The Persistence of Chronic Lead Nephropathy
2014; Elsevier BV; Volume: 64; Issue: 1 Linguagem: Inglês
10.1053/j.ajkd.2014.04.004
ISSN1523-6838
AutoresVecihi Batuman, Richard P. Wedeen,
Tópico(s)Heavy Metal Exposure and Toxicity
ResumoRelated Article, p. 25 Related Article, p. 25 Since its earliest description in 1863 in France by Lancereaux, chronic lead nephropathy has been recognized in diverse settings, including episodic high exposure in the workplace and continuous low-level environmental exposure.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar Later, clusters of chronic lead nephropathy cases between 1915 and 1935 were linked to childhood lead poisoning from ingestion of lead-based paint in Queensland, Australia,2Inglis J.A. Henderson D.A. Emmerson B.T. The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland.J Pathol. 1978; 124: 65-76Crossref PubMed Scopus (81) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar and during the 1950s, to lead-contaminated moonshine whiskey in the southern United States.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar Despite continued reports of chronic lead nephropathy from both occupational and nonoccupational settings,1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 4Brewster U.C. Perazella M.A. A review of chronic lead intoxication: an unrecognized cause of chronic kidney disease.Am J Med Sci. 2004; 327: 341-347Crossref PubMed Scopus (46) Google Scholar, 5Ekong E.B. Jaar B.G. Weaver V.M. Lead-related nephrotoxicity: a review of the epidemiologic evidence.Kidney Int. 2006; 70: 2074-2084Abstract Full Text Full Text PDF PubMed Scopus (254) Google Scholar the role of lead in kidney disease has been controversial and some authors have even questioned the very existence of chronic lead nephropathy.6Evans M. Elinder C.G. Chronic renal failure from lead: myth or evidence-based fact?.Kidney Int. 2011; 79: 272-279Crossref PubMed Scopus (44) Google Scholar, 7Evans M. Fored C.M. Nise G. Bellocco R. Nyren O. Elinder C.G. Occupational lead exposure and severe CKD: a population-based case-control and prospective observational cohort study in Sweden.Am J Kidney Dis. 2010; 55: 497-506Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar Amidst this growing skepticism, this issue of AJKD presents a study by Chowdhury et al8Chowdhury R. Darrow L. McClellan W. Sarnat S. Steenland K. Incident ESRD among participants in a lead surveillance program.Am J Kidney Dis. 2014; 64: 25-31Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar reporting an increased risk of end-stage renal disease (ESRD) in individuals exposed to lead, mostly in the occupational setting. The authors analyzed blood lead values from 58,307 men in 11 states that participated in the Adult Blood Lead Surveillance (ABLES) program sponsored by the National Institute for Occupational Safety and Health. Compared to US general population (adjusted for age, race, sex and calendar), the analysis showed an increased standardized incidence ratio of ESRD at 5 years or later in individuals with at least one blood lead value above 51 μg/dL, with a median follow-up of 17.7 years. The study adds new evidence that lead contributes to kidney disease by relying on hard outcome data, ESRD. Why then is there a dispute over the role of lead in kidney disease? The controversy may stem from a variety of misconceptions. Chronic lead nephropathy usually occurs as a consequence of continuous asymptomatic environmental lead ingestion, hobbies that involve lead-containing paints or glaze, shooting ranges, or exposure during occupations such as battery manufacture, lead smelting, or lead paint removal.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 5Ekong E.B. Jaar B.G. Weaver V.M. Lead-related nephrotoxicity: a review of the epidemiologic evidence.Kidney Int. 2006; 70: 2074-2084Abstract Full Text Full Text PDF PubMed Scopus (254) Google Scholar, 9Wedeen R.P. Malik D.K. Batuman V. Detection and treatment of occupational lead nephropathy.Arch Intern Med. 1979; 139: 53-57Crossref PubMed Scopus (154) Google Scholar Whether exposure is continuous and low dose or intermittent, asymptomatic, and high bolus, lead-associated morbidity, including kidney disease, is a function of cumulative lead exposure because of the very long half-life of lead in the body.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar Often there is a decades-long lag time between exposure and the manifestation of kidney disease, which may blur the association. This is in contrast to acute symptomatic lead poisoning, which occurs in individuals with very high blood lead levels (usually > 80 μg/dL) at the time of acute exposure and usually presents as a dramatic clinical picture with colic, seizures, peripheral nerve palsy, and acute lead nephropathy accompanied by proximal tubular defects such as Fanconi syndrome, tubular proteinuria (enzymuria and low-molecular-weight proteinuria), and acid-fast intranuclear inclusions.