Cadmium May Predispose Mice to Immune Complex-Mediated Renal Injury: Another Possible Mechanism for Cadmium-Induced Nephrotoxicity
There is strong evidence that chronic ingestion of cadmium results in tubulointerstitial nephritis with a Fanconi-type syndrome in both humans and animals (2,4). There are fewer reports of glomerulonephritis associated with cadmium exposure (1–4) . Those reports that mention glomerular damage usually attribute it to autoantibody production against tissue damaged by cadmium (1,2,4). Our laboratory has accumulated evidence that chronic cadmium ingestion can inhibit clearance of immune complexes by the mononuclear phagocytic system of mice. Such abnormalities may allow the persistence of soluble antigen antibody complexes in the circulation which in turn might lead to greater deposition of the complexes in the glomeruli of the kidney and possibly other sites potentially injurious to organ function.
KeywordsMigration Albumin Cadmium Nephritis Spectrophotometry
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- 2.H.C. Gonick and H.J. Kramer, Pathogenesis of the Fanconi Syndrome, In: “Renal Tubular Disorders. Pathophysiology, Diagnosis, and Management.” H. C. Gonick and V. M. Buckalew, Jr., eds., Marcel Dekker, New York (1985), pp. 545–607.Google Scholar
- 4.T. Kjellstrom, Renal effects, In: “Cadmium and Health: A Toxicological and Epidemiological Appraisal, Vol. II, Effects and Response.” L. Friberg, C.G. Elinder, T. Kjellstrom, and G.F. Nordberg, eds., CRC Press, Boca Raton, Florida (1986), pp. 21–109Google Scholar