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Association Between Serum Fetuin-A And Proinflammatory Cytokines In Patients With Chronic Renal Failure.

Posted on:2012-03-24Degree:MasterType:Thesis
Country:ChinaCandidate:Z P DiFull Text:PDF
GTID:2154330335499059Subject:Surgery
Abstract/Summary:PDF Full Text Request
Background and Objective:The incidence of chronic renal failure increases every year.It is the result caused by renal chronic lesion originated by kinds of reasons and progressing aggravation.Microinflammatory state in patients with CRF is characterized with high level of serum inflammatory cytokines and acute reactive protein.The patients do not have significant clinical symptoms of infection. Clinical studies have shown that:Microinflammatory state may promote complications of CRF,like malnutrition anemia and so on. It can deteriorate renal function.There was an obvious correction with the mortality and prognosis of patients.fetuin-A is known to be an inhibitor of calcification.Fetuin-A is a serum protein which is produced by liver.It also can inhibit vascular smooth muscle cell calcification,which form the circulating protein -minenal componds to inhibit phosphate or calcium deposition formed vascular calcification,but not impact on the normal physiological processes.But studies correlating levels of this glycoprotein to markers of inflammation are limited.To understand these relationships, we investigated the relationship between serum fetuin-A and proinflammatory cytokine levels in patients with chronic renal failure.Methods:33 cases of hemodialysis CRF patients were chosen as hemodialysis group.33 cases of pre-dialysis CRF patients were chosen as pre-dialysis group,participation was allowed if the creatinine clearance was below 60mL/min.18 subject with normal renal function were enrolled in this study.Gender and age matched between the experimental group and control group.Exclusion criteria included presence of diabetes mellitus, autoimmune disease or any other known condition that would alter cytokine levels, participation was allowed if the creatinine clearance was below 60mL/min.After fasting overnight, venous blood samples were drawn from all patients and controls, from the 08.00AM and 10.00AM in the morning (for HD patients, beginning of the HD session). The samples were trifuged and stored at-70℃.Serum fetuin-A, IL-1β,IL-6,TNF-a was analyzed by enzyme linked immunosorbent assay. The levels of blood urea nitrogen (BUN),creatinine,serum albumin, total cholesterol,and LDL cholesterol, triglycerides and serum calcium and phosphorus were measured meanwhile in the hemodialysis group and pre-dialysis group. Result was summarized as mean±standard deviation (x±s).All statistic analyses were performed using commercially available software for SPSS 17.0.Results:Serum fetuin-A concentrations and proinflammatory cytokine concentrations were significantly different between HD, pre-dialysis patients and control subjects (fetuin-A:P<0.001, IL-1β:P<0.001, IL-6:P<0.001).Serum fetuin-A levels were significantly lower in HD patients than in pre-dialysis patients and controls. IL-1β,IL-6,and TNF-a levels were significantly higher in HD patients than in the other groups.In the HD group and pre-dialysis group, serum fetuin-A was significantly and inversely related to IL-1β,IL-6 and TNF-a (IL-1β:P<0.01, IL-6: P<0.01, TNF-a:P<0.01). In controls, serum fetuin-A did not correlate with IL-1β,IL-6 and TNF-a (P>0.05). In the HD group and pre-dialysis group, serum fetuin-A levels correlated inversely to BUN, serum creatinine, phosphorusand calcium-phosphorus product(P<0.01). Whereas fetuin-A levels were significantly correlated (directly) with serum albumin concentrations (P<0.01).Conclusion:The serum level of fetuin-A decreases in HD and pre-dialysis patients,and is even lower in HD patients. Serum fetuin-A was significantly and inversely related to IL-1 p,IL-6 and TNF-a in pre-dialysis patients and in HD patients. It supports the hypothesis of inflammation-dependent down regulation of fetuin-A expression.It is suggesting that micro-inflammation causes reduced fetuin-A may be the cause of cardiovascular disease.
Keywords/Search Tags:Chronic renal failure, microinflammatory status, fetuin-A, IL-1β, IL-6, TNF-α
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