Skip to main content

Lead nephropathy

  • Chapter
Clinical Nephrotoxins

Abstract

Because of its stability and malleability, lead has been used by man for millennia. Although lead may be found in remnants from primitive societies, it is present in greater concentrations in industrial societies. It is widely distributed throughout the earth and accumulates in most tissues and plants.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 74.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Lancereaux E. Saturnisme chronique avec acces de goutte et arthrities uratiques. Compt Rend Soc de Biol (Paris) 1872; 2: 99–106.

    Google Scholar 

  2. Rabinowitz MB, Wetherill GW, Kopple JD. Magnitude of lead intake from respiration by normal man. J Lab Clin Med 1977; 90: 238–48.

    PubMed  CAS  Google Scholar 

  3. Rabinowitz MB, Wetherhill GW, Kopple JD. Kinetic analysis of lead metabolism in healthy humans. J Clin Invest 1976; 58: 260–70.

    Article  PubMed  CAS  Google Scholar 

  4. Van de Vyver FL, D’Haese PC, Visser WJ, Elseviers MM, Knippenberg LJ, Lamberts LV, Wedeen RP, De Broe ME. Bone lead in dialysis patients. Kidney Int 1988; 33: 601–7.

    Article  PubMed  Google Scholar 

  5. Vallee BL, Ulmer DD. Biochemical effects of mercury, cadmium and lead. Ann Rev Biochem 1972; 41: 91–128.

    Article  PubMed  CAS  Google Scholar 

  6. Fowler BA, Duval G. Effects of lead on the kidney: roles of high-affinity lead-binding proteins. Environ Health Perspect 1991; 91: 77–80.

    Article  PubMed  CAS  Google Scholar 

  7. Goyer RA. Mechanisms of lead and cadmium nephrotoxicity. Toxicol Lett 1989; 46: 153–62.

    Article  PubMed  CAS  Google Scholar 

  8. Pounds JB, Long GJ, Rosen JF. Cellular and molecular toxicity of lead in bone. Environ Health Perspect 1991; 91: 17–32.

    Article  PubMed  CAS  Google Scholar 

  9. Chisolm JJ, Harrison HC, Eberlern WR, Harrison HE. Aminoaciduria, hypophosphatemia and rickets in lead poisoning. Am J Dis Child 1955; 89: 159–68.

    CAS  Google Scholar 

  10. Chisolm JJ Jr, Mellits ED, Barrett MB. Interrelationships among blood lead concentration, quantitative daily ALA-U and urinary lead output following calcium EDTA. In: Nordberg GF, editor. Effects and dose-response relationships of toxic metals. Amsterdam: Elseviers, 1976: 416–33.

    Google Scholar 

  11. Agency for Toxic Substances and Disease Registry. Public Health Service. US Department of Health and Human Services. The nature and extent of lead poisoning in children in the United States. A report to Congress. Atlanta: US Department of Health and Human Services, Public Health Service, 1988.

    Google Scholar 

  12. National Research Council. Airborne lead in perspective. Washington: National Academy of Sciences, 1972.

    Google Scholar 

  13. Goyer RA, Leonard DL, Bream PR, Irons TG. Aminoaciduria in experimental lead poisoning. Proc Soc Exp Biol Med 1970; 135: 767–71.

    Article  PubMed  CAS  Google Scholar 

  14. Goyer RA, Leonard DL, Moore JF, Rhyne B, Kingman MR. Lead dosage and the role of the intranuclear inclusion body: an experimental study. Arch Environ Health 1970; 20: 705–11.

    Article  PubMed  CAS  Google Scholar 

  15. Goyer RA, Wilson MH. Lead-induced inclusion bodies. Results of ethylenediaminetetraacetic acid treatment. Lab Invest 1975; 32: 149–56.

    PubMed  CAS  Google Scholar 

  16. Schumann GB, Lerner SI, Weiss MA, Gawronski L, Lohiya GK. Inclusion-bearing cells in industrial workers exposed to lead. Am J Clin Pathol 1980; 74: 192–6.

    PubMed  CAS  Google Scholar 

  17. Council of the Queensland Branch of the British Medical Association. An historical account of the occurrence and causation of lead poisoning among Queensland children. Med J Aust 1922; 1: 148–52.

    Google Scholar 

  18. Nye LJJ. Chronic nephritis and lead poisoning. Sydney: Angus and Robertson, 1933.

    Google Scholar 

  19. Nye LJJ. An investigation of extraordinary incidence of chronic nephritis in young people in Queensland. Med J Aust 1929; 2: 145–59.

    Google Scholar 

  20. Fairley KD. A review of the evidence relating to lead as an etiological agent in chronic nephritis in Queensland. Med J Aust 1934; 1: 600–6.

    Google Scholar 

  21. Murray RE. Plumbism and chronic nephritis in young people in Queensland. Commonwealth of Australia, Department of Health Service Publication, 1939, no 2.