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar Conflating acute lead nephropathy characterized by transient proximal tubular defects with the interstitial nephritis of chronic lead nephropathy is another common source of confusion. The pathophysiologic mechanisms that induce vasospastic abdominal pain (lead colic) and transient hypertension associated with acute lead poisoning are very different from sustained hypertension induced by long-term lead absorption in adults who are otherwise asymptomatic. Nevertheless, acute lead nephropathy in childhood may evolve into chronic lead nephropathy in adulthood.2Inglis J.A. Henderson D.A. Emmerson B.T. The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland.J Pathol. 1978; 124: 65-76Crossref PubMed Scopus (81) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar, 10Hu H. Pepper L. Goldman R. Effect of repeated occupational exposure to lead, cessation of exposure, and chelation on levels of lead in bone.Am J Ind Med. 1991; 20: 723-735Crossref PubMed Scopus (62) Google Scholar Clinically, chronic lead nephropathy presents as decreased glomerular filtration rate with hypertension, moderate proteinuria, and sometimes gout.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar, 11Batuman V. Maesaka J.K. Haddad B. Tepper E. Landy E. Wedeen R.P. The role of lead in gout nephropathy.N Engl J Med. 1981; 304: 520-523Crossref PubMed Scopus (122) Google Scholar Kidney biopsy is nonspecific and shows interstitial fibrosis, tubule atrophy, and meager inflammatory cell infiltrate.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 2Inglis J.A. Henderson D.A. Emmerson B.T. The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland.J Pathol. 1978; 124: 65-76Crossref PubMed Scopus (81) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar, 5Ekong E.B. Jaar B.G. Weaver V.M. Lead-related nephrotoxicity: a review of the epidemiologic evidence.Kidney Int. 2006; 70: 2074-2084Abstract Full Text Full Text PDF PubMed Scopus (254) Google Scholar A milder form of the condition may include only modest elevations of blood pressure and serum creatinine level such that both are still within the generally accepted reference range.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 4Brewster U.C. Perazella M.A. A review of chronic lead intoxication: an unrecognized cause of chronic kidney disease.Am J Med Sci. 2004; 327: 341-347Crossref PubMed Scopus (46) Google Scholar, 12Batuman V. Lead chelation therapy retards the decline of renal function in patients with chronic kidney disease.Nat Clin Pract Nephrol. 2007; 3: 646-647Crossref PubMed Scopus (2) Google Scholar, 13Muntner P. He J. Vupputuri S. Coresh J. Batuman V. Blood lead and chronic kidney disease in the general United States population: results from NHANES III.Kidney Int. 2003; 63: 1044-1050Crossref PubMed Scopus (178) Google Scholar The causative role of lead can be inferred from a history of occupational exposure and confirmed by demonstrating increased body lead burden by bone lead measurement, x-ray fluorescence, or EDTA-lead mobilization test.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar, 4Brewster U.C. Perazella M.A. A review of chronic lead intoxication: an unrecognized cause of chronic kidney disease.Am J Med Sci. 2004; 327: 341-347Crossref PubMed Scopus (46) Google Scholar Because the US Renal Data System does not list lead nephropathy as a choice, lead exposure history and appropriate testing for lead are rarely pursued. Thus, ESRD due solely to lead absorption is rarely recognized.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar, 4Brewster U.C. Perazella M.A. A review of chronic lead intoxication: an unrecognized cause of chronic kidney disease.Am J Med Sci. 2004; 327: 341-347Crossref PubMed Scopus (46) Google Scholar, 14Muntner P. Menke A. Batuman V. Rabito F.A. He J. Todd A.C. Association of tibia lead and blood lead with end-stage renal disease: a pilot study of African-Americans.Environ Res. 2007; 104: 396-401Crossref PubMed Scopus (28) Google Scholar, 15Van de Vyver F.L. D'Haese P.C. Visser W.J. et al.Bone lead in dialysis patients.Kidney Int. 1988; 33: 601-607Crossref PubMed Scopus (57) Google Scholar With the introduction of industrial exposure standards and removal of lead first from paint and then gasoline, symptomatic lead poisoning became rare. Kidney disease associated with increased lead absorption looked like it might soon end up as a medical curiosity from a bygone era. However, studies continued to identify lead as a cause of kidney disease, hypertension, and gout in workers with occupational