title: Experimental lead nephropathy: treatment with calcium disodium ethylenediaminetetraacetate.
abstract: Chronic lead poisoning may cause hypertension, gout, and renal insufficiency. Most experimental poisoning studies have involved the use of high doses over short periods (ie, acute poisoning). Although chelating treatment leads to remission of acute lead nephropathy, its effects in the treatment of chronic poisoning are unclear. The aims of this study were to evaluate renal alterations produced during chronic lead poisoning and their progression when poisoning was over and to determine the efficiency of chelating treatment with calcium disodium ethylenediaminetetraacetate (EDTA). In this study, 56 male Wistar rats were administered lead in drinking water (500 ppm lead acetate) over 90 days. The control group consisted of 21 nonexposed rats. Seven rats from each group were killed on days 60 and 90. At the end of the 90-day period, 21 of the lead-exposed rats were treated with disodium monocalcium EDTA (50 mg/kg/d x 5 days) intraperitoneally, and 21 were administered serum saline by the same route. Three treatment courses were given separated by 9 days free of treatment. Seven rats from each subgroup were sacrificed at the end of each treatment course. Main findings related to poisoning were hypertrophy and vacuolization of medium and small arteries; mucoid edema and muscular hypertrophy in arterioles; loss of cell brush borders, cell loss, and intranuclear inclusion bodies in the proximal tubule; and fibrosis and the presence of infiltrates in the interstitial component. Treatment with EDTA slowed the progression of most alterations. No damage associated with the use of the chelating agent was observed. Longer term studies of the effects of this drug are required to establish whether the damage caused by lead poisoning may be reversed.
authors.affiliation: Department of Nephrology, Hospital Clínico S. Carlos, Madrid, Spain. asanchez@hcsc.insalud.es
authors.forename: Ana I
authors.initials: AI
authors.lastname: Sánchez-Fructuoso
authors.forename: Julia
authors.initials: J
authors.lastname: Blanco
authors.forename: Montserrat
authors.initials: M
authors.lastname: Cano
authors.forename: Luis
authors.initials: L
authors.lastname: Ortega
authors.forename: Miguel
authors.initials: M
authors.lastname: Arroyo
authors.forename: Christina
authors.initials: C
authors.lastname: Fernández
authors.forename: Dolores
authors.initials: D
authors.lastname: Prats
authors.forename: Alberto
authors.initials: A
authors.lastname: Barrientos
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D002467:Cell Nucleus / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D002614:Chelating Agents / Q000627:therapeutic use*; D003404:Creatinine / Q000097:blood / Q000652:urine; D004195:Disease Models, Animal; D004492:Edetic Acid / Q000627:therapeutic use*; D005355:Fibrosis; D006984:Hypertrophy; D002479:Inclusion Bodies / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D007687:Kidney Tubules, Proximal / Q000098:blood supply / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D007855:Lead Poisoning / Q000097:blood / Q000188:drug therapy* / Q000201:enzymology; D008214:Lymphocytes / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D008297:Male; D008871:Microvilli / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000098:blood supply / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D000623:Porphobilinogen Synthase / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D014617:Vacuoles / Q000187:drug effects / Q000473:pathology
chemical_list: D002614:Chelating Agents; D004492:Edetic Acid; D003404:Creatinine; D000623:Porphobilinogen Synthase