Brain-derived neurotrophic factor associated with kidney function.

BACKGROUND: We examined the relationship between brain-derived neurotrophic factor (BDNF) and chronic kidney disease (CKD). METHODS: First, a cross-sectional study was conducted in 480 participants without known diabetes. An oral glucose tolerance test (OGTT) was administered after overnight fasting, and blood samples were collected at 0, 30, and 120 min. Second, a total of 3003 participants were enrolled for the case-control genetic analysis. After assigning them to a case or a control group based on age and CKD status, we investigated the association between BDNF gene variants and susceptibility to CKD. RESULTS: A higher fasting serum BDNF quartile was significantly associated with a lower prevalence of CKD (P value for trend < 0.001). Based on the receiver operating characteristic analysis, the fasting BDNF level had a larger area under the curve for differentiating CKD (0.645, 95% CI 0.583‒0.707) than the BDNF levels at both 30 min (0.547, 95% CI 0.481‒0.612) and 120 min (0.598, 95% CI 0.536‒0.661). A significantly lower CKD prevalence (odds ratio = 0.30, 95% CI 0.12‒0.71) was observed in the highest quartile of fasting BDNF level than that in the lowest quartile, whereas no interquartile differences were observed for BDNF levels determined at 30 or 120 min during the OGTT. Furthermore, BDNF-associated variants, including rs12098908, rs12577517, and rs72891405, were significantly associated with CKD. CONCLUSIONS: The BDNF level at fasting, but not at 30 and 120 min after glucose intake, was an independent indicator of CKD. In addition, significant associations were observed between three BDNF gene variants and CKD.

Brain-Derived Neurotrophic Factor Reduces Long-Term Mortality in Patients With Coronary Artery Disease and Chronic Kidney Disease.

Objectives: Chronic kidney disease (CKD) is a risk factor for coronary artery disease (CAD). We examined the effects of circulating brain-derived neurotrophic factor (BDNF) on long-term mortality in patients with CAD and CKD. Materials and Methods: We enrolled patients with established CAD in the present study. Serum BDNF and estimated glomerular filtration rate (eGFR) were assessed after overnight fasting. All-cause mortality served as the primary endpoint. Results: All 348 enrolled patients were divided into four groups according to their median BDNF level and CKD status, defined according to eGFR <60 mL/min/1.73 m2. Forty-five patients reached the primary endpoint during the median follow-up time of 6.0 years. Kaplan-Meier survival analysis indicated that the group with low BDNF and CKD had a significantly higher mortality rate than the other three groups (log-rank test p < 0.001). Compared to the high BDNF without CKD group, the low BDNF with CKD group had a hazard ratio (HR) of 3.186 [95% confidence interval (CI): 1.482-6.846] for all-cause mortality according to the multivariable Cox proportional hazard regression analysis after adjusting for age and urine albumin-creatinine ratio (p = 0.003). Furthermore, there was a significantly interactive effect between BDNF and CKD status on the risk of the primary endpoint (odds ratio = 6.413, 95% CI: 1.497-27.47 in the multivariable logistic regression model and HR = 3.640, 95% CI: 1.006-13.173 in the Cox regression model). Conclusion: We observed a synergistic effect between low serum BDNF levels and CKD on the prediction of all-cause mortality in patients with CAD.