lead exposure, as well as in individuals with presumed “gout nephropathy” or unexplained kidney disease and hypertension who did not have an identifiable history of exposure to lead.9Wedeen R.P. Malik D.K. Batuman V. Detection and treatment of occupational lead nephropathy.Arch Intern Med. 1979; 139: 53-57Crossref PubMed Scopus (154) Google Scholar, 11Batuman V. Maesaka J.K. Haddad B. Tepper E. Landy E. Wedeen R.P. The role of lead in gout nephropathy.N Engl J Med. 1981; 304: 520-523Crossref PubMed Scopus (122) Google Scholar, 16Batuman V. Landy E. Maesaka J.K. Wedeen R.P. Contribution of lead to hypertension with renal impairment.N Engl J Med. 1983; 309: 17-21Crossref PubMed Scopus (149) Google Scholar Such studies emphasized the role of environmental lead as a source of continued exposure associated with significant kidney disease. These studies also confirmed that kidney failure per se does not cause an increase in body lead stores, thus refuting the hypothesis of reverse causation.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar, 16Batuman V. Landy E. Maesaka J.K. Wedeen R.P. Contribution of lead to hypertension with renal impairment.N Engl J Med. 1983; 309: 17-21Crossref PubMed Scopus (149) Google Scholar Fueling the controversy, in their analyses of Swedish workers, Evans et al stated that “data provide no evidence of an important role of low-level occupational lead exposure in the cause or progression of severe CKD.”6Evans M. Elinder C.G. Chronic renal failure from lead: myth or evidence-based fact?.Kidney Int. 2011; 79: 272-279Crossref PubMed Scopus (44) Google Scholar, 7Evans M. Fored C.M. Nise G. Bellocco R. Nyren O. Elinder C.G. Occupational lead exposure and severe CKD: a population-based case-control and prospective observational cohort study in Sweden.Am J Kidney Dis. 2010; 55: 497-506Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar However, in this analysis, exposure to lead was assessed by an “expert rating method”7Evans M. Fored C.M. Nise G. Bellocco R. Nyren O. Elinder C.G. Occupational lead exposure and severe CKD: a population-based case-control and prospective observational cohort study in Sweden.Am J Kidney Dis. 2010; 55: 497-506Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar and not actual lead measurements, such as blood lead, bone lead by radiographic findings, or EDTA tests. In contrast, Chowdhury et al8Chowdhury R. Darrow L. McClellan W. Sarnat S. Steenland K. Incident ESRD among participants in a lead surveillance program.Am J Kidney Dis. 2014; 64: 25-31Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar used blood lead values to assign exposure intensity and relied on ESRD as the outcome data. The authors found an increased standardized incidence risk for ESRD in the highest quintile of blood lead level (>51 μg/dL) in participants who were followed up for at least 5 years. The causative role of lead in these individuals would have been more convincing if it had been correlated with a valid estimate of body lead burden using, for example, an EDTA test or x-ray fluorescence.1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 14Muntner P. Menke A. Batuman V. Rabito F.A. He J. Todd A.C. Association of tibia lead and blood lead with end-stage renal disease: a pilot study of African-Americans.Environ Res. 2007; 104: 396-401Crossref PubMed Scopus (28) Google Scholar, 15Van de Vyver F.L. D'Haese P.C. Visser W.J. et al.Bone lead in dialysis patients.Kidney Int. 1988; 33: 601-607Crossref PubMed Scopus (57) Google Scholar Given the large number of participants included in this study, such measurements understandably are impractical. Nevertheless, elevated blood lead levels in the occupational setting place these individuals at high risk for increased cumulative absorption of lead, which correlates with lead-associated chronic kidney disease (CKD).1Batuman V. Lead nephropathy, gout, and hypertension.Am J Med Sci. 1993; 305: 241-247Crossref PubMed Scopus (73) Google Scholar, 15Van de Vyver F.L. D'Haese P.C. Visser W.J. et al.Bone lead in dialysis patients.Kidney Int. 1988; 33: 601-607Crossref PubMed Scopus (57) Google Scholar The finding of Chowdhury et al8Chowdhury R. Darrow L. McClellan W. Sarnat S. Steenland K. Incident ESRD among participants in a lead surveillance program.Am J Kidney Dis. 2014; 64: 25-31Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar that individuals in the group with the highest blood lead level are at increased risk of developing ESRD when evaluated at least 5 years later is consistent with the known behavior of lead-associated kidney disease. There is a long latency between the time of exposure and recognition of clinical disease; relying on history or the presence of symptoms often is misleading in the absence of blood or bone lead measurements. This was illustrated dramatically in studies tracing the Queensland epidemic of childhood nephritis to acute lead poisoning. Many individuals who sustained lead poisoning during childhood were shown to develop chronic lead nephropathy as young adults, confirmed by EDTA testing.2Inglis J.A. Henderson D.A. Emmerson B.T. The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland.J Pathol. 