A Beijing Hospital study suggests peroneal motor nerve damage may identify patients at risk of accelerated renal decline, while sudomotor dysfunction mainly reflects existing kidney impairment.
A real-world study from Beijing Hospital suggests that not all nerve measures in Type 2 diabetes carry the same prognostic weight for kidney disease. In patients with advanced age, long-standing diabetes and established complications, sudomotor small-fibre dysfunction tracked closely with current renal impairment, but it did not independently forecast faster future loss of kidney function once baseline kidney status was taken into account. By contrast, a lower peroneal motor amplitude, a marker of large-fibre nerve damage, remained linked to accelerated renal decline.
The research, published in a Wiley journal, drew on 1,400 inpatients with Type 2 diabetes treated between January 2020 and September 2025. After exclusions for incomplete testing, non-diabetic neuropathy, acute kidney injury and other factors, 694 patients were included in the baseline analysis. A smaller longitudinal group of 234 patients, followed for a median of two years, was used to assess annualised estimated glomerular filtration rate, or eGFR, decline. The authors defined accelerated decline as a fall of more than 3 mL/min/1.73 m2 a year, with a stricter threshold of more than 5 mL/min/1.73 m2 a year tested separately.
The study used Sudoscan to assess electrochemical skin conductance of the feet, a non-invasive measure of postganglionic sympathetic small-fibre function, alongside standard nerve conduction studies. At baseline, people in the lowest sudomotor tertile were older, had lived with diabetes longer, had poorer glycaemic control and showed worse renal and nerve function than those with better sudomotor readings. Baseline ESCF, the feet conductance measure, correlated with baseline eGFR, but that association weakened and disappeared after baseline kidney function was added to the model. In other words, the sudomotor signal appeared to reflect existing kidney injury rather than add much independent forward-looking information.
The large-fibre findings were more striking. In the longitudinal analysis, right peroneal motor amplitude emerged as an independent predictor of slower renal deterioration, even after adjustment for other clinical factors. It remained significant in a sensitivity analysis using the stricter rapid-decline threshold recommended by kidney guidelines. The signal also held up across most subgroups, although the association was stronger in patients with pre-existing diabetic kidney disease and in women. The authors said these subgroup findings are exploratory, but they may point to differences in how advanced systemic damage is expressed across patient groups.
Adding the neurofunctional data to a standard clinical model improved discrimination only modestly, but it materially improved risk reclassification. The combined model lifted the area under the receiver operating characteristic curve from 0.666 to 0.705, while also producing a continuous net reclassification improvement of 30.35%. The authors argue that this suggests the nerve tests may help identify “hidden high-risk” patients whose kidney risk is underestimated by conventional markers alone. Still, they caution that the study was retrospective, single-centre and lacked external validation, so the findings should be confirmed in larger prospective cohorts before being used routinely in practice.
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