Kidney function test: these are the most common

For humans, the kidney has a very strong storage capacity, which is one of its strongest functions. However, due to various factors in life, people's kidneys may have problems. If you want to confirm what disease your kidneys have, you need to go to the hospital for a kidney function test. So, what are the kidney function indicators?

Serum creatinine (Cr):

Adult serum Cr value: 44-132 micromoles per liter for men, 70-106 micromoles per liter for women. Because the kidney has a strong storage capacity, when blood Cr continues to increase, it indicates severe glomerular damage. Ccr (endogenous creatinine clearance): 80-120 ml/(min·1.73 m2), after the age of 40, it increases with age, and Ccr decreases year by year. At the age of 70, it is about 60% of that in young people, and there is no corresponding increase in blood Cr level. When Ccr is lower than 40 ml·min, protein intake should be limited; lower than ml·min is an indication for artificial kidney dialysis.

Serum urea (SU) and urea nitrogen (BUN):

Urea is the end product of amino acid metabolism in the body. SU for adults is 1.78-7.14 mmol/L, and BUN is 3.56-14.28 mmol/L. Similar to serum creatinine, SU will only increase significantly when the glomerular filtration rate drops below 50% of normal. Increased SU indicates: 1. Damage to the glomerular filtration function; 2. Vigorous protein metabolism or excessive protein intake.

Serum uric acid and urine uric acid (UA):

It is a metabolite of purine in nucleoprotein and nucleic acid. Adult UA concentration: 150-416 micromoles per liter for males and 89-357 micromoles per liter for females. If the influence of exogenous UA is excluded (such as fasting from purine-rich foods for 3 days), and urine UA concentration is measured at the same time, it will be more diagnostically valuable. 1. If blood UA is elevated and urine UA is reduced, it indicates damage to the glomerular filtration function; 2. Both blood and urine UA are elevated, indicating abnormal increase in UA production. It is often secondary gout caused by primary gout due to genetic enzyme deficiency, blood disease, tissue hypoxia, tumors, anticancer drugs, long-term use of diuretics and certain anti-tuberculosis drugs, chronic lead poisoning, and long-term fasting. 3. Decreased blood UA and increased urine UA indicate damage to renal tubular reabsorption of UA, and large amounts of UA are lost in the urine, which can be seen in interstitial nephritis, Fanconi syndrome, chronic cadmium poisoning, and the use of sulfonamides. 4. Decreased blood and urine UA are seen in decreased UA production, such as acute liver necrosis, hepatolenticular degeneration, and other severe liver damage, or enzyme defects involved in UA production, the use of anticancer drugs that inhibit purine synthesis, and large doses of glucocorticoids.