Chromium-Induced Kidney Disease

Wedeen, Richard P.; Qian, Lifen

doi:10.2307/3431139

Cited by 62 publications

(40 citation statements)

References 12 publications

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“…In two-thii-ds of the i-ats in the second part of the studly, thei-e were no feces in the first 6 hr. The urinai-y patterns were moi-e level in that the chiomium output at each time pei-iod was highei-fiom the soil-tieated animals.…”

Section: Experimental Design and Resultsmentioning

confidence: 89%

Oral Bioavailability of Chromium from a Specific Site

Witmer

Harris

Shupack

1991

Environmental Health Perspectives

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Analysis of soil from a specific site in New Jersey indicated a low level of sodium and chromium present as a calcium compound. Chromium was then administered orally to young, mature male rats at a level of 240,g/kg for 14 days as chromium-contaminated soil, as CaCrO4, and as an equimolar mixture of the soil and calcium salts for 14 days. The rats were sacrificed 24 hr after the last dosing, and tissues were taken immediately for chromium analysis. Blood, muscle, and liver contained the highest levels of chromium in these animals, although kidney contained the highest concentration per gram of tissue. The total amount of chromium in the tissues was less than 2% of the administered chromium. In a study of the excretion of chromium, the animals were dosed orally for 8 days (with CaCrO4 or contaminated soil, each at the level of 240 pmole Cr/ kg), and the chromium in feces and urine was determined on days 1, 2, 7, and 8. After cessation of dosing for 27 days, the same rats were dosed for 2 days at the same level, and chromium in urine and feces was determined for the 2 days. The animals administered the chromium in soil had higher levels of chromium in both urine and feces on all days compared to the group fed the CaCrO4. The total recovery of chromium in any of the 2-day periods was less than 50% of the chromium administered during that period.

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Section: Experimental Design and Resultsmentioning

confidence: 89%

Oral Bioavailability of Chromium from a Specific Site

Witmer

Harris

Shupack

1991

Environmental Health Perspectives

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“…37 Nonreadily internalized metalprotein complexes, such as albumin or metallothionein, typically act to inhibit metal bioreactivity locally by sequestering metal ions. 27 The concentrations of Cr and Ti detected in the fractionated serum of groups I, II, and III and the total protein within these same fractions were used to provide a means of characterizing the metal-protein binding affinity based on a metal to protein molar ratio. The differential pattern of Cr or Ti affinity for different serum proteins was found to be different than the metal concentration profiles depicted in Figures 3, 4, and 5.…”

Section: Discussionmentioning

confidence: 99%

“…However, other investigations have linked metal bioreactivity to both the affinity and avidity of metal ion-ligand binding. 27,31,[36][37][38] The affinity and avidity of ligand binding can both affect the bioavailability of metal ions to cell membranes, an important factor dictating the degree of uptake into cells. 36,39 Metals bound to proteins that act to facilitate metal entry into cells are generally more likely to be toxic when compared with metal-protein complexes not readily internalized by cells.…”

Section: Discussionmentioning

confidence: 99%

“…The absence of proof of such causality is not proof of absence: specific metal degradation products (and their associated ligands) generated from orthopedic implants have not been previously characterized and, additionally, no prospective cohort or case control studies of the delayed effects of low-level chronic long-term metal exposure have been published. 27 At the outset of this investigation we hypothesized that circulating metal originating from implant corrosion and wear is primarily bound by specific serum proteins that form complexes that then may mediate the biologic reactivity. We examined this hypothesis by characterizing the Cr and Ti content in fractionated serum in three groups of patients: controls without implants, patients with Cr containing CoCr alloy hip…”

Section: Introductionmentioning

confidence: 99%

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Systemic metal-protein binding associated with total joint replacement arthroplasty

Hallab

Jacobs

Skipor

et al. 2000

J. Biomed. Mater. Res.

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The distribution of titanium [Ti] and chromium [Cr] in serum protein fractions of patients with and without total joint replacements containing Cr and Ti was studied. Three groups were evaluated: 10 patients with cobalt-chromium [CoCr] alloy prostheses and known elevated levels of Cr; 10 patients with Ti containing implants and known elevated levels of Ti; and 10 age matched controls without prostheses. Metal-protein binding was also examined by adding various concentrations of Cr(+3) (CrCl(3)) to control serum. Cr and Ti were bound to serum proteins within specific molecular weight ranges in both patient groups. Two molecular weight ranges were found to bind Cr (at approximately 70 and approximately 180 kDa) in patients with CoCr alloy prostheses, whereas a single molecular weight range (at approximately 70 kDa) was found to bind Ti in patients with Ti alloy implants. This metal-protein binding was reproduced in vitro by adding CrCl(3) at concentrations of approximately 100 and 1000 ppb Cr, which is orders of magnitude higher than that contained in the serum of patients with CoCr alloy implants ( approximately 3 ppb Cr). This suggests that protein binding is initiated in the periprosthetic space where metal concentrations are typically 2-3 orders of magnitude higher than that observed systemically in the serum. In vitro, high molecular weight proteins including immunoglobulins demonstrated the highest affinity to Cr. Determination of specific protein carriers of metal degradation products is an essential component in the assessment of the long-term biological affects of total joint replacement devices.

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“…Few epidemiological studies have specifically assessed chromium and arsenic exposure as potential risk factors for kidney disease (Wedeen and Qian, 1991;Zheng et al, 2014). The lack of sufficient evidence in humans is principally due to the lack of study quality and prospective evidence, together with the use of non-sensitive kidney injury biomarkers.…”

Section: Discussionmentioning

confidence: 99%