Mercury-Induced Nephrotic Syndrome: A Correlation between Pathological Changes and Serum and Urine Biochemistry Parameters in Rats
Ibrahim, Suhaidah (1998) Mercury-Induced Nephrotic Syndrome: A Correlation between Pathological Changes and Serum and Urine Biochemistry Parameters in Rats. Masters thesis, Universiti Putra Malaysia.
Nephrotic syndrome (NS) is a renal disease featured mainly by proteinuria, hypoalbuminemia, oedema, and ascites. The etiologies could be diverse while the signs and symptoms are detected only at late stages ofthe disease. This study was conducted to assess the response of serum and urine biochemical indicators of renal failure and the compensatory mechanisrnls that may be involved in maintaining optimum renal function following repeated exposure to mercury chloride (HgCI2). A total of forty-five Sprague-Dawley rats aged between eight to ten weeks were injected intravenously through tail vein with 0.5 mg ofHgCl2/kg body weight every alternate days for ten days. The same number of rats were injected with 1 ml of normal saline/ kg body weight and served as controls. Five rats from each group were killed every four days commencing from the fourth day of the last injection. There were significant changes observed in the concentration of blood urea nitrogen (BUN), serum creatinine, serum total protein, serum albumin, urine total protein, and urine albumin during the 42-day experimental period. The concentration of BUN begun to increase significantly (P<0.05) by day 22, but returned to normal values after the initial increase on day 30. While serum creatinine concentration fluctuated with two peak values on days 34 and 42. Loss of albumin from plasma was observed to be intermittent and urine total protein showed a late increase on day 34. Urine albumin showed a significant earlier increase (p<O.05) on day 18, but decreased toward control values for the next 8 days before increasing back to a peak value on day 42. The deposition of mercury (Hg) following chronic exposure was high in the kidneys and the liver. The concentration of renal Hg was at peak values from day 14 to day 22 and gradually decreased thereafter. The renal tubular damage was observed to begin on day 18 and increased in intensity 26 days into the experiment reaching peak on day 42. There was also epithelisation of renal tubular epithelium. This response was greater on day 14 and quickly decreased thereon to disappear completely by day 28. The extensive damage of renal tubules which began on day 18 onwards could be due to an excessive loading of the metal beyond tissue elemental saturation and to the long retention of Hg in the tissues. The study suggests Hg accumulated predominantly in the kidneys and produced a biphasic response of renal-associated biochemical parameters in which urine albumin is the possible early indicator to renal damage. Tubular epithelisation could be one of the mechanisms involved in maintaining the optimum renal function.
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