Summary
In male patients with idiopathic recurrent calcium urolithiasis (RCU) the effects of oral potassium sodium citrate (PSC) on acid-base, citrate and mineral metabolism were investigated. There were 17 normocitraturic and 15 hypocitraturic patients. The examination time points in our clinical laboratory were prior to medication and after 3, 6 and over 12 months of medication. Urine collection periods were over 24 h, 2 h — after an overnight fast — 3 h postprandially. Acceptance by the patients was poor, a large number refusing to take PSC for 12 months. Compliance of the patients continuing with the study was adequate as assessed by the urinary excretion of potassium and sodium. No unwanted side effects were observed. After 3 months of PSC medication a compensated metabolic alkalosis developed; in the urine calcium was decreased, while citrate, pH and oxalate were increased, as were hydroxyapatite supersaturation and calcium phosphate particles. After more than 12 months of PSC medication, citrate and pH tended toward the pretreatment baseline values, while hydroxyapatite supersaturation and calcium had already returned to pretreatment values. Despite ongoing PSC intake, patients with pre-existing hypocitraturia had lower urinary citrate than patients with previous normocitraturia, while the concomitant pH and hydroxyapatite supersaturation in the urine of the former remained at levels close to those of the latter. Under the influence of PSC, parathyroid gland function remained unchanged, but serum levels of bone alkaline phosphatase and osteocalcin were low, and urinary hydroxyproline was high. We conclude that (1) PSC shifts the acid-base status toward metabolic alkalosis, and also modulates bone metabolism; (2) over the long term, PSC may be unable to achieve a constantly high urinary citrate, in particular in RCU with pre-existent hypocitraturia — in contrast to its short- and medium-term effects. Long-term interrupted medication with PSC is proposed for the metaphylaxis of RCU. A regimen of this type may also be expected to yield more insight into the mechanism(s) underlying hypocitraturia.
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Herrmann, U., Schwille, P.O., Schwarzlaender, H. et al. Citrate and recurrent idiopathic calcium urolithiasis. Urol. Res. 20, 347–353 (1992). https://doi.org/10.1007/BF00922747
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DOI: https://doi.org/10.1007/BF00922747