs) on liver transplantation (LT) remains unclear, especially in the field of living donor LT (LDLT). Herein, we evaluated the prevalence of preformed DSAs and their effect on graft outcome in LDLT in the first year following surgery. Using the Luminex® Single Antigen assay, we analyzed the preoperative sera of 61 adult LDLT recipients between 2014 and 2015. Clinical outcomes and pathologic findings including complement component 4d (C4d) expression in the first year after LT were retrospectively reviewed. Regardless of the class of DSA, DSAs with mean fluorescence intensity (MFI) ≥1000 were defined as positive and preformed DSA with MFI ≥5000 was defined as strongly positive. Fifteen patients (24.6%) had preformed DSAs, and 8 patients (13.1%) showed strongly positive preformed DSAs. Among 15 DSA positive patients, 2 (13.3%) showed persistent DSAs after LDLT. No de novo DSAs were noted in patients without preformed DSAs. Preformed DSAs were not related to graft dysfunction, laboratory values, or C4d expression or other pathologic findings in the first year of LDLT. In conclusion, preformed DSAs persisted during follow‐up in 13.3% of cases and did not have adverse effect on histologic or clinical outcomes in the first year of LDLT. [ABSTRACT FROM AUTHOR]

Abstract: Donor‐specific alloantibodies (DSA) have been associated with rejection and shorter graft survival after orthotopic liver transplantation (OLT). We examined the role of DSA in nonanastomotic biliary strictures (NAS) after OLT. Patients receiving first OLT who developed NAS (n = 68) and a control group without NAS (n = 83), with pre‐OLT and 12 months post‐OLT serum samples, were included. DSA were specified using the Luminex single antigen test. Risk factors for NAS and graft survival were analyzed. The presence of preformed DSA was not significantly different between patients with NAS and controls (P = .89). After 12 months, 26.5% of NAS patients and 16.9% of controls had generated de novo DSA (P = .15). Neither de novo class I DSA nor de novo class II DSA were associated with NAS. De novo DSA generally developed after the diagnosis of NAS. Time‐dependent regression analysis identified both NAS (aHR 8.05, CI 3.28 – 19.77, P < .01) and de novo class II DSA (aHR 2.84, CI 1.38 – 5.82, P < .01) as independent risk factors for graft loss. Preformed or de novo DSA were not associated with the development of NAS. However, NAS as well as de novo class II DSA were independent risk factors for graft loss after OLT. [ABSTRACT FROM AUTHOR]

Background Donor-specific antibodies ( DSAs) are an important cause of complications after solid organ transplant. Risk factors and, thus, strategies for preventing DSA development are not well defined. Methods The DSA status of 400 patients who underwent liver transplant ( LT) at the outpatient clinic of the University Hospital Essen was determined. Human leukocyte antigen ( HLA) antibodies were detected by single-antigen bead technology. The strength of DSAs was reported as mean fluorescence intensity. Results Detectable DSAs were found in 74 (18.5%) patients and significantly more often in patients who underwent LT for autoimmune liver disease than for all other indications (29.3%; P=.022), but significantly less often found in patients who underwent LT for hepatocellular carcinoma (7.6%, P=.005). The incidence of DSAs increased with time after LT, and the risk was generally higher for female patients. The frequency of DSA detection was significantly lower (10.6%) for patients receiving immunosuppressive treatment with mammalian target of rapamycin ( mTOR) inhibitors than for those receiving other regimens (20.5%; P=.025). Conclusion Autoimmune liver diseases, female sex, and time of more than 8 years since LT predispose patients to the development of DSAs. Immunosuppression with the mTOR inhibitor everolimus protects against DSA development after liver transplant. [ABSTRACT FROM AUTHOR]

