The diabetes prevalence is increasing with decades all over the world [1]. Diabetic nephropathy (DN), the most prevalent microvascular disorder of diabetes, effects about 20–40% of diabetic patients in developed countries [2]. Diabetic nephropathy (DN) is a chronic, progressive process that lastly results in renal fibrosis and end-stage renal failure (ESRD), a devastating disease that needs dialysis or kidney transplantation [3], [4]. Type 2 diabetes mellitus (T2DM) represents a leading reason of ESRD [5], [6]. The burden of diabetes and DN on society is tremendous. Recent research has examined the potential molecular pathways involved in DN. Nevertheless, the precise pathophysiology is still not explained [7].

Musclin, a novel muscle-secreted peptide, inhibited insulin-stimulated glucose uptake in C2C12 cells [8]. In addition, musclin incubation suppressed the protein kinase B (Akt) mRNA expression and Akt phosphorylation in rat muscle tissues [9]. Therefore, musclin is involved in regulation glucose metabolism and insulin resistance. Recent results displayed elevated serum musclin in T2DM patients than in controls [10]. This demonstrates that musclin may play a possible function in the pathophysiology of diabetes.

The current research aims to test the correlation between serum musclin and DN.