Risk factors for distal symmetric polyneuropathy in patients with type 2 diabetes mellitus: A retrospective study

The pathophysiology of distal symmetric polyneuropathy (DSPN) is multifactorial, involving chronic hyperglycemia, oxidative stress, accumulation of advanced glycation end products, impaired microvascular perfusion, metabolic toxicity, and nutritional deficiencies. Although previous studies have identified various risk factors, substantial heterogeneity exists across regions and populations, and most investigations have not comprehensively integrated metabolic markers, microvascular damage, and electrophysiological data. Therefore, a multidimensional assessment of DSPN risk factors is essential to improve early screening and risk-prediction strategies. A total of 120 patients with type 2 diabetes mellitus (T2DM) were enrolled, including 60 with DSPN and 60 without. Compared with the non-DSPN group, patients with DSPN were older, had longer diabetes duration, and demonstrated a higher prevalence of smoking, diabetic retinopathy (DR), and diabetic kidney disease. DSPN patients exhibited poorer glycemic control (higher fasting blood glucose, 2-hour postprandial blood glucose, and hemoglobin A1c [HbA1c]), more pronounced dyslipidemia (elevated triglycerides, reduced high-density lipoprotein cholesterol), and abnormalities in inflammatory and nutritional markers (elevated C-reactive protein and homocysteine [HCY], reduced vitamin B12). Renal function parameters (serum creatinine, estimated glomerular filtration rate, urine albumin-creatinine ratio) indicated more severe microvascular impairment in the DSPN group. Electrophysiological testing showed reduced sensory and motor nerve conduction velocities, decreased amplitudes, and prolonged latencies. Multivariable logistic regression identified diabetes duration, DR, elevated HbA1c, elevated HCY, and reduced sural nerve amplitude as independent risk factors for DSPN. Longer diabetes duration, DR, elevated HbA1c, elevated HCY levels, and reduced sural nerve amplitude were independently associated with DSPN in patients with T2DM. These findings may contribute to improved risk stratification and support further investigation of multidimensional approaches for early DSPN identification. This single-center retrospective cohort study included patients with T2DM treated at our hospital between June 2023 and June 2025. DSPN was diagnosed based on American Diabetes Association, European Federation of Neurological Societies, and diabetic neuropathy working group criteria using a combination of clinical symptoms, neurological signs, and nerve conduction studies. Demographic characteristics, lifestyle factors, diabetes-related complications, glucose and lipid metabolism indicators, renal function, inflammatory and nutritional markers, and electrophysiological parameters were collected. Group differences were assessed using the t-test, Mann-Whitney U test, or χ2 test. Variables with P < .10 in univariate analyses were entered into multivariable logistic regression to identify independent risk factors for DSPN. Sensitivity analyses and collinearity diagnostics were performed to assess the robustness of the findings.