Frontiers in endocrinology · 2026
New findings in diabetic kidney disease: correlation and enhanced combined diagnostic value of sclerostin and 25(OH)VD.
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Niu Chunfan, Yin Jianhong, Li Mina, Wu Qianqian, Liu Ming, Sun Li, Yang Jing, Xu Linxin
Аннотация
OBJECTIVE: Diabetic kidney disease (DKD) is a major microvascular complication of type 2 diabetes mellitus (T2DM), and its early identification is crucial. As a novel endocrine marker, the relationship between sclerostin and DKD, as well as its combined diagnostic value with 25-hydroxyvitamin D (25(OH)VD), remains unclear. This study aims to investigate circulating sclerostin levels in patients with DKD and its combined diagnostic value with 25(OH)VD, providing evidence for early clinical diagnosis.
METHODS: A total of 308 patients with T2DM were enrolled, including 113 with DKD (DKD group) and 195 without DKD (T2DM group). The DKD group was subdivided into microalbuminuria and macroalbuminuria groups based on UACR. General information and clinical indicators were collected for all patients. Concurrently, blood samples were collected to measure serum sclerostin levels using the ELISA method. Statistical analysis evaluated sclerostin expression differences across groups and its correlations with other indicators. Binary logistic regression analyzed the independent associations of sclerostin and 25(OH)VD with DKD. Receiver operating characteristic (ROC) curves were plotted to assess the predictive efficacy of serum sclerostin and 25(OH)VD levels for T2DM with albuminuria.
RESULTS: Compared to the T2DM group, patients in the DKD group exhibited decreased serum sclerostin and 25(OH)VD levels (P< 0.05). Further subgroup analysis of DKD revealed that serum sclerostin levels were significantly lower in both the microalbuminuria and macroalbuminuria groups compared to the normal albuminuria group (P< 0.05). Serum 25(OH)VD in the massive proteinuria group was significantly lower than in both the normal proteinuria and microalbuminuria groups (P< 0.05). Correlation analysis showed a significant negative correlation between sclerostin and UACR (r = -0.197, P< 0.001) and a significant positive correlation with 25(OH)VD (r = 0.167, P = 0.003). Binary logistic regression analysis demonstrated that serum sclerostin and 25(OH)VD remained independent predictors of DKD even after adjusting for variables. ROC curve analysis showed that the AUC for predicting DKD using serum sclerostin and 25(OH)VD was 0.73, with a sensitivity of 61.1% and specificity of 75%.
CONCLUSION: This study confirms that serum levels of sclerostin and 25(OH)VD are significantly reduced in patients with DKD, and both are independent protective factors for DKD. Their combined assessment demonstrates good predictive value for the early identification of DKD, providing clinical insights into the interaction between bone metabolism and renal pathology.
METHODS: A total of 308 patients with T2DM were enrolled, including 113 with DKD (DKD group) and 195 without DKD (T2DM group). The DKD group was subdivided into microalbuminuria and macroalbuminuria groups based on UACR. General information and clinical indicators were collected for all patients. Concurrently, blood samples were collected to measure serum sclerostin levels using the ELISA method. Statistical analysis evaluated sclerostin expression differences across groups and its correlations with other indicators. Binary logistic regression analyzed the independent associations of sclerostin and 25(OH)VD with DKD. Receiver operating characteristic (ROC) curves were plotted to assess the predictive efficacy of serum sclerostin and 25(OH)VD levels for T2DM with albuminuria.
RESULTS: Compared to the T2DM group, patients in the DKD group exhibited decreased serum sclerostin and 25(OH)VD levels (P< 0.05). Further subgroup analysis of DKD revealed that serum sclerostin levels were significantly lower in both the microalbuminuria and macroalbuminuria groups compared to the normal albuminuria group (P< 0.05). Serum 25(OH)VD in the massive proteinuria group was significantly lower than in both the normal proteinuria and microalbuminuria groups (P< 0.05). Correlation analysis showed a significant negative correlation between sclerostin and UACR (r = -0.197, P< 0.001) and a significant positive correlation with 25(OH)VD (r = 0.167, P = 0.003). Binary logistic regression analysis demonstrated that serum sclerostin and 25(OH)VD remained independent predictors of DKD even after adjusting for variables. ROC curve analysis showed that the AUC for predicting DKD using serum sclerostin and 25(OH)VD was 0.73, with a sensitivity of 61.1% and specificity of 75%.
CONCLUSION: This study confirms that serum levels of sclerostin and 25(OH)VD are significantly reduced in patients with DKD, and both are independent protective factors for DKD. Their combined assessment demonstrates good predictive value for the early identification of DKD, providing clinical insights into the interaction between bone metabolism and renal pathology.