Background Antibody-mediated rejection ( AMR) resulting from de novo donor-specific antibodies (dn DSA) leads to adverse outcomes following heart transplantation ( HTx). It remains unclear what role dn DSA to specific HLA antigens play in adverse outcomes. This study compares outcomes in patients developing dn DSA to DQ antigens with those developing non- DQ dn DSA and those free from dn DSA. Methods The present study was a single-center, retrospective analysis of 122 consecutive HTx recipients. The primary outcome was a composite of death or graft dysfunction. Results After 3.3 years of follow-up, 31 (28%) patients developed dn DSA. Mean time to dn DSA was 539 days. Of 31 patients, 19 developed DQ antibodies and 12 developed non- DQ antibodies. Compared to non- DQ dn DSA, DQ antibodies presented with higher MFI values ( P=.001) were more likely persistent ( P=.001) and appeared later post- HTx (654 vs 359 days, P=.035). In a multivariable analysis, DQ dn DSA was associated with increased risk of the primary endpoint ( HR 6.15, 95% CI 2.57-14.75, P=.001), whereas no increased risk was seen with non- DQ dn DSA ( P=.749). Conclusions dn DSA to DQ antigens following HTx are associated with increased risk of death and graft dysfunction. [ABSTRACT FROM AUTHOR]

There is limited evidence for a negative impact of preformed, donor-specific HLA antibodies ( DSA) identified by cross-matching on outcomes after liver transplantation. Three recent studies have suggested an association between preformed DSA detected by Luminex and reduced graft or recipient survival in liver transplant cohorts with a high prevalence of hepatitis C. This study investigated the impact of preformed DSA identified by Luminex in the Scottish liver transplant population. All recipients of liver transplants in Scotland between 2007 and 2015 with samples available for day of transplant antibody testing and donor HLA typing were included (n=459); 96% of the cohort were white and 19% had a primary diagnosis of hepatitis C. The median follow-up time was 36 months. Preformed DSA were detected in 88 recipients. In multivariate analysis, preformed DSA with a median fluorescent intensity ≥10 000 were associated with recipient mortality at 1 year. There was no association between DSA and overall graft or recipient survival. This study adds to the growing body of evidence supporting a detrimental impact of preformed, high-level DSA in a subset of liver transplant recipients by identifying an association in an ethnically and demographically distinct liver transplant population. [ABSTRACT FROM AUTHOR]

Background The role of anti- HLA- DP antibodies in renal transplantation is poorly defined. This study describes the impact of donor (donor-specific antibody [ DSA]) and non-donor-specific antibodies against HLA- DP antigens in renal transplant patients. Methods Of 195 consecutive patients transplanted between September 2009 and December 2011, 166 primary kidney recipients and their donors were typed (high-resolution) for DP antigens. Sera taken pre-transplant and at 1, 3, 6, 9, and 12 months, and annually post-transplant were retrospectively tested for anti- DP antibodies using single-antigen beads. Results In 81 (49%) patients, anti- DP antibodies were found; 64% (n=52) of patients were positive in the pre-transplant samples and 36% (n=29) were positive exclusively post-transplant. The median time from transplantation to antibody was 20.9 months. Fifty-five percent (n=16) of the de novo anti- DP antibodies were accompanied by another de novo DSA. Anti- DP antibody-positive patients had a higher rate of rejection (compared with anti- DP antibody-negative patients, P=.01). The estimated glomerular filtration rate declined more with anti- DP antibodies (−5.5% vs +26%). Conclusions Antibodies against HLA- DP antigens are common. De novo anti- DP antibodies commonly appear after acute rejection and accompany DSA, which makes it difficult to determine whether anti- DP antibodies are the cause or the consequence of graft injury. [ABSTRACT FROM AUTHOR]

