ORLANDO – , according to a 7-year investigation of 539 children.
Every 1-mg/dL climb in baseline serum uric acid increased the risk of subsequent elevated urine albumin excretion 1.23 fold, after adjustment for potential confounders (P = .02).
The finding adds to growing evidence that serum uric acid (SUA) isn’t just a marker of diabetic kidney disease, but a contributor to it. “There is definitely” cross-talk between gout and diabetes, said lead investigator Petter Bjornstad, MD, assistant professor of pediatric endocrinology at the University of Colorado, Aurora.
Elevated SUA is common in both conditions and a risk factor for kidney disease. Newer studies have linked higher levels to nephron number decline and other pathologies, perhaps through renal inflammation. Allopurinol, the traditional uric acid lowering agent in gout, isto prevent kidney decline in adults with type 1 diabetes mellitus. There’s also evidence that the potent uric acid lowering agent, febuxostat (Uloric), attenuates hypofiltration in early diabetic kidney disease.
The 539 children, all part of the Treatment Options for Type 2 Diabetes in Adolescents and Youth () trial, were assessed annually over a mean of 5.7 years. At baseline, they were 13.9 years old and had T2DM for 7.9 months, on average. The mean body mass index was 34.6 kg/m2, mean hemoglobin A1c was 6%.
Almost 20% of the children were hypertensive at baseline (130/80 mm Hg or higher); 26% were hyperuricemic (6.8 mg/dL or higher); and 6.1% had elevated urine albumin excretion (urine albumin creatinine ratio of at least 30 mg/g), a marker of renal pathology. At the end of follow-up, 18% had elevated albumin excretion and 37.4% were hypertensive.
“Hyperuricemia was common in youth with type 2 diabetes,” just as it’s been shown in adults with the disease. “Higher baseline SUA independently increase[s] risk for onset of hypertension and elevated urine albumin excretion,” Dr. Bjornstad said.
However, the association between SUA and elevated albumin excretion was statistically significant only in boys – 36% of the study population – and non-Hispanic whites, 20% of the subjects, after adjustment for BMI, hemoglobin A1c, estimated glomerular filtration rate, and use of ACE inhibitors and angiotensin II receptor blockers.
The National Institutes of Health funded the work. Dr. Bjornstad is a consultant for Boehringer Ingelheim.
SOURCE: Bjornstad P et al. ADA 2018, abstract