    Google Scholar 

  22. Henderson DA. A follow-up of cases of plumbism in children. Austr Ann Med 1954; 3: 219–24.

    CAS  Google Scholar 

  23. Henderson DA. Chronic nephritis in Queensland. Austr Ann Med 1955; 4: 163–77.

    CAS  Google Scholar 

  24. Henderson DA, Inglis JA. The lead content of bone in chronic Bright’s disease. Austr Ann Med 1957; 6: 145–54.

    CAS  Google Scholar 

  25. Emmerson BT. Chronic lead nephropathy: the diagnostic use of calcium EDTA and the association with gout. Aust Ann Med 1963; 12: 310–24.

    PubMed  CAS  Google Scholar 

  26. Emmerson BT. Chronic lead nephropathy. Kidney Int 1973; 4: 1–5.

    Article  PubMed  CAS  Google Scholar 

  27. Inglis JA, Henderson DA, Emmerson BT. The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland. J Path 1978; 124: 65–76.

    Article  PubMed  CAS  Google Scholar 

  28. Emmerson BT. The renal excretion of urate in chronic lead nephropathy. Austr Ann Med 1965; 14: 295–303.

    CAS  Google Scholar 

  29. Emmerson BT, Mirosch W, Douglas JB. The relative contributions of tubular reabsorption and secretion to urate excretion in lead nephropathy. Aust NZ J Med 1971; 4: 353–62.

    Article  Google Scholar 

  30. Morgan JM, Hartley MW, Miller RW. Nephropathy in chronic lead poisoning. Arch Int Med 1966; 118: 17–29.

    Article  CAS  Google Scholar 

  31. Ball GV, Sorensen LB. Pathogenesis of hyperuricemia in saturnine gout. N Engl J Med 1969; 280: 1199–1202.

    Article  PubMed  CAS  Google Scholar 

  32. Garrod AB. Second communication on the blood and effused fluids in gout, rheumatism and Brights’ disease. Med Chir Tr (London) 1854; 37: 49–61.

    CAS  Google Scholar 

  33. Garrod AB. A treatise on gout and rheumatic gout, 3rd ed. London: Longmans, Green & Co, 1876.

    Google Scholar 

  34. Wedeen RP. Poison in the pot: the legacy of lead. Carbondale, Ill: Southern Illinois University Press, 1984.

    Google Scholar 

  35. Craswell PW, Price J, Boyle PD, Heazlewood VJ, Baddeley H, Lloyd HM, Thomas BJ, Thomas BW. Chronic renal failure with gout: a marker of chronic lead poisoning. Kidney Int 1984; 26: 319–23.

    Article  PubMed  CAS  Google Scholar 

  36. Peitzman SJ, Bodison W, Ellis I. Moonshine drinking among hypertensive veterans in Philadelphia. Arch Intern Med 1985; 145: 632–4.

    Article  PubMed  CAS  Google Scholar 

  37. Emmerson BT. The clinical differentiation of lead gout from primary gout. Arthritis Rheum 1968; 11: 623–4.

    Article  PubMed  CAS  Google Scholar 

  38. Batuman V, Maesaka JK, Haddad B, Tepper E, Landy E, Wedeen RP. The role of lead in gout nephropathy. N Engl J Med 1981; 304: 520–3.

    Article  PubMed  CAS  Google Scholar 

  39. Batuman V, Landy E, Maesaka JK, Wedeen RP. Contribution of lead to hypertension with renal impairment. N Engl J Med 1983; 309: 17–21.

    Article  PubMed  CAS  Google Scholar 

  40. Sandstead HH, Michelakis AM, Temple TE. Lead intoxication: its effect on the renin-aldosterone response to sodium deprivation. Arch Environ Health 1970; 20: 356–63.

    Article  PubMed  CAS  Google Scholar 

  41. Harlan WR. The relationship of blood lead levels to blood pressure in the US population. Environ Health Persp 1988; 78: 9–13.

    Article  CAS  Google Scholar 

  42. Pirkle JL, Schwartz J, Landis JR, Harlan WR. The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. Am J Epidemiol 1985; 121: 246–58.

    PubMed  CAS  Google Scholar 

  43. Sharp DS, Becker CE, Smith AH. Chronic low level lead exposure — its role in the pathogenesis of hypertension. Med Toxicol 1987; 2: 210–32.

    Article  PubMed  CAS  Google Scholar 

  44. Ritz E, Mann J, Stoeppler M. Lead and the kidney. Adv Nephrol 1988; 17: 241–74.

    CAS  Google Scholar 

  45. Wedeen RP, Maesaka JK, Weiner B, Lipat GA, Lyons MM, Vitale LF, Joselow NM. Occupational lead nephropathy. Am J Med 1975; 59: 630–41.

    Article  PubMed  CAS  Google Scholar 

  46. Selevan SG, Landrigan PJ, Stern FB, Jones JH. Mortality of lead smelter workers. Am J Epidemiol 1985; 122: 673–83.

    PubMed  CAS  Google Scholar 

  47. Wedeen RP, Mallik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med 1979; 139: 53–7.

    Article  PubMed  CAS  Google Scholar 

  48. Cramer K, Goyer RA, Jagenburg R, Marion H. Renal ultrastructure, renal function, and parameters of lead toxicity in workers with different periods of lead exposure. Brit J Ind Med 1974; 31: 113–27.

