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Thursday, April 19, 2012
Special project of the biochemical tests in kidney disease
Biochemical examination of the kidney disease diagnosis, differential diagnosis of some kidney disease, guide therapy and prognosis is important. The following is commonly used in several checks:
(1) selective monitoring of urine protein electrophoresis and urine protein.
White electrophoresis score an integral part of the urinary protein analysis to determine the source of urinary protein, which helps the cause of the diagnosis and prognosis. If there is a mixed proteinuria, indicating impaired renal function involving the glomerular and tubular.
The risk of glomerular disease, the filtration membrane permeability and filtration role change. Mild glomerular disease, the filtration membrane "loophole" in a smaller in molecular weight protein in urine-based, high molecular weight protein excretion rarely called selective proteinuria. Obvious glomerular lesions filtration membrane "loophole" in the urine is not only a large number of albumin, and there are a lot of high molecular weight protein (such as globulin), which is called non-selective proteinuria. Selective proteinuria determination results suggest that the pathological type, predict treatment response and prognosis. Children with nephrotic syndrome, proteinuria was highly selective, of which about 97% of patients with minimal change nephropathy; adults also the majority of small lesions or minor lesions, but can also be found in membranous glomerulonephritis, focal renal small glomerulonephritis, proliferative glomerulonephritis.Van Gogh selectivity can predict a good response to steroid and immunosuppressive therapy; high selectivity and a better prognosis, otherwise poor prognosis.
(2) blood, urine complement determination.
Increased serum total complement (CH50) found in a variety of inflammatory, acute phase reactants. Some malignant tumors increased complement activity. Reduce serum CH50 is common in acute and chronic glomerulonephritis, hemolytic anemia and systemic lupus erythematosus. Blood of acute glomerulonephritis C3 decline, especially in post-streptococcal acute glomerulonephritis decreased more significantly. Mesangial proliferative glomerulonephritis, lupus nephritis and renal transplant rejection, C3 can reduce blood. Determination of urinary C3 content may indirectly reflect the permeability of the glomerular basement membrane, mesangial proliferative glomerulonephritis, lupus nephritis urinary C3 almost all positive; positive rate of membranous nephropathy and focal segmental glomerulosclerosis high, minimal change is often negative. Urine C3-positive patients compared with negative patients with severe illness and poor prognosis, the higher the content of the disease the more severe.
(3) fibrin degradation products determination.
Urinary fibrin degradation product of positive means of coagulation and fibrinolysis in the kidney, suggesting that the inflammatory lesions. Non-inflammatory diseases are mostly negative. Primary glomerular nephropathy is usually negative, chronic nephritis and more positive. Urinary fibrin degradation products was increased to reflect the degree of renal impairment. In the course of treatment of chronic nephritis, the clinical symptoms, recovery of renal function, urinary fibrin degradation product decreased gradually or negative; positive that kidney disease inflammatory process is still ongoing disease activity, continuous positive prognosis after treatment poor.
(4) of glomerular urine protein examination.
If the glomerular filtration barrier injury, will appear in the urine albumin, transferrin, immunoglobulin G; in molecular weight protein of the immunoglobulin M and α2-macroglobulin. Urinary albumin to detect the early diagnosis contribute to the glomerular lesions. When the glomerular mild lesions, increased urinary albumin; when further damaged, urinary IgA and IgG increased urine IgM increased; of glomerular serious disease. Urinary albumin and IgG glomerular lesions prompted the transition to chronic urine IgM important in predicting renal failure.
(5) renal tubular urine protein examination.
Proximal tubule epithelial cell damage, obstacles to the normal filtration of protein reabsorption, urine low molecular weight proteins, mainly α1-microglobulin, β2-microglobulin, lysozyme, acid and vitamin A binding protein. This group proteinuria displacement increase is a sign of renal proximal tubule damage.
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