Higher blood lead levels, a risk factor for cardiovascular disease, have been reported among patients with end-stage renal disease. We sought to determine whether higher lead levels in end-stage renal disease patients are due to lead being released from the skeleton. Fifty-one African American patients with end-stage renal disease were recruited from three Tulane University-affiliated dialysis clinics between January and July 2005. An interviewer-administered questionnaire, blood specimen collection, and 109Cd x-ray fluorescence measurement of tibia lead occurred during a single study visit. In addition, levels of serum parathyroid hormone (PTH), calcium, phosphorus, and albumin were abstracted from patients' charts. The distributions of tibia and blood lead were similar across levels of serum PTH. Specifically, the median tibia lead was 21 μg/g and 17 μg/g for participants with PTH levels < 300 pg/mL and ≥ 300 pg/mL, respectively (p = .70). Also, geometric mean blood lead levels were 6.7 μg/dL and 6.6 μg/dL for participants with serum PTH levels < 300 pg/mL and ≥ 300 pg/mL, respectively (p = .87). After adjustment for age, gender, education, smoking, and dialysis vintage, log-transformed blood lead was 0.022 lower in patients with serum PTH ≥ 300 pg/mL (p = .87). Additionally, no differences were noted in tibia and blood lead across levels of serum calcium, serum phosphorus, and the calcium × phosphorus product (all p > .40). The high blood lead levels observed among end-stage renal disease 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.
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