Renal impairment in experimental hemochromatosis in rats.
Parenteral administration of iron as the complex with nitrilotriacetate resulted in moderate iron deposition in the renal cortex along with heavy deposition of iron in liver, heart, and exocrine pancreas. Iron treated rats exhibited slight but significant changes in serum chemistries consistent with mild renal insufficiency: increased chloride and creatinine and decreased sodium, calcium and CO2 content as a group with isolated increases in urea nitrogen (2/9) and phosphorus (3/9). Serum albumin was decreased and the normal correlation of serum calcium with serum albumin was abolished by iron overload. Although food intake/g body weight was similar in the two groups, both water intake and urine output relative to solute load were increased in iron-overloaded rats. We conclude that the renal insufficiency occasionally reported in human hemochromatosis may reflect a direct nephrotoxic action of iron.
D000818:Animals; D002118:Calcium / Q000097:blood; D002712:Chlorides / Q000097:blood; D003404:Creatinine / Q000097:blood; D004435:Eating; D005290:Ferric Compounds; D006432:Hemochromatosis / Q000139:chemically induced / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D009571:Nitrilotriacetic Acid / Q000031:analogs & derivatives*; D051381:Rats; D011919:Rats, Inbred Strains; D012709:Serum Albumin / Q000032:analysis
D002712:Chlorides; D005290:Ferric Compounds; D012709:Serum Albumin; D003404:Creatinine; D009571:Nitrilotriacetic Acid; D002118:Calcium; C020326:ferric nitrilotriacetate