LAUSR

Background and Hypothesis: Hypocitraturia is a marker of metabolic acidosis and a risk factor for kidney stone formation. Oral citrate replacement is a mainstay therapy for hypocitraturic nephrolithiasis. We have observed that a subpopulation of hypocitraturic stone formers do not respond to oral potassium citrate (KCit) with the expected increase in urine citrate despite evidence of adherence to therapy as measured by increased urine K, citrate nonresponders (NR). We hypothesize that altered kidney handling of citrate accounts for the failure of oral citrate to result in increased urine citrate. Methods: To study this hypothesis, we compared changes in urine electrolyte excretion before and after citrate administration in citrate responder (R) and nonresponder (NR) stone formers with hypocitraturia and normal kidney function. Net gastrointestinal alkali absorption was calculated by the method of Oh (Urine Na + K + Ca + Mg) – (Urine Cl + P). Results: We identified 7 R and 8 NR with 24h urine assessments pre and post KCit. 7/8 R and 6/8 NR were female and all were White. There were no significant differences in age, weight, BMI, or dose of citrate. Baseline serum K and bicarbonate (24 +/- 3 meq/L) were similar in both groups and did not show significant changes after KCit administration. By design, 24h urine citrate increased significantly more in R (2.2 +/- 1.4 to 8.3 +/- 3.8 meq/d) than in NR (1.9 +/- 1.4 to 2.9 +/- 1.2 meq/d). Urine pH increased in both groups similarly (6.64 to 7.03 NR, 6.6 to 7.06 R) as did 24h urine K. Urine calcium did not change in either group. Ammonia excretion decreased significantly in R but not NR. However, 24h urine titratable acid excretion decreased in both groups. Net acid excretion was higher at baseline in NR and decreased in both groups but to negative levels in R. Interestingly, net gastrointestinal alkali absorption increased similarly in both groups. Conclusions: These findings suggest that R and NR have equivalent gastrointestinal absorption of KCit. NR may have a greater acid burden enhancing kidney citrate reabsorption as suggested by the higher baseline net acid excretion or altered bone utilization of citrate resulting in reduced excretion of a citrate load. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.