title: Erythrocyte aminolevulinate dehydratase activity as a lead marker in patients with chronic renal failure.
abstract: BACKGROUND
  Overexposure to lead may result in an increased risk for developing chronic renal failure (CRF) and hypertension. Subclinical lead poisoning is difficult to identify. Because the heme biosynthetic pathway is highly sensitive to lead, we considered the study of enzymes involved in this pathway as a method to detect an excessive body lead burden.
  
  
  METHODS
  Main concerns in assessing the heme pathway in patients with CRF were related to aminolevulinate dehydratase (ALAD) activity. We first selected a number of patients with CRF at a predialysis stage, subsequently dividing them into two groups after the EDTA mobilization test had determined whether lead pools were expanded. The study included 24 healthy controls, 12 patients with clinical plumbism and biochemical demonstration of lead poisoning (Pb-CONT), 18 patients with CRF with no evidence of high lead storage (CRF/-), and 8 patients with CRF with high urinary excretion of lead in contrast to normal blood lead levels (CRF/+).
  
  
  RESULTS
  As expected, symptoms of plumbism (Pb-CONT) were accompanied by an increased erythrocyte zinc-protoporphyrin-free protoporphyrin ratio and high urine coproporphyrin excretion, whereas both these values were within the normal range in all patients with CRF. CRF/- patients showed minor abnormalities of erythrocyte heme metabolism, such as low ALAD activity, both baseline and in vitro restored. The ALAD-restored ALAD ratio correlated closely with urine lead excretion; it was normal in healthy controls and CRF/- patients and significantly reduced in Pb-CONT and CRF/+ patients.
  
  
  CONCLUSIONS
  The erythrocyte ALAD-restored ALAD ratio may be a useful tool to show otherwise subclinical lead poisoning in patients with CRF.
authors.affiliation: Research Centre, Doce de Octubre Hospital, Madrid, Spain.
authors.forename: Antonio
authors.initials: A
authors.lastname: Fontanellas
authors.forename: Susana
authors.initials: S
authors.lastname: Navarro
authors.forename: María-José
authors.initials: MJ
authors.lastname: Morán-Jiménez
authors.forename: Ana I
authors.initials: AI
authors.lastname: Sánchez-Fructuoso
authors.forename: Irene
authors.initials: I
authors.lastname: Vegh
authors.forename: Alberto
authors.initials: A
authors.lastname: Barrientos
authors.forename: Rafael Enríquez
authors.initials: RE
authors.lastname: de Salamanca
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D004912:Erythrocytes / Q000201:enzymology*; D005260:Female; D006418:Heme / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000201:enzymology*; D007854:Lead / Q000097:blood* / Q000652:urine; D020263:Lead Poisoning, Nervous System / Q000097:blood / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D000623:Porphobilinogen Synthase / Q000097:blood*; D011166:Porphyrins / Q000097:blood
chemical_list: D015415:Biomarkers; D011166:Porphyrins; D007854:Lead; D006418:Heme; D000623:Porphobilinogen Synthase