Subclinical Acute Antibody-Mediated Rejection in Positive Crossmatch Renal Allografts

Haas, Mark; Montgomery, Robert A.; Segev, Dorry L.; Rahman, Mostafizur; Racusen, Lorraine C.; Bagnasco, Serena M.; Simpkins, Christopher E.; Warren, Daniel; Lepley, Diane; Zachary, Andrea A.; Kraus, Edward S.

doi:10.1111/j.1600-6143.2006.01657.x

Cited by 138 publications

(116 citation statements)

References 39 publications

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“…Also evaluated were 38 late biopsies, performed primarily for clinical reasons. As will be seen, there was indeed an impressive acceleration of arteriosclerosis in DSAϩ patients, strongly associated with the presence of the newly described entity of subclinical AMR, 8,9 including microcirculation inflammation and C4d and DSA positivity.…”

mentioning

confidence: 85%

Donor-Specific Antibodies Accelerate Arteriosclerosis after Kidney Transplantation

Hill

Nochy²,

Bruneval³

et al. 2011

Journal of the American Society of Nephrology

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In biopsies of renal allografts, arteriosclerosis is often more severe than expected based on the age of the donor, even without a history of rejection vasculitis. To determine whether preformed donor-specific antibodies (DSAs) may contribute to the severity of arteriosclerosis, we examined protocol biopsies from patients with (n ϭ 40) or without (n ϭ 59) DSA after excluding those with any evidence of vasculitis. Among DSA-positive patients, arteriosclerosis significantly progressed between month 3 and month 12 after transplant (mean Banff cv score 0.65 Ϯ 0.11 to 1.12 Ϯ 0.10, P ϭ 0.014); in contrast, among DSA-negative patients, we did not detect a statistically significant progression during the same timeframe (mean Banff cv score 0.65 Ϯ 0.11 to 0.81 Ϯ 0.10, P ϭ not significant). Available biopsies at later time points supported a rate of progression of arteriosclerosis in DSA-negative patients that was approximately one third that in DSA-positive patients. Accelerated arteriosclerosis was significantly associated with peritubular capillary leukocytic infiltration, glomerulitis, subclinical antibody-mediated rejection, and interstitial inflammation. In conclusion, these data support the hypothesis that donorspecific antibodies dramatically accelerate post-transplant progression of arteriosclerosis.

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mentioning

confidence: 85%

Donor-Specific Antibodies Accelerate Arteriosclerosis after Kidney Transplantation

Hill

Nochy²,

Bruneval³

et al. 2011

Journal of the American Society of Nephrology

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“…7,12 This could be due to the absence in our center of early protocol graft biopsies, which usually show subclinical AMR in patients with preformed DSA. 32,33 Loupy et al reported that patients with C1q+ DSAs had more microcirculation inflammation and C4d deposition than those with C1q2 DSAs or no DSAs in 1-year protocol biopsies. This association could fade over time because our late biopsies exhibited a high incidence of interstitial fibrosis, tubular atrophy, and transplant glomerulopathy, without any difference in microcirculation inflammation or C4d deposition between patients with C1q+, C1q2, or no dnDSAs.…”

Section: Discussionmentioning

confidence: 99%

Non-Complement–Binding De Novo Donor-Specific Anti-HLA Antibodies and Kidney Allograft Survival

Guidicelli¹,

Guerville²,

Lepreux³

et al. 2016

Journal of the American Society of Nephrology

125

112

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C1q-binding ability may indicate the clinical relevance of de novo donor-specific anti-HLA antibodies (DSA). This study investigated the incidence and risk factors for the appearance of C1q-binding de novo DSA and their long-term impact. Using Luminex Single Antigen Flow Bead assays, 346 pretransplant nonsensitized kidney recipients were screened at 2 and 5 years after transplantation for de novo DSA, which was followed when positive by a C1q Luminex assay. At 2 and 5 years, 12 (3.5%) and eight (2.5%) patients, respectively, had C1q-binding de novo DSA. De novo DSA mean fluorescence intensity .6237 and .10,000 at 2 and 5 years, respectively, predicted C1q binding. HLA mismatches and cyclosporine A were independently associated with increased risk of C1q-binding de novo DSA. When de novo DSA were analyzed at 2 years, the 5-year death-censored graft survival was similar between patients with C1q-nonbinding de novo DSA and those without de novo DSA, but was lower for patients with C1q-binding de novo DSA (P=0.003). When de novo DSA were analyzed at 2 and 5 years, the 10-year death-censored graft survival was lower for patients with C1q-nonbinding de novo DSA detected at both 2 and 5 years (P,0.001) and for patients with C1q-binding de novo DSA (P=0.002) than for patients without de novo DSA. These results were partially confirmed in two validation cohorts. In conclusion, C1q-binding de novo DSA are associated with graft loss occurring quickly after their appearance. However, the long-term persistence of C1q-nonbinding de novo DSA could lead to lower graft survival.

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“…Matinlauri IH, H€ ockerstedt KA, Isoniemi HM. Equal overall rejection rate in pre-transplant flow-cytometric cross- Increasing data C4d deposition in microvasculature Abundant data 37,38 Increasing data DSA subtypes, C1q binding Emerging data [67][68][69] Limited data Microvascular inflammation Emerging data [70][71][72] [77][78][79] No analogous data Therapeutic trials designed to prevent DSA-associated injury Several studies [80][81][82] None 524 TANER, STEGALL, AND HEIMBACH LIVER TRANSPLANTATION, May 2014…”

Section: Discussionmentioning

confidence: 99%

Antibody-mediated rejection in liver transplantation: Current controversies and future directions

2014

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Subclinical Acute Antibody-Mediated Rejection in Positive Crossmatch Renal Allografts

Cited by 138 publications

References 39 publications

Donor-Specific Antibodies Accelerate Arteriosclerosis after Kidney Transplantation

Donor-Specific Antibodies Accelerate Arteriosclerosis after Kidney Transplantation

Non-Complement–Binding De Novo Donor-Specific Anti-HLA Antibodies and Kidney Allograft Survival

Antibody-mediated rejection in liver transplantation: Current controversies and future directions

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