Expression of miR-155, miR-223, miR-29b, miR-142-3p, and miR-142-5p in kidney allografts with acute tubular necrosis, rejection phenotypes, and BK-polyomavirus nephropathy.

Specific tissue microRNA (miRNA) profiles may reflect biologically relevant pathways of kidney allograft injury and rejection. We analyzed the intragraft expression of five preselected miRNAs (miR-29b-3p, miR-142-3p, miR-142-5p, miR-155-5p and miR-223-3p) using qPCR in biopsies from patients with antibody-mediated rejection (ABMR; n = 26), T cell-mediated rejection (TCMR; n = 14), BK polyomavirus nephropathy (BKVN; n = 15), acute tubular necrosis (ATN; n = 8), and controls (CTRL; n = 20). miR-155-5p, miR-223-3p, and miR-142-5p/3p were significantly up-regulated in ABMR (p < 0.01), TCMR (p ≤ 0.012), and BKVN (p ≤ 0.001) compared with CTRL, while miR-223-3p levels in ATN were comparable to CTRL. These immune-related miRNAs correlated with serum creatinine, proteinuria, Banff inflammation scores (t, i, ti; all p ≤ 0.001), and transcriptomic markers of rejection and tissue injury derived from molecular analysis of biopsy samples (all p < 0.01). miR-155-5p showed the strongest and most consistent association with rejection-related parameters, whereas miR-29b-3p correlated with donor characteristics and chronic fibrosis. In classification analyses, individual miRNAs displayed moderate discrimination, with miR-223-3p performing best, while a combined multi-miRNA model markedly improved separation of rejecting and non-rejecting phenotypes (AUC = 0.954 after BKVN exclusion). Intragraft miRNA expression was associated with selected inflammatory and immune-mediated features of allograft dysfunction and may provide supportive biological information alongside histopathological and molecular assessment in future studies. However, these exploratory findings require validation in larger, independent cohorts, including paired blood or urine samples, before any diagnostic or biomarker role can be established.