Association of urinary citrate excretion, pH, and net gastrointestinal alkali absorption with diet, diuretic use, and blood glucose concentration

Urinary citrate (Ucit) protects against urinary stone formation. Acid base status and diet influence Ucit. However, the effect of demographics, diet, and glucose metabolism on Ucit excretion, urinary pH (U‐pH) and net gastrointestinal alkali absorption (NAA) are not known. Twenty‐four hour urine samples, blood glucose, creatinine, and cystatin C were obtained from non‐Hispanic white sibships in Rochester, MN (n = 446; 64.5 ± 9 years; 58% female). Diet was assessed by a food frequency questionnaire. The impact of blood glucose, demographics and dietary elements on Ucit excretion, U‐pH, and NAA were evaluated in bivariate and multivariable models and interaction models that included age, sex, and weight. NAA significantly associated with Ucit and U‐pH. In multivariate models Ucit increased with age, weight, eGFR(C) (ys), and blood glucose, but decreased with loop diuretic and thiazide use. U‐pH decreased with serum creatinine, blood glucose, and dietary protein but increased with dietary potassium. NAA was higher in males and increased with age, weight, eGFR(C) (ys) and dietary potassium. Significant interactions were observed for Ucit excretion with age and blood glucose, weight and eGFR(C) (ys,) and sex and thiazide use. Blood glucose had a significant and independent effect on U‐pH and also Ucit. This study provides the first evidence that blood glucose could influence urinary stone risk independent of urinary pH, potentially providing new insight into the association of obesity and urinary stone disease.