Plasma aluminium: a redundant test for patients on dialysis?

Gault, P M; Allen, K R; Newton, K. E.

doi:10.1258/0004563053026862

Cited by 25 publications

(30 citation statements)

References 13 publications

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“…The normal plasma aluminum concentration is around 0.1 µM, while among patients with kidney failure receiving dialysis treatment or workers in an aluminum manufacturing factory the levels can reach 3.7 µM (Becaria et al 2002; Gault et al 2005; Banks et al 2006). Thus, the levels of alumina and nano-alumina used in the present study were within the pathological range.…”

Section: Discussionmentioning

confidence: 99%

“…Alumina is among the most abundantly produced chemical in nanosized particles, estimated to account for approximately 20% of the 2005 world market of nanoparticles (Rittner 2002). Aluminum can act as a disrupter of cell membranes and has been implicated as an etiological factor in a variety of neurode-generative diseases (Vorbrodt et al 1994; Gault et al 2005). For example, a number of studies have revealed aluminum deposits in the brains of Alzheimer’s disease patients, where it may potentiate the neurotoxicity and facilitate the disease process (Yokel and McNamara 2001; Becaria et al 2002; Yokel et al 2002; Service 2004; Kawahara 2005; Lukiw et al 2005; Banks et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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Manufactured Aluminum Oxide Nanoparticles Decrease Expression of Tight Junction Proteins in Brain Vasculature

Chen

Yokel

Hennig

et al. 2008

J Neuroimmune Pharmacol

253

129

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Manufactured nanoparticles of aluminum oxide (nano-alumina) have been widely used in the environment; however, their potential toxicity provides a growing concern for human health. The present study focuses on the hypothesis that nano-alumina can affect the blood-brain barrier and induce endothelial toxicity. In the first series of experiments, human brain microvascular endothelial cells (HBMEC) were exposed to alumina and control nanoparticles in dose-and time-responsive manners. Treatment with nano-alumina markedly reduced HBMEC viability, altered mitochondrial potential, increased cellular oxidation, and decreased tight junction protein expression as compared to control nanoparticles. Alterations of tight junction protein levels were prevented by cellular enrichment with glutathione. In the second series of experiments, rats were infused with nanoalumina at the dose of 29 mg/kg and the brains were stained for expression of tight junction proteins. Treatment with nano-alumina resulted in a marked fragmentation and disruption of integrity of claudin-5 and occludin. These results indicate that cerebral vasculature can be affected by nanoalumina. In addition, our data indicate that alterations of mitochondrial functions may be the underlying mechanism of nano-alumina toxicity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Manufactured Aluminum Oxide Nanoparticles Decrease Expression of Tight Junction Proteins in Brain Vasculature

Chen

Yokel

Hennig

et al. 2008

J Neuroimmune Pharmacol

253

129

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“…Except in rare cases of equipment failure (CDC 2008) or inadvertent introduction of Al into dialysate (Berend et al 2001), elevated serum Al and risk of dialysis encephalopathy have for all practical purposes been eliminated by controlling Al concentrations in dialysate to less than 10 μg/L (ANSI/AAMI 2004, CAN/CSA-ISO 2011) and substituting Al phosphate binders with Ca acetate, Ca carbonate, sevelamer, or lanthanum. Abnormally high plasma and serum Al levels can result after daily consumption of the customary approximately 4 g of Al-based phosphate chelators even with regular clinical monitoring (Arenas et al 2008, Cárdenas et al 2010, Gault et al 2006). Those observations contrast with Jimenez et al (2011) and Mudge et al (2011) who concluded Al-based phosphate chelators are not only economical and effective, but they have a high rate of patient compliance without undue health risk.…”

