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Renal ultrastructure, renal function, and parameters of lead toxicity in workers with different periods of lead exposure
  1. Kim CramÉr,
  2. Robert A. Goyer,
  3. Rudolf Jagenburg,
  4. Marion H. Wilson
  1. Department of Hygiene, Västra Frolunda Sjukvårdscentral, USA
  2. Department of Clinical Chemistry, University of Göteborg, City of Göteborg, Sweden
  3. Department of Pathology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA

    Abstract

    Cramér, K., Goyer, R. A., Jagenburg, R., and Wilson, Marion H. (1974).British Journal of Industrial Medicine,31, 113-127. Renal ultrastructure, renal function, and parameters of lead toxicity in workers with different periods of lead exposure. Renal biopsies were obtained from five men with heavy occupational exposure to lead and compared with studies of their renal function and parameters of lead toxicity. Two men had lead exposure of less than one year while three men had been exposed for from four to more than 30 years. In addition, renal function studies were performed in two men from whom renal biopsies could not be obtained. Their lead exposures were five and 12 years, respectively. Significantly lower plasma levels, when compared with non-exposed controls, were found for proline, valine, tyrosine, and phenylalanine although no excessive aminoaciduria was found. Renal function tests were normal in all except for a reduced glomerular filtration rate (GFR) in one worker. Plasma ALA was measured by a new and highly specific method and ALA clearance was found to follow GFR closely. Those workers with prolonged lead exposure showed a lower urinary lead excreation. Typical lead-induced intranuclear inclusion bodies were found only in those with short exposure. The ultrastructural changes were localized to the proximal tubules, while the glomeruli were only nonspecifically affected. Mitochondrial changes were found in all men. Reasons for the decrease in inclusion body formation in chronic lead nephropathy are uncertain but may be due to an increased rate of renal cell turnover or a consequence of chelation therapy.

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