Outcome of patients with transplant glomerulopathy ( TG) is poor. Using B-cell targeting molecules represent a rational strategy to treat TG during chronic antibody-mediated rejection. In this pilot study, 21 patients with this diagnosis received four doses of intravenous immunoglobulins and two doses of rituximab ( IVIG/ RTX group). They were retrospectively compared with a untreated control group of 10 patients. At 24 months post-biopsy, graft survival was similar and poor between the treated and the untreated group, 47% vs. 40%, respectively, p = 0.69. This absence of response of IVIG/ RTX treatment was observed, regardless the phenotype of TG. Baseline estimated glomerular filtration rate ( eGFR) and decline in eGFR during the first six months after the treatment were risk factors associated with 24-month graft survival. The IVIG/ RTX therapy had a modest effect on the kinetics of donor-specific alloantibodies at M24, compared to the untreated group, not associated with an improvement in graft survival. The mean number of adverse events per patient was higher in the IVIG/ RTX group than in the control group (p = 0.03). Taken together, IVIG/ RTX treatment for severe TG during chronic antibody-mediated rejection does not seem to change the natural history of TG and is associated with a high incidence of adverse events. [ABSTRACT FROM AUTHOR]

Class I single-antigen flow beads ( SAFB) carry native and denatured human leukocyte antigen ( HLA) molecules. Using a cohort of 179 class I HLA-sensitized kidney recipients, we described incidence and clinical relevance of preformed denatured HLA donor-specific antibodies ( DSA) using two different assays: an acid-treated SAFB assay (anti- dHLA DSA) and the iBeads assays ( SAFB+/iBeads- DSA). Eighty-five class I DSA were found in 67 patients (median mean fluorescence intensity [ MFI] of 1729 [range 520-13 882]). Anti-dHLA and SAFB+/iBeads- DSA represented 11% and 18% of class I DSA and were mainly low MFI DSA (500-1000 MFI). Concordance between these two assays was good (90%). None of the patients with only class I anti- dHLA DSA or only SAFB+/iBeads- DSA developed acute clinical antibody-mediated rejection in the first-year post-transplantation, and their five-yr death-censored graft survival was similar to that of patients without DSA. Moreover, all these patients displayed a negative current T-cell flow cytometry cross-match. Therefore, both anti-dHLA DSA and SAFB+/iBeads- DSA appear irrelevant, which could explain the good outcome observed in some patients with preformed class I DSA. [ABSTRACT FROM AUTHOR]

Introduction Transplant glomerulopathy ( TG) is the characteristic lesion of chronic antibody-mediated rejection ( AMR). However, in some patients presents with no circulating HLA antibodies or C4d positivity. Aim Patients with TG accomplishing criteria for chronic AMR were compared to patients with isolated TG. Patients and Methods We reviewed late (>6 months) graft biopsies performed between 2007 and 2010 (n = 75). Biopsies with C4d-negative TG and no circulating donor-specific antibody were called isolated TG (n = 12), and chronic AMR was defined according to Banff consensus (n = 17). HLA antibodies were evaluated by Luminex technology. Immunohistochemistry was performed to quantify graft infiltrating cells. Results Patients with isolated TG were older (52 ± 14 vs. 35 ± 14; p = 0.0048), received grafts from older donors (54 ± 16 vs. 41 ± 18; p = 0.0554), and displayed a lower inflammation in the glomerular (g-score: 0.5 ± 0.5 vs. 1.0 ± 0.9; p = 0.0865; CD3 positive cells/glomeruli: 1.5 ± 2.9 vs. 4.4 ± 4.1; p = 0.0147), interstitial (i-score: 1.2 ± 0.9 vs. 1.9 ± 1.0; p = 0.0685; CD45 positive cells/hpf: 18 ± 11 vs. 57 ± 68; p = 0.0132), and peritubular capillary (ptc-score 0.2 ± 0.6 vs. 1.1 ± 0.9; p = 0.0089; CD45 positive cells/hpf: 3.7 ± 3.1 vs. 10.1 ± 7.4; p = 0.0290) compartments. Fifteen grafts were lost and graft survival was significantly lower in patients with chronic AMR (p = 0.0122). Conclusion Isolated TG is associated with less severe allograft inflammation and with a better outcome than chronic AMR. [ABSTRACT FROM AUTHOR]

