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CLINICOPATHOLOGICAL EVALUATION OF KIDNEY FUNCTIONS AFTER CADMIUM CHLORIDE ADMINISTRATION IN MALE RATS

BENHA VETERINARY MEDICAL JOURNAL • 2013
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Publication Information
Authors Abdel-baky, A.A., Mahmoud, A.A. and Fararh, K.M.
Keywords Cadmium chloride, Kidney, Liver, Lipid profile
Journal BENHA VETERINARY MEDICAL JOURNAL
Publisher BVMJ
Volume 24
Issue 1
Pages 1-11
publication.type International
Paper Link Not Available
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.