Abstract

To the Editor: We read with interest the review article by Evans and Elinder,1.Evans M. Elinder C.-G. Chronic renal failure from lead: myth or evidence-based fact?.Kidney Int. 2011; 79: 272-279Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar who attempted to challenge the well-established fact that lead exposure causes chronic renal failure (CRF). Nevertheless, it seems that the authors missed some important facts when citing our studies.2.Yu C.C. Lin J.L. Lin-Tan D.T. Environmental exposure to lead and progression of chronic renal diseases: a four-year prospective longitudinal study.J Am Soc Nephrol. 2004; 15: 1016-1022Crossref PubMed Scopus (85) Google Scholar, 3.Lin J.L. Lin-Tan D.T. Hsu K.H. et al.Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (219) Google Scholar, 4.Lin J.L. Lin-Tan D.T. Li Y.J. et al.Low-level environmental exposure to lead and progressive chronic kidney diseases.Am J Med. 2006; 119 (e701–709): 707Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar In the paper,1.Evans M. Elinder C.-G. Chronic renal failure from lead: myth or evidence-based fact?.Kidney Int. 2011; 79: 272-279Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar the authors commented that the studies2.Yu C.C. Lin J.L. Lin-Tan D.T. Environmental exposure to lead and progression of chronic renal diseases: a four-year prospective longitudinal study.J Am Soc Nephrol. 2004; 15: 1016-1022Crossref PubMed Scopus (85) Google Scholar, 3.Lin J.L. Lin-Tan D.T. Hsu K.H. et al.Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (219) Google Scholar, 4.Lin J.L. Lin-Tan D.T. Li Y.J. et al.Low-level environmental exposure to lead and progressive chronic kidney diseases.Am J Med. 2006; 119 (e701–709): 707Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar were limited by not measuring glomerular filtration rate (GFR) and not adjusting for confounding factors (acidosis, inflammation, and hyperparathyroidism). Furthermore, there is limited knowledge and lack of validation of ethylenediaminetetraacetic acid (EDTA) test among CRF patients. These interpretations are not entirely correct. For example, we have reported3.Lin J.L. Lin-Tan D.T. Hsu K.H. et al.Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (219) Google Scholar that GFR improved significantly by the end of the 27th month in patients receiving EDTA chelation therapy. The mean change in GFR in the chelation group was 2.1±5.7 ml/min, as compared with −6.0±5.8 ml/min in the controls (P<0.001). The rate of decline in GFR in the chelation group was also lower than that in the controls during the 24-month period of repeated chelation therapy or placebo. Anyway, we reckon that the studies2.Yu C.C. Lin J.L. Lin-Tan D.T. Environmental exposure to lead and progression of chronic renal diseases: a four-year prospective longitudinal study.J Am Soc Nephrol. 2004; 15: 1016-1022Crossref PubMed Scopus (85) Google Scholar, 3.Lin J.L. Lin-Tan D.T. Hsu K.H. et al.Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (219) Google Scholar, 4.Lin J.L. Lin-Tan D.T. Li Y.J. et al.Low-level environmental exposure to lead and progressive chronic kidney diseases.Am J Med. 2006; 119 (e701–709): 707Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar were not adjusted for the above-mentioned confounders, but we wonder if the chronic kidney disease stage 3 of the studied population2.Yu C.C. Lin J.L. Lin-Tan D.T. Environmental exposure to lead and progression of chronic renal diseases: a four-year prospective longitudinal study.J Am Soc Nephrol. 2004; 15: 1016-1022Crossref PubMed Scopus (85) Google Scholar, 3.Lin J.L. Lin-Tan D.T. Hsu K.H. et al.Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.N Engl J Med. 2003; 348: 277-286Crossref PubMed Scopus (219) Google Scholar, 4.Lin J.L. Lin-Tan D.T. Li Y.J. et al.Low-level environmental exposure to lead and progressive chronic kidney diseases.Am J Med. 2006; 119 (e701–709): 707Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar could cause any considerable acidosis, inflammation, or hyperparathyroidism. In contrast, advanced-stage chronic kidney disease or end-stage renal disease5.Lin J.L. Lin-Tan D.T. Yen T.H. et al.Blood lead levels, malnutrition, inflammation, and mortality in patients with diabetes treated by long-term hemodialysis.Am J Kidney Dis. 2008; 51: 107-115Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar might be the exception. Literature data on the validation of the EDTA test among CRF patients are few, but we have demonstrated6.Lin-Tan D.T. Lin J.L. Yen T.H. et al.Long-term outcome of repeated lead chelation therapy in progressive non-diabetic chronic kidney diseases.Nephrol Dial Transplant. 2007; 22: 2924-2931Crossref PubMed Scopus (40) Google Scholar that repeated chelation therapy slowed the progression of renal insufficiency in non-diabetic patients with high normal-body lead burden.

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