Scarce data exist regarding the incidence of donor-specific antibodies ( DSAs) in kidney transplant patients receiving everolimus-based immunosuppression without calcineurin inhibitors ( CNIs). The aim of this retrospective case-control study was to compare the incidence of de novo DSAs in patients converted to an everolimus-based regimen without CNIs with that seen in patients maintained on CNIs. Sixty-one DSA-free kidney transplant patients who had been converted to an everolimus-based regimen (everolimus group) were compared to 61 other patients maintained on CNIs-based regimen (control group). Patients were matched according to age, gender, induction therapy, date of transplantation, and being DSA-free at baseline. At last follow-up, the incidence of DSAs was 9.8% in the everolimus group and 5% in the control group (p = ns). In the everolimus group, the increased incidence of DSAs between baseline and last follow-up was statistically significant. Antibody-mediated rejection occurred in 6.5% in the everolimus group and 0% in the CNIs group. The incidence of DSAs is numerically increased in kidney transplant patients treated with an everolimus-based without CNIs. A study including a larger number of patients is required to determine whether a CNI-free everolimus-based immunosuppression significantly increases DSAs formation. [ABSTRACT FROM AUTHOR]

The significance of donor-specific antibodies ( DSA) is not well known in the setting of pancreas transplantation. Since December 2009, we prospectively followed pancreas transplant patients with single-antigen-luminex-bead testing at one, two, three, six, and then every six months for the first two yr. Thirty-five of the 92 patients that underwent pancreas transplantation (13 pancreas-alone [ PTA], 20 with a kidney [ SPK], and two after a kidney [ PAK]) agreed to participate in study. Median age at transplant was 45 yr and follow-up was 23 months. Majority were Caucasian (n = 33) and male (n = 18). Rabbit anti-thymocyte globulin induction was used. Median HLA-mismatch was 4.2 ± 1.1. Eight patients (7 SPK, 1 PAK) developed post-transplant DSA at median follow-up of 76 d (26-119), 1 SPK had pre-formed DSA. Seven patients had both class I and class II DSA, one with class I and one with class II only. Mean peak class I DSA- MFI was 3529 (±1456); class II DSA- MFI was 5734 (±3204) whereas cumulative DSA MFI ( CI + CII) was 9264 (±4233). No difference was observed in the patient and donor demographics among patients with and without DSA. One patient in non- DSA group developed acute cellular rejection of pancreas. From our data it appears that post-transplant DSA in pancreas allograft recipients may not impact the early-pancreatic allograft outcomes. The utility of prospective DSA monitoring in pancreatic transplant patients needs further evaluation and long-term follow-up. [ABSTRACT FROM AUTHOR]

Currently, the number of highly sensitized patients awaiting a renal transplant is increasing on the waiting lists of different organ exchange organizations. Due to the presence of antibodies against a broad variety of human leukocyte antigen (HLA) specificities, highly sensitized patients have a markedly reduced chance of receiving a crossmatch-negative organ. It has long been recognized that hyperacute rejection is associated with the presence of donor-specific anti-HLA antibodies at the time of transplantation. Meanwhile treatment protocols have been developed to achieve successful transplantation across antibody barriers. Therefore, the presence of donor-specific anti-HLA antibodies and a positive serological crossmatch are no longer considered as an absolute contraindication to renal transplantation. Mainly, two desensitization protocols have been established in order to overcome a positive crossmatch or to enhance the chance of highly sensitized patients to receive a crossmatch-negative organ: high-dose intravenous immunoglobulin (IVIg) or low-dose IVIg in combination with plasmapheresis. Herein, we summarize the characteristics of these two treatment regimes along with other alternative approaches that are currently used for the management of kidney graft recipients with broad alloantibody reactivity against potential kidney donors. [ABSTRACT FROM AUTHOR]

