**1. Introduction**

The prevalence of Diabetes Mellitus (DM) increases globally; in 2011, about 366 million people experienced Diabetes, and it is estimated to continue to grow to 522 million people in 2030 [1]. Diabetes Mellitus will cause damage and failure of various organs; one of these organs is the kidney. This complication of DM in the kidney is called Diabetic Nephropathy. The prevalence of Diabetic Nephropathy occurs in 20–40% of all type-2 DM patients [2]. Kidney damage in Diabetic Nephropathy is irreversible and causes an increase in morbidity, mortality, and the burden of health financing in most countries [3].

The principal risks of Diabetic Nephropathy are modifiable, namely blood pressure, blood sugar, and dyslipidemia. Meanwhile, factors that cannot be modified include age, race, and genetic profile [4]. However, the pathogenesis that contributes to Diabetic Nephropathy incidence is not fully understood, especially the role of genetics [5]. So that efforts to obtain genetic information in type-2 DM patients who are susceptible/at risk of Diabetic Nephropathy provide an opportunity to predict and diagnose this complication early [6].

The ELMO-1 gene is a functional gene that codes for the formation of the ELMO-1 protein, located on chromosome 7 of mammalian cells. ELMO-1 protein helps engulf "eating" or clean apoptotic cells and plays a role in cell motility and cell shape changes [7, 8].

ELMO-1 protein increases in hyperglycemic conditions and TGF-β1 (Tumor Growth Factor Beta-1), collagen type-1, fibronectin expression, and Extra Cellular Matrix (ECM) in the kidneys. MMP-9 also plays a vital role in diabetic nephropathy. Increased secretion of MMP-9 destroys the podocyte diaphragm, which is an essential component in maintaining the standard barrier of glomerular filtration [10].
