Kidneys chronic cadmium poisoning

RBP has been found in relatively large amounts in the urine from patients with tubular proteinuria (Peterson and Berggard, 1971). Much is known about urinary protein excretion of Japanese patients with chronic cadmium poisoning (Kanai-er al., 1972a,b). These patients manifest tubular proteinuria and the excretion of considerable amounts of low-molecular-weight proteins, including RBP. The urinary excretion of RBP has been induced in a rabbit (Muto et al., 1976) and in a rhesus monkey (Nomiyama et al., 1981) by chronic poisoning with cadmium. Studies of the role of the kidney in RBP metabolism have also been carried out in rats with various kinds of experimentally induced renal lesions (Peterson et al., 1974). These various reported observations are all consistent with the above postulated role of the kidney in RBP metabolism. 

Disturbed renal function, with proteinuria, glucosuria, and aminoaciduria, has been observed in woricers exposed to cadmium. The proteinuria in chronic cadmium poisoning is of the tubular type and is caused by decreased reabsorption of proteins. " " As mentioned previously, when the kidneys have been damaged by cadmium, the excretion of the metal increases and the kidney concentration of cadmium will diminish considerably. ... 

The most severe form of chronic cadmium (Cd) poisoning caused by prolonged oral Cd ingestion is Itai-itai disease, which developed in numerous inhabitants of the Jinzu River basin in Toyama Prefecture, Japan in the 1950s (Figure 20.7). For the first time, cadmium pollution was shown to have severe consequences on human health, particularly in women. The most important effects were softening of the bones and kidney failure. The name of the disease is derived from the painful screams (Japanese /to/) caused by the severe pain in the... 

Cadmium (Cd) is a non-essensial metal used in industry as an anti-corrosive agent, and is found as a contaminant in food and also in cigarette smoke. The most serious consequence of chronic Cd poisoning is lung- and prostate cancer but the first effect during chronic intake is kidney damage, manifested by marked proteinuria [164]. Under chronic exposure, cadmium is primarily taken up by the liver, where it induces synthesis of metallothionein (MT) and induces formation of cadmium-metallothionein complexes. 

While severe cadmium toxicity like that which occurred near Toyama has not been found elsewhere, it is suspected that mild to moderate types of chronic cadmium toxicity may cause disorders of the kidneys leading to high blood pressure. However, the milder forms of cadmium poisoning may be counteracted by such essential minerals as calcium, copper, iron, manganese, selenium, and zinc. Therefore, a few scientists believe that high ratios of cadmium to zinc in the diet and in the various tissues of the body are better indicators of potential cadmium toxicities than the dietary and tissue levels of this toxicant alone. 

The radius of Zn is 0.74 A, that of Cd is 0.95 A. Can this difference be the cause of such a dramatic reversal of biological properties The answer is that while size is not the only factor, it is very important. In the carbonic anhydrase enzyme the Zn ion is found electrostatically bonded to atoms on file protein, as shown in Figure 7.8 . It turns out that Cd binds in this same place preferentially over Zn ", thus displacing it. When Cd is present instead of Zn ", however, the reaction of CO2 with water is not facilitated. More seriously, Cd + inhibits reactions that are essential to the kidney s functioning. Moreover, cadmium is a cumulative poison, so chronic exposure to even veiy low levels over an extended time leads to poisoning. 

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