The aim of the Deterioration of Kidney Allograft Function study (DeKAF) was to identify and assess the pathologies of troubled kidney grafts, that is, those with ↑ risk for death-censored graft loss (DC-GL). The cross-sectional cohort consisted of those tx prior to 10/1/05 and having SCr ≤2 mg/dl on 1/1/06, and subsequently having deterioration of function (25% ↑ Cr or new onset proteinuria) leading to graft bx. Prelim studies(18 mo f/u) identified clusters of markers, and individual histologic markers (C4d, IATR (infl in areas of fibrosis) plus DSA markers as risks for DC-GL. In this study, we assessed whether these associations remain valid during long- term follow up. Median f/u is now 67 mos, and the findings remain similar: 1) Fig. 1a shows the clusters by extended Banff criteria. There is a signif diff (p<.0001) between clusters in DC-GL (Fig. 1b) Cluster 1 (fibrosis w/o infl), often read by local pathologists as CNI-toxicity, had the least GL. In contrast to prelim data, Cluster 2 (inflammation w/o chronic change) has HR of failure 1.96> cluster 1 (p<.0001). 2) Fig. 2a shows the outcomes grouped by C4d and DSA. C4d+/DSA+ had signif ↑ 5 yr DC-GL vs C4d-/DSA- (p=.0001); DSA+/C4d (p=.03) vs -/-; DSA-/C4d+(=.04) vs-/-.[hellip]3) Univariate analysis of time to DC-GL was signif diff by IATR score (e.g., 1 vs 0; 2 vs 3) (<.01). In addition, 2 groups (i=0, IATR=0 and i>0, IATR=0) had signif better DCGS than either i=0, IATR>0 or i>0, IATR>0 (Fig. 2b). In contrast, i=0, IATR>0 vs i>0 and IATR>0 was NS. We conclude that findings observed in prelim analysis of the DeKAF CS-cohort (cluster analysis, DSA/C4d, and IATR) remain significant with extended f/u.

CITATION INFORMATION: Matas A, Fieberg A, Leduc R, Cosio F, Gaston R, Mannon R, Cecka M, Rush D, Kasiske B, Gourishankar S, Connett J, Grande J. Long-Term Death-Censored Graft Loss in the DeKAF Study. Am J Transplant. 2016;16 (suppl 3).

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