Diabetes Risk Increased by Kidney Dysfunction
Kidney dysfunction, specifically elevated blood urea nitrogen (BUN) levels, increases the risk for type 2 diabetes, according to the findings of a recent study.
After experimental evidence suggested that higher urea levels increased insulin resistance and suppressed insulin secretion in mice, researchers conducted a large epidemiological study to examine whether this relationship existed in humans.
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The study included 1,337,452 United States veterans without diabetes at baseline. Blood samples were used to determine BUN levels and estimated glomerular filtration rate (eGFR). Using various risk models, the researchers analyzed the relationship between diabetes, eGFR, and BUN levels.
During the median 4.93 years of follow-up, 172,913 individuals developed diabetes.
While joint risk models showed that eGFR and BUN were not associated with diabetes risk among individuals with a BUN level of 25 mg/dl or lower, those with BUN levels over 25 mg/dl had a significantly elevated risk for diabetes, regardless of eGFR. Individuals with a BUN over 25 mg/dL and eGFR of 15 ml/min/1.73 m2 had the highest risk for diabetes (hazard ratio [HR] 1.68 95% CI: 1.51-1.87).
Additional analyses showed that that the risk for diabetes progressively increased as BUN levels increased and this linear relationship was confirmed in models where eGFR was included as a continuous covariate.
Overall, increases in BUN concentration by 10 mg/dL was associated with the risk for type 2 diabetes independent of eGFR levels.
“Taken together, the constellation of findings suggests that in advanced kidney disease and consistent with the experimental evidence, an elevated BUN level is associated with an increased risk of incident diabetes mellitus,” the researchers concluded.
—Melissa Weiss
Reference:
Xie Y, Bowe B, Li T, Xian H, Yan Y, Al-Aly Z. Higher blood urea nitrogen is associated with increased risk of incident diabetes mellitus [published online December 10, 2017]. Kidney International. http://dx.doi.org/10.1016/j.kint.2017.08.033.