The critical level of cadmium in human renal cortex: A reevaluation

doi:10.1016/0378-4274(83)90156-X

Toxicology Letters

Volume 15, Issue 4, March 1983, Pages 357-360

https://doi.org/10.1016/0378-4274(83)90156-X Get rights and content

Abstract

The previously published estimate (160 ppm) of the critical level of renal cortical cadmium (Cd) (Roels et al., Environ. Res., 26 (1981) 217–240) has been reassessed after the depth of the left kidney was measured in each worker by echography. The correction introduced for kidney depth demonstrates that the critical liver cadmium level of 30 ppm corresponds to a corrected critical level of cadmium in renal cortex of 216 ppm. This critical cadmium level in renal cortex (CdKc) protects probably more than 90% of male workers from developing Cd-induced renal dysfunction.

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This paper is a review of epidemiological studies in which sensitive markers of nephrotoxicity have been used to detect the early effects of chemicals on the kidney. Most of the studies are cross-sectional, and their objective was either to identify potentially nephrotoxic chemicals (organic solvents, heavy metals) in the working or general environment or to establish dose-response/effect relationships from which safe exposure levels can be defined (e.g., for cadmium and mercury vapour). A few longitudinal studies were conducted to determine the persistence of renal disturbances and to get information on their predictive value (e.g., microproteinuria in cadmium workers). Nephrotoxicity tests, which have proved to be the most useful in these epidemiological studies, rely on the determination of specific urinary proteins which, according to their size, reflect the functional integrity of the proximal tubule (e.g., retinol-binding protein or β₂-microglobulin) or the glomerulus (e.g., albumin, immunoglobulin G). An increased urinary excretion of the lysosomal enzyme N-acetyl-β-D-glucosaminidase has been reported in several studies (e.g., in lead-exposed workers), but the pathological significance of this finding remains to be clarified, particularly when it is not associated with changes in the urinary excretion of specific proteins. Further work is needed to assess the usefulness of tests introduced more recently such as the assay of renal antigens in urine and the use of red-blood-eell membrane negative charges as an index of the glomerular polyanion. With the exception of microproteinuria observed in chronic cadmium poisoning, no epidemiological data are available on the prognostic value of subclinical renal effects caused by nephrotoxic chemicals.
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