1985
DOI: 10.1016/s0022-3476(85)80344-9
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Renal function 9 to 17 years after childhood lead poisoning

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Cited by 13 publications
(4 citation statements)
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“…A case-control study from the United States found no difference in creatinine clearance in children with lead poisoning (exposure levels 100–471 μg/dl) compared to sibling controls (Moel et al, 1985). A cross-sectional study of 196 children in Morocco found no significant correlations between blood lead and urine RBP and albumin levels (Laamech et al, 2014).…”
Section: Resultsmentioning
confidence: 99%
“…A case-control study from the United States found no difference in creatinine clearance in children with lead poisoning (exposure levels 100–471 μg/dl) compared to sibling controls (Moel et al, 1985). A cross-sectional study of 196 children in Morocco found no significant correlations between blood lead and urine RBP and albumin levels (Laamech et al, 2014).…”
Section: Resultsmentioning
confidence: 99%
“…Chronic poisoning with lead (blood lead levels > 60 µg/dL) has been associated with nephropathy in children and adults (Ekong et al, 2006), and was characterized by tubulointerstitial fibrosis, tubular atrophy, glomerular sclerosis, and reduced eGFR (Morgan et al, 1966;Loghman-Adham, 1997). Childhood lead poisoning can also promote hypertension (Moel et al, 1985;Hu, 1991;Fadrowski et al, 2010), prolong partial Fanconi syndrome (Loghman-Adham, 1998), and lead to abnormal renal function (Moel and Sachs, 1992;Filler et al, 2012;Fadrowski et al, 2013). In a prospective Yugoslavian birth-cohort study, high blood pressure and proteinuria were observed in offspring born to mothers living near lead-contaminated environment (Factor-Litvak et al, 1999).…”
Section: Prenatal Exposure To Edcs and Chronic Kidney Diseasementioning
confidence: 99%
“…The kidneys of these individuals were found to be contracted and small, with histologic changes of interstitial fibrosis, hypertensive vascular changes, and “alterative glomerulitis” [47, 48], which is a term coined by Kimmelstiel and Wilson in 1936 to describe histological findings of nuclear proliferation and irregular pyknotic nuclei in the glomerular tuft adjacent to the vascular pole seen in hypertension-induced glomerulosclerosis [49]. Although subsequent studies of adults who suffered childhood lead poisoning have reported hypertension [50, 51], persistent partial Fanconi’s syndrome [52], and individual cases consistent with lead nephropathy [50], they have not demonstrated overall increased mortality or statistically significant decreased kidney function [53]. A possible explanation for this discrepancy may be that the children in the Queensland epidemic were untreated, whereas children in subsequent studies were treated with chelation therapy.…”
Section: Heavy Metal Nephrotoxicantsmentioning
confidence: 99%