Strohmaier Walter Ludwig, Seilnacht Jürgen, Schubert Gernot
Department of Urology and Pediatric Urology, Klinikum Coburg, Coburg, Germany. walter.strohmaier @ klinikum-coburg.de
Urol Int. 2012;88(3):294-7. doi: 10.1159/000335441. Epub 2012 Mar 7.
Citrate is one of the most important inhibitors in urolithiasis. Hypocitraturia is a common risk factor in stone formers. Citrate excretion is regulated - amongst others - by acidosis and protein intake. A considerable number of stone formers, however, show hypocitraturia in the presence of normal urine pH levels. This is potentially due to defects in the renal tubular citrate carriers (NaDC 1 and 3) which may be genetically determined.
350 consecutive stone formers were examined. Exclusion criteria were urinary tract infection, hypokalemia, and steatorrhea. The following parameters were measured: serum: creatinine, calcium, potassium, and uric acid; urine: pH profiles, citrate, calcium, uric acid, ammonia, urea, and creatinine.
83/350 patients were hypocitraturic (48 males, 35 females). 14/83 had low urine pH (≤ 6), 69/83 showed normal levels (>6). In the latter group there was a significantly higher recurrence rate (23 vs. 9%). The two groups were not different in serum parameters apart from uric acid. In urine, only pH and calcium (males) were significantly lower in the first group. Citrate did not correlate with urine pH and creatinine in the hypocitraturia-normal pH group, only with calcium in both sexes and urea and ammonia in females. In the hypocitraturia-low pH patients, there was no significant correlation between citrate and any other parameter tested.
Hypocitraturia with normal urine pH is an entity indicating a high risk for recurrence. Since there was no correlation between citrate and pH, urea and ammonia, respectively, citrate excretion is not regulated in these patients as usual. There may be a link to calcium excretion. Potentially, these patients have defects in the renal tubular citrate carriers which may be genetically determined. Genetic examinations should be performed to elucidate a potential genetic disorder in hypocitraturia-normal pH stone formers.
柠檬酸盐是尿石症中最重要的抑制剂之一。低枸橼酸尿是结石形成者的常见危险因素。柠檬酸盐排泄受多种因素调节,其中包括酸中毒和蛋白质摄入。然而,相当数量的结石形成者在尿液pH值正常的情况下仍表现为低枸橼酸尿。这可能是由于肾小管柠檬酸盐载体(NaDC 1和3)存在缺陷,而这种缺陷可能是由基因决定的。
对350例连续的结石形成者进行了检查。排除标准为尿路感染、低钾血症和脂肪泻。测量了以下参数:血清:肌酐、钙、钾和尿酸;尿液:pH值曲线、柠檬酸盐、钙、尿酸、氨、尿素和肌酐。
83/350例患者为低枸橼酸尿(48例男性,35例女性)。14/83例患者尿液pH值低(≤6),69/83例患者尿液pH值正常(>6)。在后一组中,复发率显著更高(23%对9%)。除尿酸外,两组血清参数无差异。在尿液中,只有第一组的pH值和钙(男性)显著较低。在低枸橼酸尿-正常pH值组中,柠檬酸盐与尿液pH值和肌酐无相关性,仅与两性的钙以及女性的尿素和氨相关。在低枸橼酸尿-低pH值患者中,柠檬酸盐与任何其他检测参数之间均无显著相关性。
尿液pH值正常的低枸橼酸尿是一种复发风险高的情况。由于柠檬酸盐与pH值、尿素和氨之间分别无相关性,这些患者的柠檬酸盐排泄不像通常那样受到调节。可能与钙排泄有关。这些患者可能存在肾小管柠檬酸盐载体缺陷,这可能是由基因决定的。应进行基因检测以阐明尿液pH值正常的低枸橼酸尿结石形成者中潜在的遗传疾病。