Diagnosis of diabetic peripheral neuropathy (DPN) depends on subjective findings, disturbing certain investigations for DPN risks. Bilirubin protects against vascular complications by reducing oxidative stress in diabetes, but not fully tested for DPN. This study aimed to evaluate sural nerve conduction impairments (SNCI) as an objective DPN marker and the contribution of bilirubin to SNCI.
Using DPN-Check, SNCI was defined as decline of amplitude potential or conduction velocity below normal limit in 150 inpatients with diabetes. The correlations between SNCI and conventional DPN diagnosis criteria, the incidence of diabetic retinopathy/nephropathy, biomarkers for atherosclerosis, cardiac function by ultrasonic cardiogram, and bilirubin were statistically tested, followed by the comparison of logistic regression models for SNCI to find confounders with bilirubin.
The incidence of SNCI was 72.0%. Sensitivity and specificity of SNCI for DPN prediagnosis by simplified criteria were 54.6% and 90.5%, respectively, similarly corresponded with diabetic retinopathy and nephropathy (sensitivity: 57.4% and 50.0%, respectively). SNCI significantly related to diabetes duration, declined estimated glomerular filtration rate, albuminuria, and total bilirubin. SNCI incidence was attenuated in the higher bilirubin tertiles (89.8/65.3/54.8%, p<0.001). Bilirubin was an independent inverse risk factor for SNCI even after adjustment by known risk factors for DPN and markers for microvascular complications.
SNCI is a comprehensive marker for diabetic complications. We first demonstrated the independent inverse relationship between bilirubin and SNCI through the independent pathway with other complications, provably reducing oxidative stress as previously reported.

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