Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease with a prevalence of 25–30 % globally [1]. This term defines a spectrum of diseases, including NAFLD, nonalcoholic steatohepatitis, liver cirrhosis, and hepatocellular cancer [2], [3]. The prevalence of NAFLD ranges between 55–70 % in patients with type 2 diabetes mellitus (DM) [4]. Other well-known risk factors associated with NAFLD are obesity, dyslipidemia, metabolic syndrome, and polycystic ovary syndrome [5]. While there is an increased risk of NAFLD in patients with type 2 DM, type 2 DM risk also increases in patients with NAFLD [6]. Studies show that NAFLD is associated with an increased risk of cardiovascular diseases and microvascular complications (nephropathy and retinopathy) in patients with type 2 DM [4], [7], [8].

The degree of fibrosis determines the prognosis of patients with NAFLD. Disease severity increases with the degree of fibrosis. Hepatic fibrosis is associated with type 2 DM, hypertension (HT), hyperlipidemia (HL), and chronic renal disease [1]. Hepatic fibrosis in NAFLD can be evaluated using various noninvasive methods. These methods include imaging such as computed tomography, magnetic resonance imaging (MRI), FibroScan, and MRI elastography, and scoring systems such as fibrosis-4 (FIB-4), aspartate aminotransferase/platelet ratio index (APRI), and NAFLD fibrosis score, which include commonly used biochemical markers. The FIB-4 score is calculated using serum aspartate aminotransferase (AST) and alanine transaminase (ALT) levels and thrombocyte numbers, which are commonly evaluated parameters in routine daily practice. Meta-analyses have shown that it is superior to other noninvasive scoring systems in diagnosing fibrosis [9], [10]. We aimed to evaluate the possible role of the FIB-4 score in predicting microvascular complications in diabetes.

Diabetic nephropathy is characterized by albuminuria, decreased glomerular filtration rate (GFR), high blood pressure, and elevated cardiovascular risk, affecting 20–40 % of individuals with type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes [11]. Approximately one-third of the patients requiring chronic renal replacement therapy in Western countries have type 2 diabetes. The prevalence of end-stage renal disease is increasing owing to the increasing incidence of type 2 diabetes and the decline in mortality from cardiovascular causes. In both types of diabetes, chronic hyperglycemia is the leading cause. In type 1 diabetes, hyperglycemia typically begins in the early decades of life and is a recognized cause of nephropathy. Conversely, in type 2 diabetes, hyperglycemia often begins after the age of 40 years, coinciding with the kidneys already experiencing the long-term effects of aging and other contributors to chronic renal injury, such as high blood pressure, obesity, dyslipidemia, and smoking. Aging leads to progressive glomerulosclerosis. When combined with other risk factors, it may result in arteriolosclerotic changes that frequently accompany or surpass the typical features of diabetic glomerulopathy, especially type 2 diabetes. Ischemic changes are also common in patients with type 2 diabetes owing to the high prevalence of accelerated atherosclerosis in the renal macrovasculature. Therefore, diabetic nephropathy encompasses a common syndrome in both types of diabetes but presents as a heterogeneous mix of diseases in type 2 diabetes, driven by different mechanisms and often coexisting in various combinations [12], [13].