Mobilization of lead from bone in end-stage renal failure patients with secondary hyperparathyroidism.
BACKGROUND
It is now recognized that long-term exposure to even low levels of lead may increase bone lead content. Lead can then be released in toxicologically significant amounts during critical states of increased bone turnover.


METHODS
Two patients with end-stage renal failure, one on haemodialysis and the other on continuous ambulatory peritoneal dialysis (CAPD), had been exposed to lead and developed secondary hyperparathyroidism. An edetate calcium disodium (EDTA) test was performed in combination with haemofiltration or CAPD before and after parathyroidectomy.


RESULTS
Before parathyroidectomy, both patients had low delta aminolaevulinic acid dehydrase (ALA-D) and high concentrations of chelated lead. After parathyroidectomy, there was a dramatic decrease in chelated lead and the ALA-D returned to normal.


CONCLUSIONS
Secondary hyperparathyroidism increases mobilization of bone lead in dialysis patients with an elevated lead burden. This may cause toxic effects.
Kessler
M
M
Departments of Nephrology and Internal Medicine and Laboratory of Pharmacology and Toxicology, University Hospital of Nancy, France.
Durand
P Y
PY
Huu
T C
TC
Royer-Morot
M J
MJ
Chanliau
J
J
Netter
P
P
Duc
M
M
D000368:Aged; D001692:Biological Transport; D001842:Bone and Bones / Q000378:metabolism*; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000150:complications*; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism* / Q000628:therapy; D007854:Lead / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010531:Peritoneal Dialysis, Continuous Ambulatory; D006435:Renal Dialysis
D007854:Lead