Clinicopathological Characteristics and Effect of Late Acute Rejection on Renal Transplant Outcomes

Rodrigues, Caroline Fabri Bittencourt; Franco, Marcello; Cristelli, Marina; Pestana, José Osmar Medina; Tedesco‐Silva, Hélio

doi:10.1097/tp.0000000000000145

Cited by 16 publications

(8 citation statements)

References 15 publications

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“…It is worth noting that 11 of these 17 ACRs occurred beyond 1 year after transplantation. Our findings that late ACR is responsible for graft failure are in broad agreement with the report of Rodrigues et al that late acute rejection is associated with graft failure …”

Section: Discussionsupporting

confidence: 93%

“…Our findings that late ACR is responsible for graft failure are in broad agreement with the report of Rodrigues et al that late acute rejection is associated with graft failure. 23 We reported that concurrent ACR and AMR rejection carries a poor prognosis. 24 In this study, only 3 of 27 graft failures due to AR were due to AMR biopsy diagnosis and 7 failures were due to mixed ACR and AMR.…”

Section: Discussionmentioning

confidence: 95%

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Kidney allograft failure in the steroid‐free immunosuppression era: A matched case‐control study

Alkadi

Kim

Aull

et al. 2017

Clinical Transplantation

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We studied the causes and predictors of death-censored kidney allograft failure among 1670 kidney recipients transplanted at our center in the corticosteroid-free maintenance immunosuppression era. As of January 1, 2012, we identified 137 recipients with allograft failure; 130 of them (cases) were matched 1-1 for recipient age, calendar year of transplant, and donor type with 130 recipients with functioning grafts (controls). Median time to allograft failure was 29 months (interquartile range: 18-51). Physician-validated and biopsy-confirmed categories of allograft failure were as follows: acute rejection (21%), glomerular disease (19%), transplant glomerulopathy (13%), interstitial fibrosis tubular atrophy (10%), and polyomavirus-associated nephropathy (7%). Graft failures were attributed to medical conditions in 21% and remained unresolved in 9%. Donor race, donor age, human leukocyte antigen mismatches, serum creatinine, urinary protein, acute cellular rejection, acute antibody-mediated rejection, BK viremia, and CMV viremia were associated with allograft failure. Independent predictors of allograft failure were acute cellular rejection (odds ratio: 18.31, 95% confidence interval: 5.28-63.45) and urine protein ≥1 g/d within the first year post-transplantation (5.85, 2.37-14.45). Serum creatinine ≤1.5 mg/dL within the first year post-transplantation reduced the odds (0.29, 0.13-0.64) of allograft failure. Our study has identified modifiable risk factors to reduce the burden of allograft failure.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 95%

Kidney allograft failure in the steroid‐free immunosuppression era: A matched case‐control study

Alkadi

Kim

Aull

et al. 2017

Clinical Transplantation

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“…Second, our cohorts show 51% of AR and 99% of “IFTA with AR” samples were diagnosed >1 year posttransplant. This finding confirms Scientific Registry for Transplant Recipients and DeKAF data and growing evidence that AR episodes often occur late posttransplant in both adult and pediatric populations .…”

Section: Discussionsupporting

confidence: 89%

Gene Expression in Biopsies of Acute Rejection and Interstitial Fibrosis/Tubular Atrophy Reveals Highly Shared Mechanisms That Correlate With Worse Long‐Term Outcomes

Modena

Kurian

Gaber

et al. 2016

American Journal of Transplantation

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Interstitial fibrosis and tubular atrophy (IFTA) is found in approximately 25% of 1-year biopsies posttransplant. It is known that IFTA correlates with decreased graft survival when histological evidence of inflammation is present. Identifying the mechanistic etiology of IFTA is important to understanding why long-term graft survival has not changed as expected despite improved immunosuppression and dramatically reduced rates of clinical acute rejection (AR) (Services UDoHaH. http://www.ustransplant.org/ annual_reports/current/509a_ki.htm). Gene expression profiles of 234 graft biopsy samples were obtained with matching clinical and outcome data. Eighty-one IFTA biopsies were divided into subphenotypes by degree of histological inflammation: IFTA with AR, IFTA with inflammation, and IFTA without inflammation. Samples with AR (n = 54) and normally functioning transplants (TX; n = 99) were used in comparisons. A novel analysis using gene coexpression networks revealed that all IFTA phenotypes were strongly enriched for dysregulated gene pathways and these were shared with the biopsy profiles of AR, including IFTA samples without histological evidence of inflammation. Thus, by molecular profiling we demonstrate that most IFTA samples have ongoing immune-mediated injury or chronic rejection that is more sensitively detected by gene expression profiling. These molecular biopsy profiles correlated with future graft loss in IFTA samples without inflammation.

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“…PCRR typically occurs one or more years after transplantation. Although PCRR has been generally considered to be a subtype of T cell–mediated rejection (TCMR), cases of florid plasma cell infiltration have been reported in association with late antibody‐mediated rejection (ABMR) . Similar to our case, the infiltrated plasma cells in this variant of ABMR are mature and polyclonal, as verified by expression of both kappa and lambda light chains by immunohistochemistry.…”

Section: Discussionsupporting

confidence: 80%

Recurrent IgG4-related tubulointerstitial nephritis concurrent with chronic active antibody mediated rejection: A case report

Chibbar

Wright

Dokouhaki

et al. 2018

American Journal of Transplantation

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IgG4-related disease is a relatively newly described entity that can affect nearly any organ, including the kidneys, where it usually manifests as tubulointerstitial nephritis (IgG4-TIN). The diagnosis can be suggested by characteristic histological features, including an inflammatory infiltrate with increased IgG4-positive plasma cells associated with "storiform" fibrosis. Serum IgG4 is usually elevated. In the native kidney and other organs, there is typically a brisk response to treatment with immunosuppression. Recurrence of IgG4-TIN after renal transplant has not been described in the literature. Here, we describe the first case of recurrent IgG4-TIN in a young patient concomitant with chronic active antibody mediated rejection five years after kidney transplant. Recurrent IgG4-TIN could be diagnosed by the characteristic histopathologic features and increased IgG4-positive plasma cells. Despite maintenance immunosuppression, this disease may recur in the kidney allograft.

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Clinicopathological Characteristics and Effect of Late Acute Rejection on Renal Transplant Outcomes

Abstract: The prevalence and recurrence of LAR are considerable and associated with increased incidence of graft loss. Patients who need dialysis during LAR should be carefully evaluated owing to the high prevalence of graft failure.

Cited by 16 publications

References 15 publications

Kidney allograft failure in the steroid‐free immunosuppression era: A matched case‐control study

Kidney allograft failure in the steroid‐free immunosuppression era: A matched case‐control study

Gene Expression in Biopsies of Acute Rejection and Interstitial Fibrosis/Tubular Atrophy Reveals Highly Shared Mechanisms That Correlate With Worse Long‐Term Outcomes

Recurrent IgG4-related tubulointerstitial nephritis concurrent with chronic active antibody mediated rejection: A case report

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