Q: WHAT IS THE CLINICAL IMPORTANCE OF URIC ACID AND CREATININE? ANSWER:
Uric acid is a weak organic acid, the end product of purine nucleotides degradation. The findings of human pathological levels of uric acid in serum and urine have in most patients serious clinical implications. Uric acid is a useful diagnostic tool as screening for most of purine metabolic disorders. The importance of uric acid measurement in plasma and urine with respect of metabolic disorders is highlighted. Not only gout and renal stones are indications to send blood to the laboratory for uric acid examination. Also familial nephritis, neurological abnormalities with mental retardation are reasons to know uric acid levels in blood and urine. Clinical significance
1) Physiologic changes in serum concentration of uric acid
About 350 mg of uric acid are daily produced by endogenous synthesis, while about 300 mg/day are taken by food. In plasma at pH 7.4, uric acid is found in the ionized form of monosodium and monopotassium urate, and only a minor portion as a free acid. A) About 90% of uric acid filtered in glomeruli is normally reabsorbed in renal tubules. Uric acid is normally excreted from the body via kidneys (80%) and intestine (20%). About 4.76 mmol (800 mg) are excreted per day. B) Extreme physical exercise induces a significant increase in the concentration of uric acid. C) Starvation and fat rich diet increase the concentration of uric acid in serum.
2) Pathologic changes in serum concentration of uric acid
A) Increased values of uric acid in:
• athetoid cerebral palsy with mental deficiency and self-mutilation, • coronary artery disease,
• diabetic keto-acidosis following intravenous fructose,
• Down’s syndrome (some cases), • excessive ethyl alcohol intake, • gout,
• gross tissue destruction, • heavy chain disease, • hemolytic anemias, • hyperlipoproteinemia type iii, • lead poisoning, • myeloid leukemia,
• pernicious anemia (especially after treatment),
• Pneumonia, • primary and secondary polycythemia, • primary hyperoxaluria, • pyrazinamide therapy, • Tangier disease, • uremia,
• von Gierke’s glycogen storage disease.
B) Decreased values of uric acid in:
• acromegaly (some cases),
• administration of uricosuric drugs,
• Fanconi syndrome,
• hepatolenticular degeneration,
1) Physiologic changes in urine concentration of uric acid
Uric acid is mostly excreted in urine (about 75%). The uric acid from glomerular filtrate is almost completely reabsorbed in proximal tubules. The urates in final urine derive from active secretion of uric acid in distal tubules. Urinary urate excretion after intake of food rich in purines or upon abundant intake of xylitol, and id decreased with low-protein and high-carbohydrate, high-fat diet.
2) Pathologic changes in urine concentration of uric acid
A) Increased urine uric acid concentration in:
• acute lymphocytic leukemia, • acute myelocytic leukemia, • adult respiratory distress syndrome, • bacterial meningitis, • cerebral embolism, • cerebral hemorrhage, • cerebral infarction, • cerebral thrombosis, • chronic myelocytic leukemia, • cystinosis,
• encephalomyelitis, • familial periodic paralxsis, • gout, • hepatolenticular degeneration, • Leach-Nyhan syndrome, • manic depressive disorder, • myelofibrosis, • osteomalacia, • paranoid states and other psychoses, • polycythemia rubra vera, • proximal renal tubular acidosis • regional enteritis or ileitis, • sickle cell disease, • tuberculous meningitis, • ulcerative colitis, • viral hepatitis.
B) Decreased urine uric acid concentration in:
• folic acid deficiency,
• toxic effects of...
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