Cadmium renal toxicity

Cadmium (soft, Cd2+) Renal toxicity Blocks sulfhydryl groups in enzymes and competes with zinc. Stimulates metallothionein synthesis and interferes with Cu(II) and Zn(II) metabolism. 

Griffin JL, Walker LA, Troke J, Osborn D, Shore RE, Nicholson JK. The initial pathogenesis of cadmium induced renal toxicity. FEBS Lett. 2000 478 147-150. 

Fowler BA, Nordberg GF. Renal toxicity of cadmium metallothionein morphometric and X-ray microanalytical studies. Toxicol AppI Pharmacol 1978 46 609-623. 

El-Sharaky AS, Newairy AA, Badreldeen MM, Eweda SM, Sheweita SA. Protective role of selenium against renal toxicity induced by cadmium in rats. Toxicology 2007 235 185-93. 

Chan HM, Satoh M, Zalups RK, et al. 1992. Exogenous metallothionein and renal toxicity of cadmium and mercury in rats. Toxicology 76(1) 15-26. 

Satarug, S., M. R. Haswell-Elkins, and M. R. Moore. 2000. Safe levels of cadmium intake to prevent renal toxicity in human subjects. Br. J. Nutr. 84(6) 791-802. 

Chromium-zinc mixtures were more-than-additive in toxicity to Tisbe holothuriae, a marine copepod. Zinc in combination with chromium was more toxic to copepods than were mixtures of zinc with copper, lead, nickel, or cadmium. Renal tubular absorption of zinc in mice was impaired by certain diuretics and was further influenced by dietary proteins. Zinc absorption in rats was depressed after consumption of high levels of inorganic iron absorption was normal with organoirons. Mercury-zinc mixtures were more-than-additive in toxicity to... 

The notion of reserve capacity is not confined to one toxicant or target organ. For example, the renal toxicant cadmium imparts nephrotoxicity both directly in the form of proximal tubule dysfunction and through reducing the kidney s significant reserve capacity to deal with myriad other factors affecting kidney function as one ages (WHO, 1992). 

Cadmium is absorbed more efficiently by the lungs (30 to 60%) than by the gastrointestinal tract. For inhalation exposure, both the lungs and kidneys are target organs for cadmium-induced toxicity. Inhalation exposure to cadmium and cadmium compounds may result in effects including headache, chest pains, muscular weakness, pulmonary edema, and death. Renal toxicity (tubular proteinosis) may also result from inhalation exposure to cadmium. 

The most common toxic metals in industrial use are cadmium, chromium, lead, silver, and mercury less commonly used are arsenic, selenium (both metalloids), and barium. Cadmium, a metal commonly used in alloys and myriads of other industrial uses, is fairly mobile in the environment and is responsible for many maladies including renal failure and a degenerative bone disease called "ITA ITA" disease. Chromium, most often found in plating wastes, is also environmentally mobile and is most toxic in the Cr valence state. Lead has been historically used as a component of an antiknock compound in gasoline and, along with chromium (as lead chromate), in paint and pigments. 

Numerous substances detected in drinking waters are known to induce toxicity but usually at dose levels much higher than those found in water. Nitrates or nitrites can cause infant methemoglobinemia, lead can affect the hematopoetic or nervous system, cadmium can cause renal damage, and some organohalogens may cause liver toxicity (12). 

Cadmium Weak evidence for ultratrace essentiality in rats.7 Moderately toxic to all organisms a cumulative poison in mammals, causing renal failure possibly linked with hypertension in man. Has caused serous disease f ita] itai") in Japan from pollution. May also pose pollution problem associated with industrial use of zinc, e.g., galvanization. 

The results of studies on animals show that cadmium is an extremely toxic metal. Cadmium is poorly excreted by the human body and although only 5-10% of that ingested is absorbed, it does accumulate in the body over time with renal damage being caused by long-term exposure.14 One sign of this damage is proteinuria (the appearance of increased levels of unaltered proteins in the... 

It is well known that a large number of chemical substances, including toxic metals and metalloids such as arsenic, cadmium, lead, and mercury, cause cell injury in the kidney. With metal-induced neurotoxicity, factors such as metal-binding proteins, inclusion bodies, and cell-specific receptor-like proteins seem to influence renal injury in animals and humans. It is of interest to note that certain renal cell populations become the targets for metal toxicity, while others do not. In fact, the target cell populations handle the organic and common inorganic nephrotoxicants differently. ... 

Exposures to chemical substances such as carbon tetrachloride, 1,1-dichloroeth-ylene, paradichlorobenzene, ethylbenzene, monochlorobenzene, tetrachloroethyl-ene, toluene, 1,1,2-trichloroethane, xylenes, cadmium, and lead are known to canse adverse effects on the kidney. The kidney is unusually susceptible because of its role in filtering harmful substances from the blood. Some of these toxicants canse acnte injury to the kidney, while others produce chronic changes that can lead to end-stage renal failure or cancer. Furthermore, evaluation of the nephrotoxicity of complex industrial waste mixtures with organic chemicals and metals reqnires more stndies. 

Cadmium is an environmental and occupational pollutant that is associated with nephrotoxicity (1) and bone toxicity (2) even low concentrations can impair renal function and/or increase bone fragihty. Cadmium is also an adulterant in infant formulas and weaning foods. 

In some Chinese areas there are combined exposures to cadmium and inorganic arsenic. It was shown that there is a strong interaction between these two toxicants for induction of adverse renal effects in terms of tubular markers like increased p2-microglobuIin and glomerular marker urinary albumin [158]. 

Buchet JP, Eauwerys R, Roels El, Bernard A, Bruaux P, Claeys F, DucofFre G, De Plaen P, Staessen J, Amery A, Eijnen P, Thijs L, Rondia D, Sator F, Saint-Remy A, Nick L. Renal effects of cadmium body burden of the general population. Eancet 1990 336 699-702. Nordberg GF, Goyer RA, Nordberg M. Comparative toxicity of cadmium metallothionein and cadmium chloride on mouse kidney. Arch Pathol 1975 99 192-197. 

Fowler BA, Akkerman M.The role of Ca++ in cadmium-induced renal tubular cell injury. In Cadmium in the human environment toxicity and carcinogenicity. Nordberg G, Elerber R, Alessio E (editors). International Agency for Research on Cancer (lARC) Scientific Publications, Vol 118, Lyon 1992 p. 271-277. 

The association between metal exposure and renal failure can be approached from two points of view. On the one hand environmental/industrial exposure to heavy metals, more particularly, lead, cadmium and mercury and other inorganic substances such as silicon has been linked to a reduced renal function and/or the development of acute or chronic renal failure [1]. This issue has been dealt with in other chapters of this book. On the other hand patients with chronic renal failure, especially those treated by dialysis are at an increased risk for trace element disturbances (Figure 1). Indeed in these subjects the reduced renal function, the presence of proteinuria, metabolic alterations associated with renal insufficiency, the dialysis treatment, medication etc. all may contribute to either accumulation or deficiency of trace metals. With regard to aluminum intensive research on the element s toxic effects has been performed in the past. Recently, new metal-containing medications have been introduced of which the potential toxic effects should be considered and put in a justified context. 

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