1978; 124: 65-76Crossref PubMed Scopus (81) Google Scholar, 3Emmerson B.T. Chronic lead nephropathy.Kidney Int. 1973; 4: 1-5Crossref PubMed Scopus (105) Google Scholar Finding a higher incidence of ESRD in patients with a high probability of elevated body lead stores is also consistent with the idea that lead may not be the sole cause of the kidney disease, but may have been the facilitator-accelerator factor in individuals with a propensity to kidney disease, as suggested in the studies from Taiwan.12Batuman V. Lead chelation therapy retards the decline of renal function in patients with chronic kidney disease.Nat Clin Pract Nephrol. 2007; 3: 646-647Crossref PubMed Scopus (2) Google Scholar, 17Lin J.L. Lin-Tan D.T. Hsu K.H. Yu C.C. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (241) Google Scholar, 18Weaver V.M. Fadrowski J.J. Jaar B.G. Does calcium disodium EDTA slow CKD progression?.Am J Kidney Dis. 2012; 60: 503-506Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar, 19Huang W.H. Lin J.L. Lin-Tan D.T. Hsu C.W. Chen K.H. Yen T.H. Environmental lead exposure accelerates progressive diabetic nephropathy in type II diabetic patients.Biomed Res Int. 2013; 2013: 742545PubMed Google Scholar Randomized placebo-controlled trials from Taiwan have consistently demonstrated that using chelation treatment with calcium disodium EDTA in patients with moderately elevated body lead burdens, including patients with diabetic kidney disease, slows the progression of CKD.12Batuman V. Lead chelation therapy retards the decline of renal function in patients with chronic kidney disease.Nat Clin Pract Nephrol. 2007; 3: 646-647Crossref PubMed Scopus (2) Google Scholar, 17Lin J.L. Lin-Tan D.T. Hsu K.H. Yu C.C. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (241) Google Scholar, 19Huang W.H. Lin J.L. Lin-Tan D.T. Hsu C.W. Chen K.H. Yen T.H. Environmental lead exposure accelerates progressive diabetic nephropathy in type II diabetic patients.Biomed Res Int. 2013; 2013: 742545PubMed Google Scholar, 20Chen K.H. Lin J.L. Lin-Tan D.T. et al.Effect of chelation therapy on progressive diabetic nephropathy in patients with type 2 diabetes and high-normal body lead burdens.Am J Kidney Dis. 2012; 60: 530-538Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar, 21Lin-Tan D.T. Lin J.L. Yen T.H. Chen K.H. Huang Y.L. Long-term outcome of repeated lead chelation therapy in progressive non-diabetic chronic kidney diseases.Nephrol Dial Transplant. 2007; 22: 2924-2931Crossref PubMed Scopus (47) Google Scholar These studies suggested that cumulative lead exposure may be a factor contributing to the progression of diabetic and nondiabetic CKD.12Batuman V. Lead chelation therapy retards the decline of renal function in patients with chronic kidney disease.Nat Clin Pract Nephrol. 2007; 3: 646-647Crossref PubMed Scopus (2) Google Scholar, 17Lin J.L. Lin-Tan D.T. Hsu K.H. Yu C.C. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (241) Google Scholar, 18Weaver V.M. Fadrowski J.J. Jaar B.G. Does calcium disodium EDTA slow CKD progression?.Am J Kidney Dis. 2012; 60: 503-506Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar, 20Chen K.H. Lin J.L. Lin-Tan D.T. et al.Effect of chelation therapy on progressive diabetic nephropathy in patients with type 2 diabetes and high-normal body lead burdens.Am J Kidney Dis. 2012; 60: 530-538Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar, 21Lin-Tan D.T. Lin J.L. Yen T.H. Chen K.H. Huang Y.L. Long-term outcome of repeated lead chelation therapy in progressive non-diabetic chronic kidney diseases.Nephrol Dial Transplant. 2007; 22: 2924-2931Crossref PubMed Scopus (47) Google Scholar Careful studies using appropriate measurements continue to reveal lead as either a causative or facilitating factor in the pathogenesis of CKD.15Van de Vyver F.L. D'Haese P.C. Visser W.J. et al.Bone lead in dialysis patients.Kidney Int. 1988; 33: 601-607Crossref PubMed Scopus (57) Google Scholar, 18Weaver V.M. Fadrowski J.J. Jaar B.G. Does calcium disodium EDTA slow CKD progression?.Am J Kidney Dis. 2012; 60: 503-506Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar, 19Huang W.H. Lin J.L. Lin-Tan D.T. Hsu C.W. Chen K.H. Yen T.H. Environmental lead exposure accelerates progressive diabetic nephropathy in type II diabetic patients.Biomed Res Int. 2013; 2013: 742545PubMed Google Scholar In light of