From AKI to CKD: Role of miRNAs in disease progression

Abstract

Acute kidney injury (AKI) and chronic kidney disease (CKD) are closely linked, with AKI often accelerating CKD development through sustained inflammation, fibrosis, and tubular damage. Identifying biomarkers that track this transition is essential for early diagnosis and intervention. Recent research highlights microRNAs (miRNAs) as key regulators of AKI-to-CKD progression, with distinct expression patterns across experimental models and clinical samples. Given this context, this review consolidates recent advances in miRNA research related to the AKI-to-CKD transition. Animal studies demonstrate that miRNAs such as miR-101, miR-196a-5p, miR-874-3p, and miR-486-5p contribute to fibrosis, inflammatory signaling, and tubular cell injury-hallmarks of CKD progression. In vitro models further reveal that miRNAs drive pathological processes like epithelial-mesenchymal transition (EMT) and apoptosis, underscoring their role in kidney dysfunction at the cellular level. Clinically, miR-21 has emerged as a particularly promising biomarker, with elevated levels in urine and blood correlating with AKI severity and CKD advancement, suggesting its potential for early detection and disease monitoring. Despite growing evidence of miRNA involvement in AKI-to-CKD progression, research remains limited, particularly in translating findings into predictive diagnostic tools. Future studies should focus on validating miRNA signatures in large patient cohorts and uncovering their precise molecular mechanisms to refine therapeutic strategies.