Sulfate anion: its origins and its clearance

The sulfate anion originates from methionine metabolism, and is responsible for some of the high anion gap metabolic acidosis associated with uraemia.

Origin of the sulfate anion

The tetrahedral sulfate anion is SO42- , and it seems to be retained in amounts which are proportionate to the loss of renal function (at least in children). This makes sense, as this highly charged anion is distributed mainly in the extracellular fluid (as intracellular sulfate is typically complexed with proteins, as phosphate is.) The sulfate in one’s precious bodily fluids comes mainly from the metabolism of methionine, which can be converted into cysteine, homocysteine and taurine. These are the four sulfur-containing amino acids.

sulfur-containing amino acids origin of the sulfate anion

The roles played by these amino acids are far from trivial; pretty much all of your protein synthesis begins with a methionine, and without cysteine there would be no disulfide bonds between peptides, and therefore no protein folding. S-adenosylmethionine (SAM) is an intermediate product of methionine metabolism that is said to be second only to ATP in its versatile utility in biosynthetic processes. Thus the rate of sulfate production in the human body must be considerable. The vast majority of it originates from the catabolism of these amino acids, and in fact it is possible to estimate total body protein catabolism by measuring sulfate excretion. The subjects in the quoted study produced about 10-25mmol of sulfate per day while they weren't diet-restricted.

Sulfate clearance

Your sulfate levels are kept fairly constant; however, after consuming a sulfur-heavy meal, one can expect the serum sulfate to almost double, and then to gradually return to normal within about 12 hours. There is no renal secretion of sulfate as far as we know; rather, there is a constant resorption by a sulfate-sodium cotransporter in the proximal tubule.

sulfate resoprtion

Thus, sulfate delivered to the glomerulus is filtered freely, and under conditions of normal homeostasis it is completely reabsorbed. Increased levels of sulfate, beyond a certain threshold (who knows what that is) are not reabsorbed, and drift out with the urine, hopefully reducing sulfate concentrations to a normal level. As glomerular filtration decreases, the filtered sulfate above that threshold is cleared at a rate roughly proportional to the glomerular filtration rate - but, at a late stage in renal failure, this rate is very low, and therefore sulfate is retained.


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