accumulating evidence that lead may not only directly cause kidney and cardiovascular disease, but also may accelerate the progression of nondiabetic CKD, it is time for nephrologists to reconsider the present approach to CKD. As the present study by Chowdhury et al8Chowdhury R. Darrow L. McClellan W. Sarnat S. Steenland K. Incident ESRD among participants in a lead surveillance program.Am J Kidney Dis. 2014; 64: 25-31Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar shows, patients with high blood lead levels documented in their medical history are at risk of kidney disease. Determining blood lead level or, even better, estimating it in patients with kidney disease of unknown cause who present with hypertension, gout, and meager proteinuria may be rewarding.5Ekong E.B. Jaar B.G. Weaver V.M. Lead-related nephrotoxicity: a review of the epidemiologic evidence.Kidney Int. 2006; 70: 2074-2084Abstract Full Text Full Text PDF PubMed Scopus (254) Google Scholar, 12Batuman V. Lead chelation therapy retards the decline of renal function in patients with chronic kidney disease.Nat Clin Pract Nephrol. 2007; 3: 646-647Crossref PubMed Scopus (2) Google Scholar, 18Weaver V.M. Fadrowski J.J. Jaar B.G. Does calcium disodium EDTA slow CKD progression?.Am J Kidney Dis. 2012; 60: 503-506Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar, 22Kosnett M.J. Wedeen R.P. Rothenberg S.J. et al.Recommendations for medical management of adult lead exposure.Environ Health Perspect. 2007; 115: 463-471Crossref PubMed Scopus (269) Google Scholar Chelation therapy is appropriate for rapidly lowering body lead stores in the presence of acute symptomatic lead poisoning22Kosnett M.J. Wedeen R.P. Rothenberg S.J. et al.Recommendations for medical management of adult lead exposure.Environ Health Perspect. 2007; 115: 463-471Crossref PubMed Scopus (269) Google Scholar and may be a potential strategy to slow the progression of kidney disease in patients with CKD of diverse causes with moderately elevated body lead stores.8Chowdhury R. Darrow L. McClellan W. Sarnat S. Steenland K. Incident ESRD among participants in a lead surveillance program.Am J Kidney Dis. 2014; 64: 25-31Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 14Muntner P. Menke A. Batuman V. Rabito F.A. He J. Todd A.C. Association of tibia lead and blood lead with end-stage renal disease: a pilot study of African-Americans.Environ Res. 2007; 104: 396-401Crossref PubMed Scopus (28) Google Scholar, 15Van de Vyver F.L. D'Haese P.C. Visser W.J. et al.Bone lead in dialysis patients.Kidney Int. 1988; 33: 601-607Crossref PubMed Scopus (57) Google Scholar, 17Lin J.L. Lin-Tan D.T. Hsu K.H. Yu C.C. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (241) Google Scholar, 18Weaver V.M. Fadrowski J.J. Jaar B.G. Does calcium disodium EDTA slow CKD progression?.Am J Kidney Dis. 2012; 60: 503-506Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar, 19Huang W.H. Lin J.L. Lin-Tan D.T. Hsu C.W. Chen K.H. Yen T.H. Environmental lead exposure accelerates progressive diabetic nephropathy in type II diabetic patients.Biomed Res Int. 2013; 2013: 742545PubMed Google Scholar The results from the study by Chowdhury et al8Chowdhury R. Darrow L. McClellan W. Sarnat S. Steenland K. Incident ESRD among participants in a lead surveillance program.Am J Kidney Dis. 2014; 64: 25-31Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar add to the evidence that intermittent exposure to lead resulting in high blood lead concentrations is associated with ESRD. This report confirms previous observations on similar associations that focused on earlier stages of CKD. The data not only confirm the existence of chronic lead nephropathy as a definable clinical entity, but also affirm its persistence in the occupational setting. These findings also raise doubts about the prudence of the current Occupational Safety and Health Administration guidelines that allow occupational exposure with blood lead levels up to 60 μg/dL and return to work when blood lead level decreases to <40 μg/dL.23Occupational Safety and Health Administration. Occupational Safety and Health Standards. Standard Number: 1910.1025. 2014. http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=10030. Accessed March 17, 2014.Google Scholar The contents of this editorial do not represent the views of the Department of Veterans Affairs or the US government. Support: None. Financial Disclosure: The authors declare that they have no relevant financial interests. Incident ESRD Among Participants in a Lead Surveillance ProgramAmerican Journal of Kidney DiseasesVol. 64Issue 1PreviewVery high levels of lead can cause kidney failure; data about renal effects at lower levels are limited. Full-Text PDF
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