Uric acid
Clinical significance:
Analytical methodology:
Men with uric acid level exceeding 9.0 mg/dl are approximately 150 times more likely to have coexisting gouty arthritis.
In humans approximately 75% of uric
acid excreted is lost in the urine and most of the remained is secreted into
GIT where it is degraded to allantoin by bacterial enzymes. Renal handling of
uric acid is complex and involves four sequential steps: (1) glomerular
filtration of virtually all the uric acid (2) reabsorption in PCT of about 98%
of filtered UA, (3) subsequent secretion of UA into lumen in the distal portion
of PCT about 50% (4) further reabsorption in distal tubule about 35-40%. The
net urinary excretion of UA is 6-12% of the amount filtered. At pH <5.56
uric acid exist as urate ion, soluble than uric acid and at urine pH <5.75
uric acid is predominant form and is insoluble.
Clinical significance:
Hyperuricaemia: It is defined as
plasma uric acid more than 7 mg/dl in men or >6 mg/dl in women. The major
causes of hyperuricemia are due to increased formation like in excess dietary
intake, tissue hypoxia, alcoholism, inherited metabolic disease, psoriasis,
leukemia, myeloma, etc. and due to decreased excretion like in kidney disease,
reduced secretion and increased absorption, lead poisoning, organic acids,
salicylate, etc.
Measurement of plasma uric acid is
predominantly used in the investigation of gout and it is also used in
diagnosis and monitoring of pregnancy induced hypertension (preeclamptic
toxemia). Primary gout occurs due to overproduction of uric acid and secondary
gout occurs due to retention of uric acid. Patients excreting >600 mg uric
acid/day are treated with allopurinol and secreting <600 mg/day are treated
with uricosuric drugs.
Kidney disease associated with
hyperuricemia may be gouty nephropathy with urate deposition in renal
parenchyma or acute intratubular deposition or urate crystals and urate
nephrolithiasis. Urate stone are formed during acidotic conditions where
urinary pH is <6.
Preeclamptic toxemia is condition
associated with increasing plasma uric acid concentration caused by
uteroplacental tissue breakdown and decreased kidney perfusion.
Hypouricemia: Plasma urate concentrations
<2 mg/dl. It may be seen during inadequate synthesis due to hepatic disease
or mutation in Xanthine oxidase. There may be defective renal tubular
reabsorption. Over treatment of hyperuricemia with allopurinol or uricosuric
drugs.
Analytical methodology:
Chemical method: Phosphotungstic acid oxidizes uric acid to allantoin. The reduction
product of phosphotungstate in an alkaline medium is blue and can be
quantitated by measuring absorbance at approximately 700 nm.
Uricase method: Enzymatic end point.
The color formed is measured at 600
nm. Use of HESPT acts as electron acceptor and enhance molar absorptivity. Use
of ferrocyanide is done to nullify bilirubin interference.
Dry chemistry system: It uses uricase as dry reagent. A multilayer film system
employs uricase and peroxidase separated by semipermeable membrane from a leuco
dye that is oxidized to form colored product. The quantitation of color is done
by reflectance meter system. Another system incorporates separation of plasma
from red cells and uricase peroxidase and substituted phenol to measure uric
acid.
Reference interval:
Men = 3.5-7.2 mg/dl
Women = 2.6-6.0 mg/dl
Men with uric acid level exceeding 9.0 mg/dl are approximately 150 times more likely to have coexisting gouty arthritis.
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