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Objective: The incidence of chronic renal failure (chronic renal failure, CRF) increased year by year, a variety of primary and secondary causes can lead to kidney damage and deterioration. Recent studies found that patients with CRF widespread micro-inflammatory state plays an important role in leading to further deterioration of renal function. The CRF patients microinflammation showed only a factor of inflammation in the body, mild acute phase protein continues to rise, and no obvious clinical symptoms of infection. Clinical studies have shown that patients with this ongoing micro-inflammatory state can promote malnutrition, arterial atherosclerosis and anemia complications and significantly associated with mortality and prognosis. Fetuin A (fetuin-A) is a well known calcification inhibitor of vascular smooth muscle calcification fetuin-A is produced by the liver can be suppressed, to prevent the occurrence of cardiovascular calcification and suppressed serum supersaturated calcium phosphate deposition, without affecting the normal bone mineralization, and fetuin-A is a negative acute phase response proteins, but on chronic kidney disease correlation between fetuin-A with proinflammatory cytokines was small, we examined patients with chronic renal failure fetuin- the relationship between A and inflammatory factors to investigate to find the correlation. Materials and Methods: 33 patients with chronic renal failure in maintenance hemodialysis patients in hemodialysis (HD group), 33 patients with chronic kidney disease (Chronic kidney disease, CKD) non-dialysis patients for dialysis group, requirements glomerular filtration over rate of less than 60mL/min. Also, select your gender, age-matched 18 patients with normal renal function in healthy subjects as normal control group. Exclusion criteria: under the age of 18, more than 70 years of age, clinical obvious infection, liver dysfunction, malnutrition, cancer, diabetes, rheumatological disease patients. All subjects fasting venous blood was collected and placed in the blood samples were centrifuged at -70 ℃ cryopreservation be measured. All serum samples were measured by ELISA assay fetuin-A, IL-1, IL-6 and TNF-alpha level, HID group and non-dialysis group simultaneous determination of urea nitrogen (BUN), creatinine (Cr), serum albumin (Alb) total cholesterol (TC), low-density lipoprotein (LDL), triglycerides (TG), calcium (Ca) and phosphorus (P). Data are presented as mean ± standard deviation (chi ± s), all of the data by SPSS17.0 statistical software for statistical processing. RESULTS: Plasma fetuin-A and proinflammatory cytokines concentration in the H1D group, non-dialysis group and the control group was significantly different (fetuin-A: P lt; 0.001; IL-1 beta: P lt; 0.001; IL-6: P LT ; 0.001; TNF-alpha: P lt; 0.001), HD patients fetuin-A was significantly lower than the other two groups, the IL-113, IL-6 and TNF-alpha in HD patients was significantly higher than the other two groups, the HD group serum fetuin-A and non-dialysis group, respectively, with IL-1beta, IL-6 and TNF-alpha negative correlation (IL-1β: P lt; 0.01, IL-6: P lt; 0.01, TNF-α: P lt; 0.01). Fetuin-A with three proinflammatory cytokines in the normal control group, no correlation (P gt; 0.05) HD group and non-dialysis group, fetuin-A negative correlation with BUN, Cr, P and Ca × P (P lt; 0.01), fetuin-A with Alb positive correlation (P lt; 0.01). Conclusion: Chronic renal failure is not dialysis patients and patients with HD group fetuin-A level lower than control group, the HD group decreased significantly; IL-1beta, IL-6 and TNF-alpha levels are elevated in patients with HD group most obvious, Not dialysis group was higher than in the HD group and non-dialysis group found fetuin-A negative correlation with the proinflammatory cytokines IL-1, IL-6, TNF-alpha levels to support the inflammatory response inhibition of fetuin-A expression, the prompt microinflammation lead to lower fetuin-A may also be its lead to one of the mechanisms of cardiovascular disease.
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