Loss of allografts over time remains a barrier to achieving successful outcomes in solid organ transplantation. Although the role of donor-specific alloantibody-mediated mechanisms in hyperacute rejection is well known, research and management of early and late post-transplant rejection have traditionally focused on T cell-mediated mechanisms. However, available agents that affect T-cell pathways have minimal impact on long-term graft survival, suggesting that other effector mechanisms are involved. A growing body of evidence now supports a role for alloantibody-mediated mechanisms in early and late graft rejection, which can significantly impact on long-term graft survival. The important role of B cells in generating and perpetuating alloantibody production provides a rationale for B-cell depletion therapy as an approach to prevent or reduce alloantibody formation before transplantation and to treat or prevent early and late alloantibody-mediated rejection. The use of monoclonal antibodies that directly target B cells, in combination with standard alloantibody-depleting therapies and/or immunosuppression, has been investigated in several small non-controlled studies. Promising results suggest that this strategy warrants further investigation in larger controlled studies. [ABSTRACT FROM AUTHOR]

Lederer SR, Friedrich N, Banas B, von Welser G, Albert ED, Sitter T. Effects of mycophenolate mofetil on donor-specific antibody formation in renal transplantation.Clin Transplant 2005 DOI: 10.1111/j.1399-0012.2005.00261.x© Blackwell Munksgaard, 2005Mycophenolate mofetil (MMF) is a routinely used immunosuppressive agent that selectively blocks T- and B-lymphocyte proliferation. The present study was designed to investigate the effects of this drug on human leukocyte(HLA) antibody production in general and donor-specific antibody (DSA) formation in particular in 154 recipients of renal allografts.Renal allograft recipients were subdivided into three groups. Group 1 patients (n = 60) had received MMF since transplantation in combination with either cyclosporin A or tacrolimus and steroids. Group 2 patients (n = 29) had received an MMF-free immunosuppressive regimen initially followed by addition of MMF some time later. Group 3 patients (n = 65) had received no MMF. Cyclosporin A or tacrolimus in combination with azathioprine and/or steroids were used for immunosuppression. DSA were demonstrated by enzyme-linked immunosorbent assay (ELISA) for detection of panel-reactive antibodies of HLA class I and II specificity.The HLA antibodies were found in 16.7%, 27.6% and 30.8% of transplant recipients in groups 1, 2 and 3, respectively. DSA were found in 8.3%, 17.2% and 20.0%, and non-DSA in 10.0%, 20.7% and 24.6%, of patients in groups 1, 2 and 3, respectively.The MMF reduces anti-HLA class I and II antibody production and consequently DSA production in renal allograft recipients. Our data indicate this effect to be more pronounced in patients given MMF immediately after transplantation than in those in whom MMF is introduced some time later. The presence of DSA in the serum of renal allograft recipients is associated with poorer graft function (higher serum creatinine and more rejection episodes). [ABSTRACT FROM AUTHOR]

Background: Crossmatching (XM) between organ donors and recipients is correlated with clinical outcomes. This study evaluates the results of HLA‐incompatible kidney transplant (HLA‐i KT) according to pre‐transplant XM modalities. Methods: This study included 731 consecutive patients. HLA‐i KT was defined as a transplant under conditions of complement‐dependent cytotoxicity (CDC) XM positivity, flow‐cytometric XM (FCXM) positivity, and/or maximal donor‐specific antibody (DSA) mean fluorescence intensity (MFI) ≥5000. Results: The incidence of antibody‐mediated rejection (AMR) within 1 year after transplant was significantly higher in the HLA‐i group than in the HLA compatible (HLA‐c) group (15 vs 9 patients, 14.2% vs 1.4%; P < 0.01). Multivariate analysis indicated that a DSA MFI ≥5000 (odds ratio [OR] = 2.63; 95% confidence interval [CI], 1.00‐6.98; P = 0.05) was significantly associated with acute rejection (AR), whereas CDC (OR = 2.09; 95% CI, 0.55‐7.99; P = 0.28) and FCXM positivity (OR = 2.07; 95% CI, 0.73‐5.87; P = 0.17) were not. Similarly, DSA MFI ≥ 5000 (OR = 4.14; P = 0.02) was the only significant factor affecting the risk of AMR. Conclusions: Of the various XM tests, DSA MFI ≥5000 was the most prominent predictor of AR in patients undergoing HLA‐i KT. [ABSTRACT FROM AUTHOR]