Sulfate and acid-base balance

It has been acknowledged for years that compounds containing sulfur (S) are an important source of endogenous acid production. In the metabolism, S is oxidized to sulfate, and therefore the mEq sulfate excreted in the urine is counted as acid retained in the body. In this study we show that pH in fluids with constant [Na] and [HEPES] declines as sulfate ions are added, and we show that titratable acidity increases exactly with the equivalents of sulfate. Therefore, sulfate excretion in urine is also acid excretion per se. This is in accordance with the down-regulation of proximal sulfate reabsorption under acidosis and the observation that children with distal renal tubular acidosis may be sulfate depleted. These results are well explained using charge-balance modeling, which is based only on the three fundamental principles of electroneutrality, conservation of mass, and rules of dissociation as devised from physical chemistry. In contrast, the findings are in contrast to expectations from conventional narratives. These are unable to understand the decreasing pH as sulfate is added since no conventional acid is present. The results may undermine the traditional notion of endogenous acid production since in the case of sulfur balance, S oxidation and its excretion as sulfate exactly balance each other. Possible clinical correlates with these findings are discussed.

多年来，人们公认含硫（S）化合物是内源性酸生产的 重要来源。在代谢过程中，硫被氧化成硫酸盐，因此尿液中排出的当量硫酸盐被视为体内保留的酸。在本研究中，我们揭示了在[Na]和[HEPES]浓度恒定的液体中，随着硫酸根离子的加入，pH值逐渐下降，并且我们发现可滴定酸度与硫酸盐的当量成正比。因此，尿液中硫酸盐的排泄本身也是酸的排泄。这与酸中毒时近端硫酸盐重吸收的下调以及远端肾小管酸中毒儿童可能存在硫酸盐耗竭的观察结果相一致。这些结果可用电荷平衡模型得到充分解释，该模型仅基于电中性、质量守恒和来自物理化学的解离规则等三个基本原理。相比之下，这些发现与传统叙述的预期相悖。传统叙述无法理解硫酸盐加入时pH值的下降，因为其中不存在常规酸。在硫平衡的情况下，硫的氧化及其以硫酸盐形式排泄的平衡恰好相互抵消，这可能会动摇传统的内源性酸生产观念。此外，对这些发现可能具有的临床相关性进行了讨论。