Risk Factors for the Development of Antibody-mediated Rejection (AMR) after Lung Transplantation

Sunder, Suraj; Witt, Chad A.; Byers, Derek E.; Hachem, Ramsey R.

doi:10.1016/j.healun.2019.01.1039

Cited by 2 publications

(4 citation statements)

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“…There is a possibility that the aforementioned crosstalk between the innate and adaptive responses contributes to the association between Pseudomonas and CLAD, specifically through DSA driving antibody‐mediated rejection (AMR). To that effect, we have previously reported in an abstract that Pseudomonas isolation may be a trigger for AMR . Because DSA is an integral component of the clinical definition of AMR and is thought to be the cause of AMR, one would expect a clear association between Pseudomonas , DSA, AMR, and CLAD.…”

Section: Discussionmentioning

confidence: 99%

“…To that effect, we have previously reported in an abstract that Pseudomonas isolation may be a trigger for AMR. 53 is often difficult to make this distinction prospectively in clinical practice. For this reason, we elected to use the term "isolation" to avoid implying that an invasive infection was present.…”

Section: Pseudomonas Aeruginosa Our Multivariable Analysis Also Idenmentioning

confidence: 99%

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Pseudomonas aeruginosa and acute rejection independently increase the risk of donor-specific antibodies after lung transplantation

Kulkarni

Tsui

Sunder

et al. 2020

American Journal of Transplantation

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Factors contributing to donor‐specific HLA antibody (DSA) development after lung transplantation have not been systematically evaluated. We hypothesized that the isolation of Pseudomonas aeruginosa in respiratory specimens would increase the risk of DSA development. Our objective was to determine the risk of DSA development associated with the isolation of Pseudomonas aeruginosa after lung transplantation. We conducted a single‐center retrospective cohort study of primary lung transplant recipients and examined risk factors for DSA development using Cox regression models. Of 460 recipients, 205 (45%) developed DSA; the majority developed Class II DSA (n = 175, 85%), and 145 of 205 (71%) developed DSA to HLA‐DQ alleles. Univariate time‐dependent analyses revealed that isolation of Pseudomonas from respiratory specimens, acute cellular rejection, and lymphocytic bronchiolitis are associated with an increased risk of DSA development. In multivariable analyses, Pseudomonas isolation, acute cellular rejection, and lymphocytic bronchiolitis remained independent risk factors for DSA development. Additionally, there was a direct association between the number of positive Pseudomonas cultures and the risk of DSA development. Our findings suggest that pro‐inflammatory events including acute cellular rejection, lymphocytic bronchiolitis, and Pseudomonas isolation after transplantation are associated with an increased risk of DSA development.

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Section: Discussionmentioning

confidence: 99%

Section: Pseudomonas Aeruginosa Our Multivariable Analysis Also Idenmentioning

confidence: 99%

Pseudomonas aeruginosa and acute rejection independently increase the risk of donor-specific antibodies after lung transplantation

Kulkarni

Tsui

Sunder

et al. 2020

American Journal of Transplantation

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“…Prior to 2016, there was no uniform consensus on a definition for AMR or standardized diagnostic criteria posing challenges to identifying and reporting true incidence of this disease process. Risk factors for AMR include preformed DSA, the development of de novo DSA post transplantation, pseudomonal infections and lymphocytic bronchiolitis [20,25]. In one study, an independent risk factor for AMR was seen in patients with cystic fibrosis [25].…”

Section: Antibody-mediated Rejectionmentioning

confidence: 99%

“…Risk factors for AMR include preformed DSA, the development of de novo DSA post transplantation, pseudomonal infections and lymphocytic bronchiolitis [20,25]. In one study, an independent risk factor for AMR was seen in patients with cystic fibrosis [25].…”

Section: Antibody-mediated Rejectionmentioning

confidence: 99%

Acute rejection post lung transplant

Hanks,

Girard,

Sehgal

2024

Current Opinion in Pulmonary Medicine

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Purpose of Review To review what is currently known about the pathogenesis, diagnosis, treatment, and prevention of acute rejection (AR) in lung transplantation. Recent Findings Epigenomic and transcriptomic methods are gaining traction as tools for earlier detection of AR, which still remains primarily a histopathologic diagnosis. Summary Acute rejection is a common cause of early posttransplant lung graft dysfunction and increases the risk of chronic rejection. Detection and diagnosis of AR is primarily based on histopathology, but noninvasive molecular methods are undergoing investigation. Two subtypes of AR exist: acute cellular rejection (ACR) and antibody-mediated rejection (AMR). Both can have varied clinical presentation, ranging from asymptomatic to fulminant ARDS, and can present simultaneously. Diagnosis of ACR requires transbronchial biopsy; AMR requires the additional measuring of circulating donor-specific antibody (DSA) levels. First-line treatment in ACR is increased immunosuppression (pulse-dose or tapered dose glucocorticoids); refractory cases may need antibody-based lymphodepletion therapy. First line treatment in AMR focuses on circulating DSA removal with B and plasma cell depletion; plasmapheresis, intravenous human immunoglobulin (IVIG), bortezomib, and rituximab are often employed.

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Risk Factors for the Development of Antibody-mediated Rejection (AMR) after Lung Transplantation

Cited by 2 publications

References 0 publications

Pseudomonas aeruginosa and acute rejection independently increase the risk of donor-specific antibodies after lung transplantation

Pseudomonas aeruginosa and acute rejection independently increase the risk of donor-specific antibodies after lung transplantation

Acute rejection post lung transplant

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