Although inorganic sulfate is an essential and ubiquitous anion in human bi
ology, it is infrequently assayed in clinical chemistry today. Serum sulfat
e is difficult to measure accurately without resorting to physicochemical m
ethods, such as ion chromatography, although many other techniques have bee
n described. It is strongly influenced by a variety of physiological factor
s, including age, diet, pregnancy, and drug ingestion. Urinary excretion is
the principal mechanism of disposal for the excess sulfate produced by sul
fur amino acid oxidation, and the kidney is the primary site of regulation.
In renal failure, sulfoesters accumulate and hypersulfatemia contributes d
irectly to the unmeasured anion gap characteristic of the condition. In con
trast, sulfate in urine is readily assayed by a number of means, particular
ly nephelometry after precipitation as a barium salt. Sulfate is most commo
nly assayed today as part of the clinical workup for nephrolithiasis, becau
se sulfate is a major contributor to the ionic strength of urine and alters
the equilibrium constants governing saturation and precipitation of calciu
m salts. Total sulfate deficiency has hitherto not been described, although
genetic defects in sulfate transporters have been associated recently with
congenital osteochondrodystrophies that may be lethal. New insights into s
ulfate transport and its hormonal regulation may lend to new clinical appli
cations of sulfate analysis in the future.