Protective anti-donor IgM production after crossmatch positive liver-kidney transplantation

McAlister, Chloe C.; Gao, Zu–Hua; McAlister, Vivian C.; Gupta, Rekha; Wright, James R.; Macdonald, A. S.; Peltekian, Kevork M.

doi:10.1002/lt.20062

Cited by 18 publications

(10 citation statements)

References 10 publications

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“…This study is in agreement with previous reports that the presence of DSA before transplantation or its development afterward is associated with an increased risk of hyperacute or acute cellular rejection 1–7, 9–14. Our novel observation is that IgG3 may be the responsible subclass.…”

Section: Discussionsupporting

confidence: 93%

“…In contrast, a study specifically looking at class switch found posttransplantation IgG DSA to be associated with rejection and IgM DSA with freedom from rejection after liver transplantation 13. We have noted the development of IgM DSA after crossmatch‐positive liver‐kidney transplantation, which failed to fix complement and appeared to protect the grafts 14. Protective IgM DSA has been reported in kidney transplantation in a study that also suggested that not all FCXM‐detected IgG DSA was detrimental to the graft 15.…”

mentioning

confidence: 68%

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Immunoglobulin-G subclass antidonor reactivity in transplant recipients

Gao¹,

McAlister²,

Wright³

et al. 2004

Liver Transpl

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Outcomes may differ after kidney transplantation compared to combined liver-kidney transplantation. In animal models, distinct patterns of antidonor immunoglobulin (Ig) G subclasses are associated with either rejection or transplant tolerance. Flow cytometry has increased the sensitivity of antidonor immunoglobulin detection. We compared antidonor IgG subclass responses in kidney transplant recipients to those in recipients of liver or multiorgan grafts. In this study of 19 organ (kidney, liver, pancreas) transplantations, recipient serum incubated with donor splenocytes was tested by flow cytometry for the presence of IgM, IgG, or IgG subclass 1 -4. Sera before transplantation and 10 days and 100 days after transplantation were used. No differences were seen in antidonor IgM, IgG, or IgG subclass antibodies among recipients of kidney transplants and liver grafts or combination grafts, either before or after transplantation. IgG4 gradually but significantly increased after transplantation in all groups. High levels of antidonor IgG3 either before transplantation or produced after it were found in 3 kidney recipients who experienced acute rejection. No other patients experienced rejection, and no other increase in IgG3 was seen. In conclusion, antidonor IgG subclass profiles may be useful to distinguish populations at risk of rejection but they do not differentiate the immunological response after kidney transplantation from that after liver or combined transplantation. A late rise in antidonor IgG4 is consistent with decreased antidonor reactivity thought to occur late after transplantation. (Liver

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Section: Discussionsupporting

confidence: 93%

mentioning

confidence: 68%

Immunoglobulin-G subclass antidonor reactivity in transplant recipients

Gao¹,

McAlister²,

Wright³

et al. 2004

Liver Transpl

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“…The high prevalence of both isotypes is justified by the high sensitivity of the detection technique (28) used. Additionally, we show that islet transplant outcome was improved in patients with pretransplant DSA, particularly IgM against major histocompatibility complex II, a finding not reported so far, to our knowledge, for islet transplantation but consistent with previously reported beneficial effects of recipient sensitization to donor-specific transplant antigens (39–42). …”

Section: Discussionsupporting

confidence: 91%

Alloantibody and Autoantibody Monitoring Predicts Islet Transplantation Outcome in Human Type 1 Diabetes

et al. 2013

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Long-term clinical outcome of islet transplantation is hampered by the rejection and recurrence of autoimmunity. Accurate monitoring may allow for early detection and treatment of these potentially compromising immune events. Islet transplant outcome was analyzed in 59 consecutive pancreatic islet recipients in whom baseline and de novo posttransplant autoantibodies (GAD antibody, insulinoma-associated protein 2 antigen, zinc transporter type 8 antigen) and donor-specific alloantibodies (DSA) were quantified. Thirty-nine recipients (66%) showed DSA or autoantibody increases (de novo expression or titer increase) after islet transplantation. Recipients who had a posttransplant antibody increase showed similar initial performance but significantly lower graft survival than patients without an increase (islet autoantibodies P < 0.001, DSA P < 0.001). Posttransplant DSA or autoantibody increases were associated with HLA-DR mismatches (P = 0.008), induction with antithymocyte globulin (P = 0.0001), and pretransplant panel reactive alloantibody >15% in either class I or class II (P = 0.024) as independent risk factors and with rapamycin as protective (P = 0.006) against antibody increases. DSA or autoantibody increases after islet transplantation are important prognostic markers, and their identification could potentially lead to improved islet cell transplant outcomes.

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“…One yr follow-up of crossmatch positive recipients of either liver or combined liverkidney transplants did not demonstrated different graft survival, acute cellular rejection or defined ''steroid resistant rejection'' episodes when compared to crossmatch negative recipients (1). One case report has suggested that CLKT may produce non-complement fixing antibody as one possible mechanism of protection of the renal allograft in a positive crossmatch combination (12). Another analysis of 99 CLKT recipients demonstrated one-yr rejection rates of 10% for renal allografts and 23% for hepatic allografts (11).…”

Section: Discussionmentioning

confidence: 98%

Antibody‐mediated rejection of renal allograft in combined liver–kidney transplant

Barth¹,

Campos²,

Kukuruga

et al. 2009

Clinical Transplantation

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Liver transplantation is performed based on ABO blood type compatibility without dependence on crossmatch results. Combined liver-kidney transplantation (CLKT) is similarly performed without dependence of crossmatch results as the liver is thought to confer protection to the renal allograft against alloantibody. We report a case of CLKT in a sensitized patient with antibody-mediated rejection (AMR) of the renal allograft. AMR was confirmed with C4d staining and serial monitoring of donor-specific antibody (DSA). Despite intensive therapy directed against AMR and the presence of the liver allograft, the patient demonstrated increasing titers of alloantibody, never demonstrated adequate renal function, and ultimately expired after two months. This result demonstrates the potential for AMR of the renal allograft in sensitized recipients of CLKT.

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Protective anti-donor IgM production after crossmatch positive liver-kidney transplantation

Abstract: The mechanism by which a liver transplantation might protect a simultaneous kidney transplant in a crossmatchpositive recipient is unknown. Flow cytometry crossmatch (FCXM) has increased the sensitivity of donorspecific antibody (

Cited by 18 publications

References 10 publications

Immunoglobulin-G subclass antidonor reactivity in transplant recipients

Immunoglobulin-G subclass antidonor reactivity in transplant recipients

Alloantibody and Autoantibody Monitoring Predicts Islet Transplantation Outcome in Human Type 1 Diabetes

Antibody‐mediated rejection of renal allograft in combined liver–kidney transplant

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