TY - JOUR
T1 - Association of urinary citrate excretion, pH, and net gastrointestinal alkali absorption with diet, diuretic use, and blood glucose concentration
AU - Perinpam, Majuran
AU - Ware, Erin B.
AU - Smith, Jennifer A.
AU - Turner, Stephen T.
AU - Kardia, Sharon L.R.
AU - Lieske, John C.
N1 - Funding Information:
This work was supported by R01 DK077950, R01 DK073537, U01 HL054457, R01 HL087660, R01 HL119443, the Mayo Clinic O'Brien Urology Research Center P50 DK083007, and Grant Number UL1 TR000135 from the National Center for Advancing Translational Sciences (NCATS), all funded by the National Institutes of Health. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.
Publisher Copyright:
© 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
PY - 2017/10
Y1 - 2017/10
N2 - 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, eGFRCys, 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, eGFRCys and dietary potassium. Significant interactions were observed for Ucit excretion with age and blood glucose, weight and eGFRCys, 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.
AB - 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, eGFRCys, 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, eGFRCys and dietary potassium. Significant interactions were observed for Ucit excretion with age and blood glucose, weight and eGFRCys, 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.
KW - Citrate
KW - diabetes mellitus
KW - diet
KW - glucose
KW - nephrolithiasis
KW - pH
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U2 - 10.14814/phy2.13411
DO - 10.14814/phy2.13411
M3 - Article
C2 - 29038354
AN - SCOPUS:85047776509
SN - 2051-817X
VL - 5
JO - Physiological Reports
JF - Physiological Reports
IS - 19
M1 - e13411
ER -