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Studies on the Pathogenesis of Type I (Distal) Renal Tubular Acidosis as Revealed by the Urinary Pco2 Tensions

机译:尿中Pco2张力揭示的I型(远端)肾小管性酸中毒的发病机制研究

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摘要

This study was designed to investigate the pathogenesis of type I (distal) renal tubular acidosis.Urinary and blood Pco2 tensions were determined when the pH of the urine was equal to or exceeded the corresponding blood pH. This provided an indication of net hydrogen ion secretion in the distal nephron. In 16 normal subjects, the Pco2 of the urine exceeded blood values (U-B Pco2) by 32.7±3.1 mm Hg. In contrast, the urinary Pco2 tensions in 10 patients with type I (distal) renal tubular acidosis were not significantly greater than blood values (U-B Pco2 = 2.0±2.2 mm Hg). These results indicate that type I (distal) renal tubular acidosis is caused by failure of the cells of the distal nephron to secrete hydrogen ions rather than to gradient-limited hydrogen ion addition to the urine. This is suggested by the fact that urinary Pco2 levels should be higher than blood Pco2 levels when hydrogen ions are secreted into urine containing bicarbonate in the distal nephron and they were not in this study despite the presence of a favorable hydrogen ion gradient (tubular fluid pH exceeded blood pH).
机译:本研究旨在研究I型(远端)肾小管酸中毒的发病机理。当尿液的pH值等于或超过相应的血液pH值时,测定尿液和血液中Pco2的张力。这提供了远端肾单位中净氢离子分泌的指示。在16名正常受试者中,尿液的Pco2超过血值(U-B Pco2)32.7±3.1 mm Hg。相反,在10例I型(远端)肾小管性酸中毒患者中,尿中Pco2的张力并没有显着大于血液值(U-B Pco2 = 2.0±2.2 mm Hg)。这些结果表明,I型(远端)肾小管性酸中毒是由远端肾单位的细胞无法分泌氢离子而不是向尿液中梯度限制的氢离子分泌所致。这是由以下事实提示的:当远端肾单位中含有碳酸氢根的尿中分泌氢离子时,尿中Pco2水平应高于血液Pco2水平,尽管存在有利的氢离子梯度(肾小管液pH超过血液pH值)。

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