Bone lead in dialysis patients

Vyver, F L Van de; D’Haese, Patrick C.; Visser, W. J.; Elseviers, Monique; Knippenberg, L. J.; Lamberts, Ludwig V.; Wedeen, Richard P.; Broe, Marc E. De

doi:10.1038/ki.1988.39

Cited by 79 publications

(53 citation statements)

References 19 publications

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“…Other studies also support the finding that renal dysfunction per se does not increase BLL (4,20,23,24). Chemical and histologic studies of transiliac biopsies obtained from 153 dialysis patients showed that chronic renal failure and dialysis do not cause accumulation of lead in bone (25). Moreover, the present longitudinal work demonstrates that after adjustment of other factors, including the renal function at baseline, both BLB and BLL are the most significant predictors of the progression of renal insufficiency.…”

Section: Discussionsupporting

confidence: 84%

Environmental Exposure to Lead and Progression of Chronic Renal Diseases

Lin²,

Lin-Tan³

2004

Journal of the American Society of Nephrology

114

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Abstract. Previous retrospective research suggests that lowlevel environmental lead exposure is associated with an acceleration of age-related impairment of renal function. For elucidating the long-term relationship between low-level environmental lead exposure and progression of chronic renal diseases in patients without diabetes, 121 patients who had chronic renal insufficiency, a normal body lead burden (BLB), and no history of exposure to lead were observed prospectively for 48 mo. Associations of both BLB and blood lead level (BLL) with renal function were evaluated, with reference to other covariates. The primary end point was an increase in the serum creatinine level to double the baseline value. Sixty-three patients had BLB Ն80 g and Ͻ600 g (high-normal group), and 58 patients had BLB Ͻ80 g (low-normal group). The primary end point occurred in 17 patients. Fifteen of them had high-normal BLB, whereas two patients had low-normal BLB (hazard ratio [95% confidence interval]: 1.01 [1.00 to 1.01] for each increment of 1 g; P ϭ 0.002). The BLB and BLL at baseline were the most important risk factors to predict progression of renal insufficiency. Each increase of 10 g in the BLB or 1 g/dl in the BLL reduced the GFR by 1.3 (P ϭ 0.002) or 4.0 ml/min (P ϭ 0.01) during the study period. In conclusion, low-level environmental lead exposure is associated with accelerated deterioration of renal insufficiency. Even at levels far below the normal ranges, both increased BLL and BLB predict accelerated progression of chronic renal diseases.A high occupational lead exposure is well documented to be able to induce nephropathy (1,2). Several studies have indicated a strong association between blood lead levels (BLL) and agerelated decline in renal function of the general population (3-6). However, these studies either were retrospective or did not adjust other confounding factors that affect the progression of renal function, such as hypertension, urinary protein excretion, and usage of angiotensin-converting enzyme (ACE) inhibitors.Furthermore, most of these studies measured BLL as an indicator of lead exposure. However, the BLL reflects recent lead exposure rather than the actual body lead burden (BLB). Calcium disodium EDTA mobilization tests and bone x-ray fluorescence studies are the most reliable methods for measuring the BLB (7). A BLB of Ͼ600 g (2.9 mol), as assessed by calcium disodium EDTA mobilization tests, indicates lead poisoning. The authors' previous studies, using EDTA-mobilization tests to assess the BLB, suggested that low-level environmental lead exposure may be associated with the progression of renal insufficiency in patients without known lead exposure (8 -10). Our recent work further established that repeated chelation therapy to reduce the BLB may slow the progression of renal insufficiency in a 27-mo clinical trial (11). However, the long-term relationship between low-level environmental lead exposure and the progression of chronic renal diseases remains unknown. A 48-mo prospective longitudinal stu...

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Section: Discussionsupporting

confidence: 84%

Environmental Exposure to Lead and Progression of Chronic Renal Diseases

Lin²,

Lin-Tan³

2004

Journal of the American Society of Nephrology

114

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“…In 20 and 24% of CaNa2EDTA-negative and CaNa2-EDTA-positive children, respectively, cortical bone lead values were similar to lead concentrations measured in bone biopsies from normal adults (16,17). Remarkably, an additional 40% of CaNa2EDTA-positive children had bone lead concentrations observed in industrially exposed adults (16,17). In this longitudinal study, lead-toxic children who did not qualify for treatment and other children who underwent one or two courses of CaNa2EDTA treatment were re-evaluated 6 weeks and 24 weeks postenrollment.…”

Section: Resultssupporting

confidence: 63%

“…By using net corrected LXRF counts and PbB values to predict CaNa2EDTA outcomes, the specificity and sensitivity of these two predictors were 86 and 93%, respectively (Table 5) (13). In 20 and 24% of CaNa2EDTA-negative and CaNa2-EDTA-positive children, respectively, cortical bone lead values were similar to lead concentrations measured in bone biopsies from normal adults (16,17). Remarkably, an additional 40% of CaNa2EDTA-positive children had bone lead concentrations observed in industrially exposed adults (16,17).…”