Section: Environmental and Occupational Exposurementioning

confidence: 99%

Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

Willhite¹,

Karyakina²,

Yokel³

et al. 2014

Critical Reviews in Toxicology

338

201

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Aluminum (Al) is a ubiquitous substance encountered both naturally (as the third most abundant element) and intentionally (used in water, foods, pharmaceuticals, and vaccines); it is also present in ambient and occupational airborne particulates. Existing data underscore the importance of Al physical and chemical forms in relation to its uptake, accumulation, and systemic bioavailability.Address for correspondence: Calvin C. Willhite, Risk Sciences International, 55 Metcalfe Street, Suite 700, Ottawa, ON, Canada. calvinwillhite@hotmail.com. Declaration of interestPartial funding for this work was provided by a contract to review the recent scientific literature on health effects of aluminum between the International Aluminium Institute (IAI, www.world-aluminium.org), the Aluminium Reach Consortium (ARC, www.aluminium-reach-consortium.eu), and Risk Sciences International (RSI, www.risksciences.com), a Canadian company established in 2006 in partnership with the University of Ottawa. Additional financial support was provided by the Natural Sciences and Engineering Research Council of Canada (NSERC) to D. Krewski, who holds the NSERC Chair in Risk Science at the University of Ottawa. C.C. Willhite, N.A. Karyakina, F. Momoli, and N. Yenugadhati were compensated by RSI for their contributions to the review. I. Arnold, T. Wisniewski and R. Yokel received no compensation from RSI for their contributions to this work. The authors, whose affiliations are shown on the title page, had sole responsibility for preparation of this paper, including determining the strategy for reviewing the scientific literature summarized in this article, synthesizing the findings, and drawing conclusions. Scientists associated with IAI/ARC were given the opportunity to review and offer technical comments on the paper, prior to submission to Critical Reviews in Toxicology. I. Arnold serves as a consultant to the International Aluminium Institute. None of the authors have appeared before regulatory agencies on behalf of the sponsors, or appeared as experts in legal proceedings concerning matters reviewed in this paper. The scientific opinions and conclusions expressed in the paper are exclusively those of the authors, and are independent of the sources of financial support. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptThe present review represents a systematic examination of the peer-reviewed literature on the adverse health effects of Al materials published since a previous critical evaluation compiled by Krewski et al. (2007). The scientific literature on the adverse health effects of Al is extensive. Health risk assessments for Al must take into account individual co-factors (e.g., age, renal function, diet, gastric pH). Conclusions from the current review point to the need for refinement of the PTWI, reduction of Al contamination in PN solutions, justification for routine addition of Al to vaccines, and harmonization of OELs for Al substances.

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“…Some experts reasoned that this may be largely attributed to the improvement in water quality [8,21,22]. There was still a question about the role of aluminum monitoring in patients with long-term HD [22], whereas mild to moderate aluminum exposure from aluminum-base phosphate binder was still observed [23,24].…”

Section: Discussionmentioning

confidence: 99%

Effect of aluminum on markers of bone formation resorption in chronic hemodialysis patients

et al. 2014

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Background:The prevalence of aluminum (Al)-related toxicity in hemodialysis (HD) patients has declined. However, some HD patients continue to receive Al-based phosphate binders, in part because of the expense of Al-free binders. Objective: To explore the effect of Al-based binders and their discontinuation on iron status, and markers of bone formation resorption in HD patients. Methods: Following an initial screen of serum Al levels in 37 HD patients, a second screening was performed after discontinuation of Al-based binders in a 2-year follow-up. A desferrioxamine (DFO; 5 mg/kg) test, and assessment of iron status and bone markers were conducted in the second screening. Results: Mean serum Al level was initially 27.8 ± 10.3 μg/L. Thirteen patients had a serum Al >30 μg/L, a level considered possibly toxic. There was a positive correlation between serum Al levels, HD duration, and cumulative dose of Al-based binder. At the second screening, the mean serum Al level decreased to 12.5 ± 7.4 μg/L. The mean serum Al level increased to 26.0 ± 14.7 μg/L post-DFO, but in none of the patients did the change in serum Al exceed the 50 μg/L threshold associated with Al-induced bone disease. The decrease in serum Al level was associated with a significant increase in intact parathyroid hormone (iPTH) whereas total alkaline phosphatase did not change. Conclusions:We recommend that if Al-based phosphate binders are used in HD patients, serum Al level, iron, and markers of bone formation resorption be closely monitored to ensure safe use of these drugs.

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Plasma aluminium: a redundant test for patients on dialysis?

Abstract: Addresses

Cited by 25 publications

References 13 publications

Manufactured Aluminum Oxide Nanoparticles Decrease Expression of Tight Junction Proteins in Brain Vasculature

Manufactured Aluminum Oxide Nanoparticles Decrease Expression of Tight Junction Proteins in Brain Vasculature

Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

Effect of aluminum on markers of bone formation resorption in chronic hemodialysis patients

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