Serum miR-21 could help detect kidney damage caused by type 2 diabetes, evidence shows
Measuring the serum levels of microRNAs (miRNAs) may reflect early renal involvement in people with type 2 diabetes, new research has revealed.
Progressive increases of miR-21 serum expression levels with albuminuria and strong associations with clinical parameters suggest that the molecular regulators could act as an indicator of diabetic nephropathy.
Albuminuria is a widely used clinical marker for diabetic nephropathy; however, its limited sensitivity and specificity in detecting early renal alterations highlight the need for additional indicators.
According to prior studies, miRNAs are emerging as molecular regulators involved in the pathogenesis of diabetic nephropathy and may provide insight into early renal involvement in type 2 diabetes.
This study aimed to evaluate the serum expression levels of miR-21 and miR-192 in normo- and microalbuminuric people with type 2 diabetes and explore their associations with metabolic and renal parameters. It included 104 individuals, including 60 people with type 2 diabetes and 44 age- and sex-matched healthy controls.
Individuals with type 2 diabetes were further classified into 30 normoalbuminuric and 30 microalbuminuric individuals based on the urinary albumin-to-creatinine ratio. Serum levels of miR-21 and miR-192 were quantified using real-time quantitative reverse transcription PCR.
The results have shown that both miR-21 and miR-192 were significantly upregulated in people with type 2 diabetes compared to healthy controls. Notably, miR-21 expression exhibited a stepwise increase from normo- to microalbuminuria and showed strong correlations with metabolic and renal parameters, including HbA1c, ACR and lipid profile.
The analysis has highlighted that miR-21 demonstrated better discriminative ability between study groups compared to miR-192.
Researchers have said that further prospective studies are needed to validate the clinical applicability.
The research study is available here.