Section: Resultssupporting

confidence: 57%

Sequential Measurements of Bone Lead Content by L X-Ray Fluorescence in CaNa 2 EDTA-Treated Lead-Toxic Children

Rosen¹,

Markowitz²,

Bijur³

et al. 1991

Environmental Health Perspectives

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With the development of L X-ray fluorescence (LXRF) to measure cortical bone lead directly, safely, rapidly, and noninvasively, the present study was undertaken to a) evaluate LXRF as a possible replacement for the CaNa2EDTA test; b) quantify lead in tibial cortical bones of mildly to moderately lead-toxic children before treatment; and c) quantify lead in tibial cortical bones of lead-toxic children sequentially following one to two courses of chelation therapy. The clinical research design was based upon a longitudinal assessment of 59 untreated lead-toxic children. At enrollment, if the blood lead (PbB) was 25 to 55 jg/dL and the erythrocyte protoporphyrin (EP) concentration was 2 35 glg/dL, LXRF measurement of tibial bone lead was carried out. One day later, each child underwent a CaNa2EDTA provocative test. If this test was positive, lead-toxic children were admitted to the hospital for 5 days of CaNa2EDTA therapy. These tests were repeated 6 weeks and 6 months after enrollment. Abatement of lead paint hazards was achieved in most apartments by the time of initial hospital discharge.The LXRF instrument consists of a low energy X-ray generator with a silver anode, a lithium-doped silicon detector, a polarizer of incident photons, and a multichannel X-ray analyzer. Partially polarized photons are directed at the subcutaneous, medial mid-tibial cortical bone. The LXRF spectrum, measured 900 from the incident beam, reveals a peak in the 10.5 KeV region, which represents the lead La line. The effective dose equivalent using tissue weighting factors according to guidelines of the National Council on Radiation Protection and Measurements (1989), was 2.5 FSv. The reproducibility of replicate LXRF measurements, including the day-to-day variation of the instrument, in 26 lead-toxic children, after repositioning the instrument within 5 cm of the first LXRF measurements, was ±9.2 (9 5% confidence limits). For an overlying tibial skin thickness of 5 mm, the minimum detection limit was 7 Ag of lead/g (wet weight) at the 95% confidence interval.Based upon a discriminant analysis, 90% of lead-toxic children were predicted correctly as being CaNa2EDTA-positive or CaNa2EDTA-negative. Using LXRF and PbB values to predict CaNa2EDTA outcomes, the specificity and sensitivity of these two predictors were 86 and 93%, respectively. In a significant fraction of CaNa2EDTA-positive and CaNa2EDTA-negative children, cortical bone lead values were similar to lead concentrations measured via bone biopsy in normal adults and lead workers in industry. By 24 weeks after enrollment, PbB, EP, and urinary lead/EDTA ratios were similar in all groups. The most dramatic decreases in net corrected photon counts by LXRF occurred in children treated twice. Mean values of cortical bone lead by LXRF at 24 weeks in all three groups of children were similar to the mean concentration in untreated CaNa2EDTA-negative children at enrollment but still three to five times greater than those measured in the tibia or whole teeth of normal European children using...

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“…However, in a similar study, PCA -chelatable lead was not related to the lead levels predicted by K-shell X-ray fluorescence for finger bone , while there was an association with biopsy specimens from the vertebra (14). Moreover, there were associations between CaNazEDTA-chelated lead and biopsies from the ileum (15).…”

mentioning

confidence: 83%

“…However, if we exclude both the retired worker and the one removed from active lead work (on the grounds that the lead distribution between different pools may have been different from that of currently active workers), then the correlation between calcaneus and chelated lead, for example, increases significantly, to r = 0.62 (N = 18). Recently, rather poor associations were reported between CaNa 2EDTA-chelated lead on one hand and either finger lead in patients with renal impairment (29) or tibia lead in lead workers (13) on the other, while there was a rather good correlation with lead in ileum biopsies (15).…”

Section: Skeletal Leadmentioning

confidence: 99%

Chelated lead and bone lead.

Tell¹,

Lj²,

Nilsson³

et al. 1992

Scand J Work Environ Health

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SKERFVING S. Chelated lead and bone lead. Scand J Work En viron Health 1992;18:113-9. In this study a close correlation [correlation coefficient (r) = 0.86, P < 0.001) was found between the blood lead level of 20 lead workers and their urinary excretion of lead for 24 h after intravenous infusion with I g of the chelating agent calcium disodium edetate, In addition , there were significant associations between lead levels in different bones (tibia /calcaneus: r=0.93, P

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Bone lead in dialysis patients

Cited by 79 publications

References 19 publications

Environmental Exposure to Lead and Progression of Chronic Renal Diseases

Environmental Exposure to Lead and Progression of Chronic Renal Diseases

Sequential Measurements of Bone Lead Content by L X-Ray Fluorescence in CaNa 2 EDTA-Treated Lead-Toxic Children

Chelated lead and bone lead.

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