    CAS  Google Scholar 

  49. Fanning D. A mortality study of lead workers — 1926–1985. Arch Environ Health 1988; 43: 247–51.

    Article  PubMed  CAS  Google Scholar 

  50. Gerhardsson L, Chettle DR, Englyst V, Nordberg GF, Nyhlin H, Scott MC, Todo AC, Vesterberg O. Kidney effects in long term exposed lead smelters workers. Brit J Ind Med 1992; 49: 186–92.

    CAS  Google Scholar 

  51. Buchet J-P, Roels H, Bernard A, Lauwerys R. Assessment of renal function of workers exposed to inorganic lead, cadmium or mercury vapor. Am J Occup Med 1980; 22: 741–50.

    CAS  Google Scholar 

  52. Vacca C. Heavy metal nephrotoxicity: lead differentiated from cadmium and mercury. Am J Clin Pathol 1980; 73: 308.

    Google Scholar 

  53. Omae K, Sakurai H, Higashi T, Muto T, Ichikawa M, Sasaki N. No adverse effects of lead on renal function in lead-exposed workers. Ind Health 1990; 28: 77–83.

    Article  PubMed  CAS  Google Scholar 

  54. Mueller PW, Paschal DC, Hammel RR, Klincewicz SL, Macneil ML, Spierto B, Steinberg KK. Chronic effects in three studies of men and women occupationally exposed to cadmium. Arch Environ Cont Toxicol 1992; 23: 125–36.

    Article  CAS  Google Scholar 

  55. Cardenas A, Roels H, Bernard AM, Barbon R, Buchet JP, Lauwerys RR, Rosello J, Ramis I, Mutti A, Franchini I, Fels LM, Stolte H, De Broe ME, Nuyts GD, Taylor SA, Price RG. Markers of early renal changes induced by industrial pollutants. II. Application to workers exposed to lead. Brit J Ind Med 1993; 50: 28–36.

    CAS  Google Scholar 

  56. Endo G, Horiguchi S, Kiyota I. Urinary N-acetyl-ß-D-glucosaminidase activity in lead-exposed workers. J Appl Toxicol 1990; 10: 235–8.

    Article  PubMed  CAS  Google Scholar 

  57. Hong CD, Hanenson IG, Lerner S, Hammond PB, Pesce AJ, Pollak VE. Occupational exposure to lead: effects on renal function. Kidney Int 1980; 18: 489–94.

    Article  PubMed  CAS  Google Scholar 

  58. Leckie WJH, Tomsett SL. The diagnostic and therapeutic use of edathamil calcium disodium (EDTA Versene) in excessive inorganic lead absorption. Q J Med 1958; 27: 65–82.

    PubMed  CAS  Google Scholar 

  59. Wedeen RP. Occupational and environmental renal diseases. Curr Nephrol 1988; 11: 65–105.

    Google Scholar 

  60. Chamberlain AC. Prediction of response of blood lead to airborne and dietary lead from volunteer experiments with lead isotopes. Proc R Soc Lond [Biol] 1985; 244: 149–82.

    Article  Google Scholar 

  61. Ahlgren L, Mattsson S. An x-ray fluorescence technique for in vivo determination of lead concentration in a bone matrix. Phys Med Biol 1979; 24: 136–45.

    Article  PubMed  CAS  Google Scholar 

  62. Craswell PW, Price J, Boyle PD, Heazlewood VJ, Baddeley H, Lloyd HM, Thomas BJ, Thomas BW, Williams GM. Chronic lead nephropathy in Queensland: alternative methods of diagnosis. Aust NZ J Med 1986; 16: 11–9.

    Article  CAS  Google Scholar 

  63. Wedeen RP. In vivo tibial XRF measurement of bone lead. Arch Environ Health 1990; 45: 69–71.

    Article  PubMed  CAS  Google Scholar 

  64. Ashouri OS. Hyperkalemic distal tubular acidosis and selective aldosterone deficiency: combination in a patient with lead nephropathy. Arch Intern Med 1985; 145: 1306–7.

    Article  PubMed  CAS  Google Scholar 

  65. Wedeen RP, Batuman V, Landy E. The safety of the EDTA lead-mobilization test. Environ Res 1983; 30: 58–62.

    Article  PubMed  CAS  Google Scholar 

  66. Germain MJ, Braden GL, Fitzgibbons JR. Failure of chelation therapy in lead nephropathy. Arch Intern Med 1984; 144: 2419–20.

    Article  PubMed  CAS  Google Scholar 

Download references

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1998 Springer Science+Business Media Dordrecht

About this chapter

Cite this chapter

Wedeen, R.P., Emmerson, B.T. (1998). Lead nephropathy. In: De Broe, M.E., Porter, G.A., Bennett, W.M., Verpooten, G.A. (eds) Clinical Nephrotoxins. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9088-4_26

Download citation

  • DOI: https://doi.org/10.1007/978-94-015-9088-4_26

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-015-9090-7

  • Online ISBN: 978-94-015-9088-4

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics