Parathyroid hormone status does not influence blood and bone lead levels in dialysis patients.

Elevated blood lead levels, a risk factor for cardiovascular disease, have been reported among patients with end-stage renal disease. We evaluated whether these higher levels are due to release of lead from the skeleton because of uremic bone disease. Fifty-one African-American patients with end-stage renal disease were recruited from 3 Tulane University dialysis programs between January and July 2005. An interviewer-administered questionnaire, blood specimen collection and 109Cd-based x-ray fluorescence measurement of tibia lead occurred during a single study visit. Levels of serum parathyroid hormone (PTH), calcium, phosphorus, and albumin were abstracted from the patients' charts. The distributions of tibia and blood lead were similar across levels of serum PTH. Specifically, for participants with serum PTH <300 pg/mL and > or =300 pg/mL, median tibia lead was 21 microg/g and 17 microg/g, respectively, and geometric mean blood lead levels were 6.7 microg/dL and 6.6 microg/dL, respectively (P = 0.70 and 0.87, respectively). After adjustment for age, gender, education, cigarette smoking, and dialysis vintage, natural log transformed blood lead was 0.022 lower in patients with serum PTH > or =300 pg/mL (P = 0.87). There were no differences in tibia and blood lead across levels of serum calcium, serum phosphorus, and the calcium phosphorus product (all P > 0.40). The high blood lead levels observed among dialysis patients do not appear to be the result of increased bone turnover. The causes of higher blood lead levels for these patients need to be identified and attenuated.