Human kidney has a strong reserve capacity in the early stage of the disease is often little or no signs, the diagnosis depends largely on laboratory examination. The blood samples of renal function tests alone, can often see such several items: Cr, BUN, UA and so on.
Serum creatinine (Cr): Cr value: 44 male adult serum micro - 132 mmol per liter, 70 female micro - 106 mmol per liter. Because kidney has strong ability of storing blood, when Cr increased, suggesting that.Ccr has severe glomerular damage (CCR) (120 ml /:80 points - 1.73 square meters), after 40 years of age with age increasing, Ccr decreased year by year, about 60% young adults at the age of 70, the blood Cr level increased. When Ccr less than 40 ml, when protein intake should be limited; less than - ml, artificial kidney dialysis indications.
Serum urea (SU) and urea nitrogen (BUN) in amino acid catabolism: urea is the end product of adult SU1.78 7.14 mmol per liter, BUN 3.56 - 14.28 mmol per liter. Same with serum creatinine, only when the glomerular filtration rate is below the normal 50%, SU will significantly increase of.SU said: 1. glomerular filtration function damage; 2. protein catabolism strong or excessive protein intake.
The blood uric acid and uric acid (UA) metabolites: purine nuclear protein and nucleic acid in the adult. The concentration of UA: male 150 - 416 micromoles per liter, 89 women - 357 micromoles per liter. If to exclude the effect of exogenous UA (containing purine rich foods such as fasting 3 days), and measured the urine the concentration of UA has more diagnostic value of.1. if the increase of serum UA and the urinary UA decreased, suggesting that injury of glomerular filtration function; 2. blood, urine UA increased, suggesting that UA generates abnormal increase. Often hereditary enzyme defect caused by primary gout, blood disease, tissue hypoxia, tumor, anticancer drugs, long-term use of diuretics and some anti tuberculosis drugs, chronic lead poisoning and other secondary gout long fasting blood UA and urine.3. reduced the increase of UA, suggesting that renal tubular reabsorption of UA damage, UA urine loss, can be found in the interstitial nephritis, Vankoni syndrome, chronic cadmium poisoning, the use of sulfa.4. blood, urine UA decrease in U The decrease of A production. Such as acute hepatic necrosis, serious hepatolenticular degeneration, liver damage, or participate in the formation of UA enzyme defect, use of anticancer drugs inhibit purine synthesis, large dose of glucocorticoids.