(i) Creatinine clearance
Creatinine (molecular weight 113d) can be freely filtered from the glomerulus without being reabsorbed by the renal tubules and is not excreted from the renal tubules when renal function is normal, so creatinine clearance (CCr) is commonly used clinically to express glomerular filtration rate (GFR). However, the following should be noted in the specific application: the change of CCr is most sensitive in the early stage of glomerular function injury, and SCr rises only when CCr decreases more than 1/2 of the normal value, but the change (decrease) of CCr value is less sensitive than the change (increase) of SCr value in severe renal failure. Therefore, when glomerular function is damaged, early observation of CCr should be focused, while later observation of SCr changes is more important; when glomerular function is restored, SCr alone cannot be tested, but must be followed until CCr is normal.
In addition, attention should be paid to the effect of renal impairment on the CCr assay value. When the glomerular function is normal, creatinine is not excreted from the tubules, so the CCr value can reflect the ARF, but when the glomerular function is severely impaired, some of the serum creatinine can be excreted from the tubules into the urine, resulting in a higher CCr value than the actual ARF, and its value cannot accurately reflect the degree of glomerular impairment. In this case, to accurately determine ARF, 99mTc-DTPA (99mTc-diethylenetriaminepentaacetic acid) nuclear test is required.
In 1976, Cockcroft et al. proposed a formula for calculating CCr from SCr, which has some application when urinary creatinine cannot be measured, but it is not applicable to the elderly, children and overly obese people. This formula for CCr calculation is as follows (ml/min).
(140 – age) × weight (kg) (male)
72×0.0113×SCr(μ
(140 – age) × weight (kg) (female)
85×0.0113×SCr(μ
(ii) Serum creatinine
SCr is about to rise when glomerular function is impaired to the decompensated stage of renal insufficiency (i.e., when the pre-narrative CCr decreases by more than 1/2 of the normal value).
The source of SCr includes endogenous creatinine (generated by the breakdown of creatine in muscles in the body) and exogenous creatinine (creatine from lean animal meat in food), with the former predominating and the latter taking up a small percentage. When renal function is normal, if too much meat is consumed, SCr can be temporarily increased, but it is soon excreted by the kidneys and does not affect early morning fasting SCr measurement. In renal failure, the kidney’s ability to excrete creatinine is reduced, so it is still appropriate for patients to avoid eating too much meat before the test.
Endogenous creatinine is influenced by muscle volume. In patients with muscle atrophy, creatine metabolism in the body is weakened and creatinine production is reduced, so the SCr value will be lower; in addition, protein synthesis in pregnant women is increased and the body is in positive nitrogen balance, so the SCr value will also be lower than normal people. The above factors should be taken into consideration when analyzing the clinical results of SCr measurement.
(iii) Blood urea nitrogen
Blood urea nitrogen (BUN), like SCr, will increase in renal insufficiency in the decompensated phase.
Urea nitrogen (molecular weight 28d) is the end product of protein metabolism of the body, and all of it is filtered from the glomerulus under normal conditions, so its value can reflect the glomerular function to a certain extent. However, the BUN value of the body can be influenced by many factors, which must be noted when analyzing the measurement results. Firstly, the BUN value can be affected by protein intake and protein catabolism rate, which is especially obvious in renal insufficiency; secondly, the filtered urea nitrogen can be partially (about 30%-40% under normal condition) reabsorbed by renal tubules, and a small amount of urea nitrogen can be excreted from renal tubules in renal failure.
(B) Measurement of serum β2-microglobulin or α1-microglobulin
1, blood β2 microglobulin measurement β2 microglobulin (β2-MG) is a protein with a molecular weight of 11800d, which can be freely filtered from the glomerulus, so the serum β2-MG concentration can reflect the glomerular filtration function. Contrast studies confirm that blood β2-MG concentration is already elevated when CCr begins to decline, so the test is no less sensitive than CCr in detecting glomerular function.
It must be noted that certain inflammatory (such as lupus erythematosus, rheumatoid arthritis, nodular disease and hepatitis, etc.) and tumor (such as myeloma, leukemia and Hodgkin’s disease, etc.) diseases of the body can also lead to an increase in serum β2-MG, at which time the serum β2-MG concentration does not reflect the glomerular function status and should be differentiated.
2, blood α1-microglobulin determination α1-microglobulin (α1-MG) is a protein with a molecular weight of 33,000d, which exists in serum in both free form and bound form (combined with IgA), and its free form can be freely filtered from the glomerulus, so serum α1-MG concentration will increase when glomerular function is impaired.
α1-MG is widely present on the surface of lymphocytes in the body, if there is a large number of lymphocyte destruction in the body (such as lymphatic leukemia, especially when chemotherapy), α1-MG will be released into the blood in large quantities, resulting in an increase in its blood concentration, and at this time, the serum α1-MG concentration certainly does not reflect the glomerular filtration function, and should also be noted.