Potential Role of Gastrointestinal Alkali Loss in Patients with Uric Acid Nephrolithiasis
Our hypothesis is that higher endogenous acid production in UA nephrolithiasis is, in part, due to increased GI alkali loss. This study will utilize a cross-sectional metabolic balance design to determine GI alkali loss and endogenous acid production by analyzing dietary, urinary, and fecal constituents in patients with UA nephrolithiasis and matched lean normal subjects.
Subjects will be recruited as referrals from the UT Southwestern Mineral Metabolism and Urology Clinics as well as the Parkland Health and Hospital System Mineral Metabolism Clinic. Normal, healthy volunteers will be recruited via campus and community-wide advertising.
The study will consist of a 4-day equilibration period on an isocaloric metabolic diet followed by a 4-day timed stool collection. Three 24-hour urine specimens will be obtained to provide a quantitative analysis of urinary organic anions and stone risk analysis and measurement of urinary acid-base profiles. Two fasting blood samples will be drawn for chemistries, insulin, and free fatty acids. A total body DXA will be performed for the analysis of body fat content and composition.
Group 1: Subjects with Uric Acid Nephrolithiasis.
Adult subjects with uric acid nephrolithiasis, age > 21 years of either sex, of any ethnicity. .
Group 2: Lean normal subjects.
Lean adult subjects (BMI<25), gender-matched and age-matched (within 5 years) to UA stone former subjects from group 1, with no known history of kidney stones.
Group 3: Obese normal subjects.
Obese adult subjects (BMI>30), gender-matched and age-matched (within 5 years) to UA stone former subjects from group 1, with no known history of kidney stones or diabetes.