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publication name CLINICOPATHOLOGICAL EVALUATION OF KIDNEY FUNCTIONS AFTER CADMIUM CHLORIDE ADMINISTRATION IN MALE RATS
Authors Abdel-baky, A.A., Mahmoud, A.A. and Fararh, K.M.
year 2013
keywords Cadmium chloride, Kidney, Liver, Lipid profile
journal BENHA VETERINARY MEDICAL JOURNAL
volume 24
issue 1
pages 1-11
publisher BVMJ
Local/International International
Paper Link Not Available
Full paper download
Supplementary materials Not Available
Abstract

The present study was conducted on male albino rats to evaluate the effects of renal toxicity induced by cadmium chloride (CdCl2) on hematological, some biochemical blood parameters as well as the associated histopathological effects on kidney and liver. Ninety male rats were randomly divided into three equal groups (each group contained 30 rats) as follow: group A (control), group B (1 mg CdCl2/kg, S/C), group C (2 mg CdCl2/kg, S/C). Cadmium chloride injection to male rats leads to significant increases in creatinine, urea, uric acid and cystatin C indicating kidney damage. Potassium and inorganic phosphorus showed significant increases in cadmium treated groups, while calcium and sodium revealed significant decreases. Hypoproteinemia, hypoalbuminemia and elevation of cholesterol, trigrlycerides and LDL-cholesterol levels were observed in cadmium-treated groups. Liver enzymes activities including alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) showed significantly increased indicating liver damage. Hematological parameters revealed significant decreases in red blood cells (RBCs), hemoglobin concentration (Hb) and hematocrit values (HCT) inducing anemia. Cadmium-treated groups showed leukocytosis, lymphocytosis and monocytosis indicating activation of the animal’s immune system due to renal and hepatic toxicity by cadmium chloride. Platelets count showed a significant increase indicating reactive thrombocytosis induced by renal toxicity. Histopathological picture of the kidneys in cadmium-treated groups showed vacuolization in the lining endothelium of glomeruli with focal fibrosis in between atrophied tubules and glomeruli. Liver showed diffuse kupffer cells proliferation in the hepatic parenchyma and hyperplasia and cystic dilatation in the bile duct. From the obtained results, we could conclude that renal toxicity induced by CdCl2 causes reduction in serum albumin concentration and oncotic pressure. Reduction in plasma oncotic pressure stimulates the hyperlipidemic response. So, renal damage is accompanied by hypoproteinemia and hyperlipidemia.

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