Urinary Lead Excretion in Uremic Patients

Behringer, D.; Craswell, Peter W.; Mohl, C.; Stoeppler, M.; Ritz, Eberhard

doi:10.1159/000183696

Cited by 36 publications

(30 citation statements)

References 23 publications

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“…In the EDTA mobilization test, Batuman et al [4] noted an increased amount of mobilizable Pb in patients with gout and renal impairment and in patients with hypertension and neph rosclerosis [5], confirming previous reports of children exposed to Pb carbonate paint [6,7] and consumers of contaminated moonshine whiskey [8], We have seen the same finding in patients with chronic interstitial nephri tis, gout and hypertension [9], Behringer et al [10] found an unexpectedly high prevalence of Pb accumulation in patients without gout but with impaired renal function secondary to several renal diseases. There is a correlation between hypertension and the Pb content of drinking water [11], At the usual environmental Pb exposure for the general population, some investigators have found a direct relationship between blood Pb levels and blood pressure [12,13], while others have not [14].…”

Section: Introductionsupporting

confidence: 88%

Blood Lead in Hemodialysis Patients

Colleoni

Arrigo²,

Gandini³

et al. 1993

Am J Nephrol

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Blood lead corrected for hematocrit (PbC) was measured in 115 hemodialysis (HD) patients. Information was collected with a questionnaire about personal and environmental factors thought to influence blood Pb levels. HD patients had significantly higher mean blood Pb than healthy subjects (p < 0.001). A non-negligible percentage of the HD population (13%) had values over 30 µg/ dl, the threshold for risk in occupational exposure, and 4% over 40 µg/dl which reflects Pb intoxication. No association was found between sex, age, duration of HD and PbC. The prevalence of high diastolic blood pressure was associated with PbC over 30 µg/dl (p < 0.01). Also, at blood Pb levels generally considered as ‘nontoxic’ (less than 40 µg/dl), we found a low correlation with diastolic blood pressure (r = 0.19, p = 0.049). A correlation was found between PbC and parathyroid hormone (r = 0.22, p = 0.01) and between PbC and mean corpuscular volume (r = -0.21, p = 0.02). The patients with individual risk factors (smoke, alcohol consumption and alkyl Pb from air contamination) had PbC levels higher than patients without (p = 0.001). The patients with environmental risk factors (professional exposure, tap water consumption and older houses) had PbC levels higher than patients without (p = 0.01). Patients with past occupational exposure had the highest mean PbC levels (34.1 µg/dl = 1.65nM/ml).

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Section: Introductionsupporting

confidence: 88%

Blood Lead in Hemodialysis Patients

Colleoni

Arrigo²,

Gandini³

et al. 1993

Am J Nephrol

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“…BLB was measured by EDTA-mobilization tests developed by Emmerson and modified by Behringer et al (14). BLL and BLB were assessed by 72-h urinary lead excretion after the intravenous infusion of 1 g of calcium disodium EDTA (edetate calcium disodium [Calcium Disodium Versenate]; Abbott Laboratories).…”

Section: Measurements Of Bll and Blbmentioning

confidence: 99%

Environmental Exposure to Lead and Progression of Chronic Renal Diseases

Lin²,

Lin-Tan³

2004

Journal of the American Society of Nephrology

110

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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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“…8] had suggested that an elevated body lead burden may be related to the progression of renal failure in patients with some preexisting renal disease. Both Behringer et al [9] and Ritz et al [10] have described significantly elevated post-EDTA urinary lead excretion in a group of patients with known renal disease such as glomerulonephritis and polycystic kidney diseases.…”

Section: Discussionmentioning

confidence: 99%

Disappearance of Immune Deposits with EDTA Chelation Therapy in a Case of IgA Nephropathy

Lin

Lim

1992

Am J Nephrol

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In this report, we describe the development of renal function impairment in a 33-year-old patient with mesangial IgA nephropathy and a history of recent gout. Increased body lead burden was identified with a positive EDTA mobilization test. The patient was treated with 1 g of edetate disodium calcium weekly for 2 months until normalization of urinary lead excretion. Improvement of renal function and proteinuria were noted. It was even more interesting to find that both immunofluorescence and electron microscopy studies of the second biopsy specimen revealed the loss of previous mesangial immune deposits. Our case demonstrated that lead may be a nonspecifically damaging factor related to the deterioration of renal function in patients with preexisting renal disease. Moreover, the disappearance of mesangial immune deposits after chelation therapy has not been previously documented. The pathogenetic basis of this observation is unknown, and its causal relationship with lead requires further elucidation.

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Urinary Lead Excretion in Uremic Patients

Cited by 36 publications

References 23 publications

Blood Lead in Hemodialysis Patients

Blood Lead in Hemodialysis Patients

Environmental Exposure to Lead and Progression of Chronic Renal Diseases

Disappearance of Immune Deposits with EDTA Chelation Therapy in a Case of IgA Nephropathy

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