Background: Chronic kidney disease describes loss of kidney function gradually; it may not become apparent in early stages until chronic kidney disease reaches an advanced stage that lead to accumulation of fluid, electrolytes and wastes and development of anemia Aim of study: The aim of this study was to investigate the possible role of fetuin A in improving anemia resulting from adenine induced chronic kidney disease in male rat. methods: Group A: rats feed normal diet for 21 days. Group B: rats feed normal diet with adenine for 21 days. Group C: rats feed normal diet with adenine for 21 days after that intraperitoneal administration of fetuin A every other day for 2 weeks. Serum samples were assayed for: creatinine, urea, iron , total iron binding capacity, ferritin, tumor necrosis factor, hepcidin. Hemoglobin content, blood indices were determined, and estimated Glomerular filtration rate was measured in addition, histopathology of the kidney was done Results: In group B: there was significant increase in serum creatinine, urea and ferritin decrease in serum iron, total iron binding capacity, hemoglobin content and estimated Glomerular filtration rate and no significant change in blood indices .Regarding inflammatory markers significant increase .Regarding renal histopathology there was moderate tubular necrosis, tubular dilatation, and mononuclear leucocytes infiltration. In group C we observed that fetuin A ameliorated these changes. . Conclusion: Fetuin A improve anemia in chronic renal failure in rat model, may be due to reduction of hepcidin or it is anti-inflammatory and anti fibrotic effect.

Background and objective: Diabetic nephropathy (DN) is a common and serious diabetic complication. Asprosin is a protein secreted by white adipose tissue and induces hepatic glucose release. The purpose of this study was designed to evaluate the potential protective effect of asprosin blockage against progression of nephropathy in type II diabetic rats.Methods: Type II diabetes mellitus was induced by feeding rats on high fat-diet for four weeks followed by injecting them with low dose of streptozotocin (STZ). We randomly divided thirty rats into three different groups: group I (control), group II (non-treated experimentally induced type II diabetic group) and group III (treated type II diabetic group with anti-asprosin antibody). Rats in group III were divided into three equal subgroups. Group (IIIA), (IIIB) and (IIIC): in which rats were given daily intraperitoneal injections of anti-asprosin antibody at doses of 10, 20 and 30 μg / kg body weight respectively for 8 weeks. After the experiments were finished, serum and kidney tissue samples were gathered. In all groups, body weights (BW), thoracic and abdominal circumferences (TC and AC) were measured. Body mass index (BMI) and AC/TC ratio were calculated. After eight weeks duration, rats were euthanized. Serum levels of insulin, glucose, lipid profile, creatinine, urea, C-reactive protien (CRP) and plasminogen activator inhibitor-1 (PAI-1) were measured; homeostasis model assessment of insulin resistance (HOMA-IR) and creatinine clearance (ml/min) were calculated. Protein in urine was estimated. Moreover, the animal was connected to the Power Lab after carotid artery cannulation to record mean arterial blood pressure (MAP). In addition, the changes in the histopathological aspects of the kidney were examined.Results: Eight weeks after induction of DM, the mean values of final BMI, final AC/TC ratio, serum levels of glucose, HOMA-IR, triglycerides (TG), total cholesterol (TC), LDL-c, urea, creatinine, CRP, PAI-1, proteinuria and MAP were significantly high (P < 0.001). However, the mean values of serum insulin, HDL-