Both antibody mediated (AMR) and T-cell mediated (TCMR) rejections either acute or chronic represent the main reason for late graft dysfunction. In this study we aimed to evaluate differences in the intrarenal expression patterns of immune system related genes in acute and chronic rejections. Graft biopsies were performed and evaluated according to Banff classification. Using the TaqMan Low Density Array, the intrarenal expressions of 376 genes relating to immune response (B-cell activation, T-cell activation, chemokines, growth factors, immune regulators, and apoptosis) were analyzed in the four rejection categories: chronic AMR, chronic TCMR, acute AMR, and acute TCMR. The set of genes significantly upregulated in acute TCMR as compared to acute AMR was identified, while no difference in gene expressions between chronic rejections groups was found. In comparison with functioning grafts, grafts that failed within the next 24 months after the chronic rejection morphological confirmation presented at biopsy already established severe graft injury (low eGFR, higher proteinuria), longer followup, higher expression of CDC20, CXCL6, DIABLO, GABRP, KIAA0101, ME2, MMP7, NFATC4, and TGFB3 mRNA, and lower expression of CCL19 and TRADD mRNA. In conclusion, both Banff 2007 chronic rejection categories did not differ in intrarenal expression of 376 selected genes associated with immune response.

Transplant Laboratory Institute for Clinical and Experimental Medicine Vídeňská 1958 9 14021 Prague Czech Republic

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Solez K, Colvin RB, Racusen LC, et al. Banff 07 classification of renal allograft pathology: updates and future directions. The American Journal of Transplantation. 2008;8(4):753–760. PubMed

Sis B, Jhangri GS, Bunnag S, Allanach K, Kaplan B, Halloran PF. Endothelial gene expression in kidney transplants with alloantibody indicates antibody-mediated damage despite lack of C4d staining. The American Journal of Transplantation. 2009;9(10):2312–2323. PubMed

Sarwal M, Chua MS, Kambham N, et al. Molecular heterogeneity in acute renal allograft rejection identified by DNA microarray profiling. The New England Journal of Medicine. 2003;349(2):125–138. PubMed

Viklicky O, Hribova P, Volk HD, et al. Molecular phenotypes of acute rejection predict kidney graft prognosis. Journal of the American Society of Nephrology. 2010;21(1):173–180. PubMed PMC

Mueller TF, Einecke G, Reeve J, et al. Microarray analysis of rejection in human kidney transplants using pathogenesis-based transcript sets. The American Journal of Transplantation. 2007;7(12):2712–2722. PubMed

Reeve J, Einecke G, Mengel M, et al. Diagnosing rejection in renal transplants: a comparison of molecular- and histopathology-based approaches. The American Journal of Transplantation. 2009;9(8):1802–1810. PubMed

Racusen LC, Solez K, Colvin RB, et al. The Banff 97 working classification of renal allograft pathology. Kidney International. 1999;55(2):713–723. PubMed

Solez K, Colvin RB, Racusen LC, et al. Banff ’05 meeting report: differential diagnosis of chronic allograft injury and elimination of chronic allograft nephropathy (“CAN”) The American Journal of Transplantation. 2007;7(3):518–526. PubMed

Homs S, Mansour H, Desvaux D, et al. Predominant Th1 and cytotoxic phenotype in biopsies from renal transplant recipients with transplant glomerulopathy. The American Journal of Transplantation. 2009;9(5):1230–1236. PubMed

Einecke G, Reeve J, Sis B, et al. A molecular classifier for predicting future graft loss in late kidney transplant biopsies. Journal of Clinical Investigation. 2010;120(6):1862–1872. PubMed PMC

Havasi A, Borkan SC. Apoptosis and acute kidney injury. Kidney International. 2011;80(1):29–40. PubMed PMC