DYSFUNCTION IN RENAL ACIDIFICATION PROCESS BY CADMIUM ADMINISTRATION IN THE RAT

Abstract

In order to investigate the effect of cadmium on the regulatory system of the acid-base balance in the kidney, the urinary pH and urinary excretion of acids and alkali were examined in rats. Thirty male Wistar rats were divided into 6 injection dose groups of 0, 0.1, 0.3, 0.6, 1.0 and 1.5 mg of Cd (as CdCl₂) per kg of body weight. Subcutaneous injections were given 6 days a week for 4 weeks. The 24-hr urine specimens were collected using a metabolic cage. After 4 weeks urinary pH significantly increased in the 0.6 and 1.0 mg dose groups, but apparently showed a near control value in the 1.5mg dose group. In the 1.0 mg dose group, a rise in urinary pH began at 3 weeks. These results suggest that continuous administration of cadmium causes dysfunction in renal acidification. Since the renal ability to excrete hydrogen ions into urine can be evaluated by measurment of urinary excretion of bicarbonate, titratable acid and ammonium ions, quantitative analysis was done by the alkali titration method. At 4 weeks the amount of titratable acid excretion was significantly decreased in the 0.6 mg dose group and showed the same level as the control in the 1.5 mg dose group. Bicarbonate excretion in the urine was detected in the 0.6 and 1.0 mg dose groups, and the amount of excretion was small in the 1.5 mg dose group. The amount of ammonium ion excretion increased with the increase of the dosage of cadmium. Thus, a change in urinary pH corresponded to the change in excretion of acids and alkali. The near controllevel of urinary pH, and acids and alkali excretion in the higher dose groups suggests that exposure to cadmium does not cause any changes in the ability of the kidney to secrete hydrogen ions in the distal tubule ; however a higher level of bicarbonate in the urine excretion suggests that there was severe damage to the proximal tubule. Moreover, the changes in the renal ability to regulate the acid-base balance was consistent with the change of the renal function of reabsorption of glucose, amino acids and protein.