Published online Apr 15, 2025. doi: 10.4239/wjd.v16.i4.101966
Revised: December 14, 2024
Accepted: January 9, 2025
Published online: April 15, 2025
Processing time: 148 Days and 3.8 Hours
Increased blood urea nitrogen (BUN) levels have been demonstrated to be asso
To examine the relationship between BUN levels and peripheral nerve function in patients with T2D.
This observational study involved the systematic recruitment of 585 patients with T2D for whom BUN levels and estimated glomerular filtration rate were mea
Across the quartiles of BUN levels, the overall composite Z-score for latency (F = 38.996, P for trend < 0.001) showed a significant increasing trend, whereas the overall composite Z-scores for amplitude (F = 50.972, P for trend < 0.001) and NCV (F = 30.636, P for trend < 0.001) exhibited a significant decreasing trend. Moreover, the BUN levels were closely correlated with the latency, amplitude, and NCV of each peripheral nerve. Furthermore, multivariate linear regression analysis revealed that elevated BUN levels were linked to a higher overall composite Z-score for latency (β = 0.166, t = 3.864, P < 0.001) and lower overall composite Z-scores for amplitude (β = -0.184, t = -4.577, P < 0.001) and NCV (β = -0.117, t = -2.787, P = 0.006) independent of the estimated glomerular filtration rate and other clinical covariates. Additionally, when the analysis was restricted to sensory or motor nerves, elevated BUN levels remained associated with sensory or motor peripheral nerve dysfunction.
Increased BUN levels were independently associated with compromised peripheral nerve function in patients with T2D.
Core Tip: Blood urea nitrogen (BUN) is a well-established biomarker utilized in clinical diagnostic evaluations. When renal function is relatively normal, an increase in BUN may indicate a negative nitrogen balance, underlying metabolic disorders, and potential adverse outcomes. In the present study, our findings indicated that increased BUN levels were independently associated with compromised peripheral nerve function in patients with type 2 diabetes and may serve as a potential risk factor for peripheral nerve dysfunction in these patients. Future interventions to lower BUN levels by improving nutritional status and balancing protein metabolism may alleviate peripheral nerve dysfunction in patients with type 2 diabetes.