TY - JOUR
T1 - Sulfate and acid-base balance
AU - Ring, Troels
AU - Frische, Sebastian
AU - Rees, Stephen Edward
AU - Nybo, Jette
AU - Kristensen, Søren Risom
PY - 2023/5
Y1 - 2023/5
N2 - 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.
AB - 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.
KW - Acid-base equilibrium
KW - HEPES
KW - biological
KW - buffers
KW - chemistry
KW - computer simulations
KW - electrochemistry
KW - ions
KW - models
KW - physical
KW - sulfates
KW - water-electrolyte balance
UR - http://www.scopus.com/inward/record.url?scp=85152068640&partnerID=8YFLogxK
U2 - 10.1080/00365513.2023.2188607
DO - 10.1080/00365513.2023.2188607
M3 - Journal article
C2 - 36988149
SN - 0036-5513
VL - 83
SP - 166
EP - 172
JO - Scandinavian Journal of Clinical and Laboratory Investigation
JF - Scandinavian Journal of Clinical and Laboratory Investigation
IS - 3
ER -