Abstract
Introduction: Steroids are considered first-line therapeutic opportunities in cases with idiopathic nephrotic syndrome (INS). The trustworthy biomarkers for steroid-resistant NS (SRNS) would permit more precise decisions in the treatment of INS.
Objectives: This study aimed to evaluate the miR-15 and miR-16 levels in NS cases.
Patients and Methods: Adult cases with primary NS (n=60) including 30 FSGS (Focal segmental glomerulosclerosis) and 30 membranous glomerulonephritis (MGN) patients and 24 healthy individuals were included. The evaluation of miR-15 and miR-16 expression in blood cells was performed using real-time polymerase chain reaction (qPCR). Moreover, gene ontology analysis and prediction of the miRNA targets were completed to recognize the biological procedures and signaling pathways involved in the pathophysiology of NS.
Results: A significant increase was observed in miR-15a-5p expression in cases with primary MGN and FSGS compared with healthy subjects. Conversely, the miR-16-5p expression was significantly decreased in both conditions compared with healthy controls. In the clinical subdivision of FSGS group to steroid-resistant-FSGS and steroid-responsive-FSGS, significant elevated levels of miR-15a-5p and diminished levels of miR-16-5p were observed in both groups compared to normal controls. Gene annotation demonstrated that these miRNAs contribute to cell cycle, ion transport, biological adhesion, cation transport, cellular response to endogenous stimulus, and regulation of small GTPase-related signal transduction.
Conclusion: Dysregulated levels of miR-15 and miR-16 may be involved in the pathogenesis and response to steroid therapy in patients with INS.