Detection Of Serum Prealbumin Levels In Patients With Primary Nephrotic Syndrome And Their Clinical Significance

In 1932 ,Christian summarized nephrotic syndrome (NS) as a varietyes of kidney disease due to damage caused by the severe proteinuria, and a group of corresponding clinical manifestations. Protein metabolism disorder is the obvious highlight performance of the disease. the pathogenesis of concrete is not clear yet, with the development of modern medicine, PNS etiology and pathogenesis was researched more in-depth. the current impact of this disease etiology and prognostic factors is complex. NS glomerular diseases common is the performance of all glomerular lesions ,and various diseases may occur NS. Clinical practice will be divided into primary NS (PNS) and secondary NS. PNS is that the original lesion in glomerular diseases. Secondary NS is secondary to systemic disease, The causes is extensive and complex, its clinical manifestations and pathological types probably has no causal relationship, Due to a higher incidence of kidney, its actively researched in recent years, And found a number of valuable research results.currently,it's recognized PNS as an immune complex-mediated glomerulonephritis. The following factors may be relevant:1, T-cell dysfunction: For a long time people have speculated it. Early in the 20th century, the 1970s-Shai-houb proposed T-cell dysfunction and simple nephrotic syndrome. After a large number of animal experiments and clinical research ,We found that T-cell not only in the number of abnormal distribution, but also the interaction between the regulation of cell disorder. Daniel has studied 29 cases of hormone-sensitive Simple nephropathy (Steroid-sensitive and simple nephrotic syndrome, SSSNS), results showed that SSSNS T cell function in children defects, and found that T n / T i ( CD4 +) and T s / T c (CD8 +) ratio declined, sIL-2R levels increased, CD4 + decreased, CD8 + increased. Cao Li, by MTT colorimetric method of idiopathic nephrotic syndrome patients active and ease of peripheral blood lymphocytes (PBL) response to the proliferation of testing and found that the proliferation activities of PBL response capacity than the control group, the remission group decreased, and with T-lymphocyte subsets of CD4 + / CD8 + ratio was positively related to the activation of IL-2R expression and IL-2 production capacity decline, and plasma and cell culture supernatant of sIL-2R increased. Richard has studied 32 cases of patients with PBL and its subsets percentage statistical analysis show the patients with recurrent acute phase of the number of T-lymphocytes decreased significantly compared with the normal control, increased CD8 + and CD4 + decline. The new research results show that patients with PNS cell immune dysfunction, abnormal cellular immune mechanisms in the PNS, plays an important role in the inhibition of T-cells increased ,And lead to the creation of a glomerular basement membrane (GBM) toxic effects Lymphokines , overcast charge weakened barriers so that the basement membrane permeability caused proteinuria; helper T lymphocyte function and reduce the decrease in the number of B cells to produce antibodies.2, Abnormal expression of cytokines in experimental animals and humans that PNS patients with nephropathy,The studying of blood circulation in cytokines show these cells with vascular permeability factor activity, and PNS have abnormal expression may be involved in the occurrence of proteinuria. It is certainty that the significance of cytokine interleukin-major (ILs), tumor necrosis factor (TNF). TNF: by mononuclear cells, T lymphocytes, glomerular mesangial cells (GMSC) generation, the study also found that patients with active PNS compared to the control group, the serum levels of TNF-αsignificantly increased, TNF-αmRNA expression. Savin's studying in vitro found that TNF-αcan inhibit the synthesis of glomerular epithelial cell protein heparin sulfate polysaccharide, cyclosporin A may prevent this effect. Tip of TNF-αin the PNS proteinuria have a role to play. Recent studies show that PNS patients with IL-2, IL-6, IL-8 expression was significantly higher: IL-8 may affect the metabolism of sulfur compounds GMB. Garin's studies show that IL-8 may influencing the metabolism sulfide on the GMB to change its negative charge barriers, increased the permeability of the GMB, resulting in proteinuria. Wada's animal experiments show that anti-IL-8 antibody role in the prevention of proteinuria. Suggesting that IL-8 is closely related to the incidence