Long non-coding RNA in IgA nephropathy: a comprehensive review.

Immunoglobulin A nephropathy (IgAN) stands as the most prevalent primary glomerulonephritis globally, almost half of patients progress to end-stage kidney disease (ESKD). However, the precise pathogenesis of IgAN remains elusive. Long non-coding RNAs (lncRNAs), non-protein-coding transcripts that regulate gene expression, have been found to exhibit distinct expression patterns in various disease states. Comprehensive bioinformatic analyses from IgAN patients have uncovered differential expression of lncRNAs such as HOTAIR, H19, and MALAT1. Furthermore, a single nucleotide polymorphism in MIR31HG has been linked to IgAN susceptibility and correlated with clinical markers like urinary red blood cells and hemoglobin levels. Lnc-TSI and lnc-CHAF1B-3, specifically expressed in the kidneys of IgAN patients, exhibit associations with renal fibrosis indices and the degree of kidney function deterioration, influencing the progression of renal fibrosis through distinct signaling pathways. Additionally, renal intercellular adhesion molecule 1 (ICAM-1) related long noncoding RNA (ICR) levels positively correlate with IgAN severity and contribute to renal fibrosis, whereas serum H19 serves as an independent protective factor against IgAN. Notably, experiments have validated the involvement of PTTG3P, lnc-CHAF1B-3, and CRNDE in the pathogenesis of IgAN. Nevertheless, data on the roles of lncRNAs in IgAN pathogenesis and their potential as biomarkers remain limited, and effective therapeutic options for IgAN are similarly rare. Therefore, there is an urgent need to bridge this knowledge gap. This article presents a review of current literature on lncRNAs related to IgAN, aiming to consolidate existing findings and identify future research avenues.