{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T20:31:24Z","timestamp":1786480284949,"version":"build-2736575974"},"reference-count":29,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2022,7,28]]},"abstract":"\n Key Points<\/jats:title>\n \n \n \n Impaired kidney function is associated with higher lead blood levels yet, simultaneously, lower amounts of urinary lead excretion.<\/jats:p>\n <\/jats:list-item>\n \n These findings suggest an increased susceptibility to progressive lead accumulation from even low levels of environmental exposure.<\/jats:p>\n <\/jats:list-item>\n \n Further research into the public health consequences of heavy metal exposure is needed, particularly among vulnerable populations.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n The consequences of low levels of environmental heavy metal exposure, as found widely in the United States, in those with impaired renal function remain underexplored.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We examined the cross-sectional association of indices of renal function with lead and cadmium levels in blood and urine among National Health and Nutrition Examination Survey (NHANES) participants. We used the 1999\u20132002 cycle, which included measures of cystatin C, in order to quantify renal function most precisely and defined chronic kidney disease (CKD) as an estimated glomerular filtration rate (eGFR) <60 ml\/min per 1.73 m\n 2<\/jats:sup>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n In weighted and adjusted analyses of 5638 participants, lead levels were 0.23 (95% CI, 0.03 to 0.42)\n \u03bc<\/jats:italic>\n g\/dl higher among participants with CKD, and 0.05 (95% CI, 0.01 to 0.09)\n \u03bc<\/jats:italic>\n g\/dL higher per 10 ml\/min per 1.73 m\n 2<\/jats:sup>\n lower eGFR. Cadmium levels were 0.02 (95% CI, 0.01 to 0.03)\n \u03bc<\/jats:italic>\n g\/L higher per 10 ml\/min per 1.73 m\n 2<\/jats:sup>\n lower eGFR. Black race significantly modified the association of lower eGFR with higher circulating lead levels (\n P<\/jats:italic>\n interaction <0.001). A 10 ml\/min per 1.73 m\n 2<\/jats:sup>\n lower eGFR was associated with a 0.13 (95% CI, 0.06 to 0.21)\n \u03bc<\/jats:italic>\n g\/dl higher lead level among Black participants compared with 0.03 (95% CI, \u20130.04 to 0.11)\n \u03bc<\/jats:italic>\n g\/dl higher level among White participants. Among the 1852 participants with urinary metal measurements, despite higher circulating levels, those with CKD had significantly lower urinary lead levels (\u20130.16 [95% CI, \u20130.30 to \u20130.01] ng\/ml) and urinary lead\/creatinine ratios (\u20130.003 [95% CI, \u20130.004 to \u20130.001]).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n CKD is associated with higher blood lead levels, particularly among Blacks, and simultaneously, lower urinary lead levels, consistent with the hypothesis that CKD confers a state of heighted susceptibility to heavy metal environmental exposure by reducing its elimination. Given that low levels of exposure remain highly prevalent in the United States, further efforts to protect patients with CKD from heavy metal toxicity may be warranted.<\/jats:p>\n <\/jats:sec>","DOI":"10.34067\/kid.0006782021","type":"journal-article","created":{"date-parts":[[2022,5,11]],"date-time":"2022-05-11T00:25:22Z","timestamp":1652228722000},"page":"1191-1196","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":26,"title":["Susceptibility to Environmental Heavy Metal Toxicity among Americans with Kidney Disease"],"prefix":"10.34067","volume":"3","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2550-2368","authenticated-orcid":false,"given":"John","family":"Danziger","sequence":"first","affiliation":[{"name":"Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4024-2034","authenticated-orcid":false,"given":"Laura E.","family":"Dodge","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"},{"name":"Harvard T.H. Chan School of Public Health, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3676-2707","authenticated-orcid":false,"given":"Howard","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Preventative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8450-6970","authenticated-orcid":false,"given":"Kenneth J.","family":"Mukamal","sequence":"additional","affiliation":[{"name":"Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2022,7,28]]},"reference":[{"key":"B3-20250825","doi-asserted-by":"crossref","first-page":"1171","DOI":"10.1001\/jama.1996.03530390037031","article-title":"The relationship of bone and blood lead to hypertension. 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