of PNS.Currently , the clinical observate the patients with PNS is still based on the plasma albumin, serum lipids, and 24-hour urine protein. According to reports: NF-κBmRNA in renal expression of cytokines TNF-αand IL-6, IL-8 expression, as well as TGF-βand VGF expression levels may also be chenged nephrotic syndrome disease to a certain extent tips.Animal experiments and clinical observation has showed that renal damage is promoting glomerulosclerosis ,renal tubular damage , renal interstitial fibrosis ,inflammatory cell infiltration, renal units gradually reduce , eventually developed to CRF. Mechanism is a complex, proteinuria induced glomerulosclerosis think that the mechanism is by changing the glomerular hemodynamics, glomerular capillary wall injury (GCW) glomerular mesangial cells (GMs). Of tubular proteinuria, interstitial damage mechanisms can be broadly adopted two ways:①secondary to glomerular damage or consistent with the role of both pathogenic role in the glomerular and tubular;②a large number of protein tubular Components of the renal tubular damage and mesenchymal role. At the same time, a large number of proteinuria, resulting in decreased plasma albumin, further aggravating condition.NS with hyperlipidemia (HLP) mechanism is not clear and is generally considered to be more liver lipoprotein synthesis and lipid remove obstacles .Hyperlipidemia of chronic progressive renal kidney damage in the main: to stimulate mesangial cell proliferation, increased extracellular matrix synthesis, and promote renal interstitial fibrosis, affecting glomerular hemodynamics.Hypoproteinemia major consideration for the current reduction of the liver, and kidneys filter out more, a decrease in the re-absorption. Hypoproteinemia body can have complex effects. Mainly include the following:①hypoalbuminemia the plasma of patients with nephrotic syndrome protein components of other effects, such as those lipoprotein a [lipoprotein (a), lysophosphatidic choline (lyso-phosphatidylcholine, LPC),α2 Giant globulin (α2-macroglobulin,α2 M),α1 giant myosin inhibitor 3 (α1 - Inhibitor3,α1-I3), the impact of body metabolism;②hypoalbuminemia patients with nephrotic syndrome can also affect LDL catabolism, and indirectly to hyperlipidemia.③hypoalbuminemia of patients with nephrotic syndrome coagulation and fibrinolytic function in promoting patients hypercoagulable state plays an important role.④hypoalbuminemia on renal function in patients with nephrotic syndrome,⑤hypoalbuminemia participate in patients with nephrotic syndrome edema and ascites formation, thus speeding up the progress of kidney diseaseSince serum PA is moving faster than albumin of 8.6 in the p H electrophoresis ,it is named, the molecular weight is about 55,000, sedimentation coefficient is 3.9. Serum albumin is the thyroxine and Retinol-binding protein, of vitamin A and thyroxine transporter, the protein has a very short half-life of only 12 hours, when liver function is impaired, or chronic lack of nutrition ,it should be decreased, reported that: PNS patients, due to extensive ALB leakage, resulting in the colloid osmotic pressure drop, which led to the synthesis PA liver, liver at the same time also increase lipid synthesis, and both of them have a certain relevance. This article is a retrospective clinical analysis of the hospital on January 1, 2007 to December 1, 2007, 60 patients that was diagnosed with idiopathic nephrotic syndrome by albumin, lipids, and 24-hour urine protein test results, the application of statistical software for data SPSS14.0 statistical analysis,the results showed that:1.PNS Group, PA increased significantly, compared with CGN group, there were significant differences (P <0.05).2. Serum PA and serum albumin were negatively correlated (r =- 0.887, P <0.01).3. Serum PA and serum lipids (TC, TG, LDL-c, apoB) were positively correlated (r values were 0.498,0.542,0.796,0.484, P <0.05).4. Serum PA and 24-hour urine protein had no significant correlation.5. After treatment, the illness was alleviated, serum TG, CHOL, LDL-C, apoB, PALB, UP decreased significantly , there were significant differences (P <0.05); ALB significantly higher than before treatment, there was significant difference (P <0.05).Statistical results indicate that: morbidity in patients with nephrotic syndrome can occur early on the increase in blood PA, and its increased value ALB, lipids (TC, TG, LDL-c, apoB) both have a certain relevance, After treatment, PA gradually returning to normal, PA'level could evaluate the PNS's activity and developmen.