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Effect of Acute Vascular Inflammation (v) on Death Censored Graft Failure (DCGF) Following Kidney Transplant (KTx)

J. Grande,1 L. Hunsicker,2 R. LeDuc,3 A. Matas, The DeKAF Consortium.

1Pathology, Mayo Clinic, Rochester, MN
2Int. Med., U Iowa, Iowa City, IA
3Biostatistics and Surgery, U Minnesota, Minneapolis, MN.

Meeting: 2018 American Transplant Congress

Abstract number: 313

Keywords: Biopsy, Kidney transplantation, Multicenter studies, Rejection

Session Information

Session Name: Concurrent Session: Kidney Complications: Diagnostic Considerations

Session Type: Concurrent Session

Date: Monday, June 4, 2018

Session Time: 4:30pm-6:00pm

 Presentation Time: 5:18pm-5:30pm

Location: Room 6C

The impact of acute vascular inflammation in acute cellular or humoral rejection following KTx, and the effect of isolated vascular inflammatory lesions on late DCGF, have not been adequately defined. We sought to define the relationship between v and other markers of acute and chronic injury (Banff scores) in KTx biopsies and the role of v on DCGF in patients enrolled two DeKAF study cohorts.

Methods: The prospective cohort (PC) included patients with kidney biopsy (KTxBx) for increase in serum creatinine (Scr) or new onset proteinuria at >3 months post KTx. The cross-sectional cohort (CSC) included patients >6 months after Tx with stable SCr before Jan 2006 who underwent KTxBx for later rise in Scr or new proteinuria. KTxBx were read by a central pathologist in blinded fashion according to expanded Banff criteria. Patients with biopsies showing BK virus or recurrent disease were excluded from analysis.

Results: 1,095 biopsies were analyzed. DCGF following KTxBx in the PC and CSC was identical up to 20 months post-index biopsy. Only 5% of biopsies (58/1095) had v scores >0. Where present, v was more strongly correlated with the markers of acute cellular rejection (ACR) t and i (Kendall correlations 0.23-0.25) than with the markers of microvascular inflammation (MVI) g, cg, and ptc (correlations 0.01 to 0.10). v>0 was strongly correlated with acute cellular rejection (i>1 or t>1) (Chisq 53.7; p < 0.0001). In multivariable Cox analysis including g, ptc, cg, v, and cohort, the presence of v>0 was the single strongest predictor of DCGF (coef 0.745, p = 0.003), showing independence of its effect from those of g, cg, and ptc. In patients with ACR the impact of v>0 on DCGF was only modest (coef 0.29, p=0.073), suggesting an effect mostly overlapping with t and i. There were only 3 biopsies with “isolated v lesions” (v>0 with no MVI or ACR).

Conclusions: The presence of v lesions is a strong predictor of DCGF. v>0 is most strongly correlated with ACR, but v had a modest independent effect on graft outcome in patients with ACR consistent with injury from AMR. In this cohort, the presence of “isolated v” lesions was rare.

CITATION INFORMATION: Grande J., Hunsicker L., LeDuc R., Matas A., The DeKAF Consortium Effect of Acute Vascular Inflammation (v) on Death Censored Graft Failure (DCGF) Following Kidney Transplant (KTx) Am J Transplant. 2017;17 (suppl 3).

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To cite this abstract in AMA style:

Grande J, Hunsicker L, LeDuc R, Matas A, Consortium TheDeKAF. Effect of Acute Vascular Inflammation (v) on Death Censored Graft Failure (DCGF) Following Kidney Transplant (KTx) [abstract]. https://atcmeetingabstracts.com/abstract/effect-of-acute-vascular-inflammation-v-on-death-censored-graft-failure-dcgf-following-kidney-transplant-ktx/. Accessed May 12, 2025.

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