Cadmium nephropathy.
Cadmium, an important environmental toxic agent has the kidney as its most important target organ. It is concentrated mainly in the renal cortex. Excessive renal accumulation of cadmium causes well defined morphological and ultrastructural pathological changes in the proximal tubules. Functional changes accompanying cadmium nephropathy include proteinuria, enzymuria, aminoaciduria, glycosuria, polyuria, hepercalciuria, increased urinary uric acid, and cadmium. The observed proteinuria has two components: low molecular weight proteinuria of tubular origin (excess excretion of proteins such as B2-microglobulin) and high molecular weight proteinuria of glomerular origin, (excretion of proteins such as albumin, IgG, transferrin, etc.) The proposed mechanisms of cadmium nephropathy are reviewed. The involvement of metallothionein in cadmium nephropathy and the  nephrotoxic effects of cadmium-thionein are discussed.
D000818:Animals; D002104:Cadmium / Q000378:metabolism; D002105:Cadmium Poisoning / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D002352:Carrier Proteins / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007674:Kidney Diseases / Q000473:pathology*; D007687:Kidney Tubules, Proximal / Q000473:pathology; D008668:Metallothionein / Q000378:metabolism / Q000633:toxicity
D002352:Carrier Proteins; C004203:cadmium-binding protein; D002104:Cadmium; D008668:Metallothionein