Abstract
This study was conducted to test the hypothesis that the margin of safe fluoride exposure is narrowed in rats that are physiologically compromised by renal dysfunction. The study objective was to determine whether increases in fluoride retention and tissue fluoride levels in rats with surgically induced renal insufficiency result in toxic fluoride effects not ordinarily observed in healthy animals. Uremic and sham-operated control rats received 0 microg/ml, 5 (0.26 mmol/l), 15 (0.79), or 50 microg/ml (2.63 mmol/l) of fluoride in their drinking water for 3 or 6 months. Fluoride retention was monitored, and, following euthanasia, tissue fluoride and biochemical markers of tissue function were analyzed. Selected tissues were saved for histology, and bone marrow cells were harvested for determining the frequency of sister chromatid exchange, a marker of genetic damage. In spite of significantly higher levels of fluoride in the tissues of the animals with renal insufficiency, there were no clinically adverse, fluoride-induced, extraskeletal physiological, biochemical, or genetic effects of chronic exposure to common levels of fluoride in these rats.
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Fluoride metabolism and renal osteodystrophy in regular dialysis treatment
Fluoride in plasma, urine and bone tissue ash were estimated using a fluoride-ion electrode in 20 control persons (CP), 32 patients with compensated chronic renal failure (CRFP) and 59 patients in RDT (RDTP). The increase in plasma fluoride (CP: 2.4 +/- 1.4, CRFP: 6.5 +/- 2.2, RDTP: 12.3 +/- 4.5
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Enamel hypoplasia in children with renal disease in a fluoridated area
The aim of this study was to compare the frequency of enamel hypoplasia in children with renal disease and healthy children, all of whom live in a fluoridated area. A cross-sectional study was made in 42 children divided into 2 groups. To describe enamel changes, 3 diagnostic criteria were applied:
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Renal failure and fluorosis
Two patients had a combination of renal insufficiency and systemic fluorosis. One had bilateral vesicoureteral reflux and recurrent pyelonephritis, with resulting renal atrophy; the other had probable renal dysgenesis of indeterminate origin. Both patients had polydipsia, polyuria, and markedly reduced renal function. Both also had clinical and roentgenographic evidence of
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Ionic serum fluoride concentrations and age in a low-fluoride community
Some previous studies indicate extra fluoride retention in human bones caused by severe renal insufficiency. Plasma and serum fluoride concentrations may also be elevated in a fluoridated community. The results from low-fluoride areas are less consistent. The first aim of the present study was thus to test the relation between
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The effects of fluoride on the bones and teeth from ICR-derived glomerulonephritis (ICGN) mice and ICR mice after subacute exposure
Dental fluorosis and osteofluorosis from using drinking water contaminated with the fluoride ion (F) have been reported from many countries including the People’s Republic of China and India. Because fluoride is excreted by the kidney and the toxic effects of F are more severe when renal failure is present, Imprinting
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Similarities between Skeletal Fluorosis and Renal Osteodystrophy
It is quite possible, and indeed likely, that some kidney patients diagnosed with renal osteodystrophy are either suffering from skeletal fluorosis or their condition is being complicated/exacerbated by fluoride exposure.
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Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
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Dental Fluorosis & Enamel Hypoplasia in Children with Kidney Disease
Children with kidney disease are known to have high levels of fluoride in their blood and to be at risk for disfiguring tooth defects. Research suggests that high levels of fluoride in blood, which can cause the tooth defect known as dental fluorosis, can contribute to the defects that occur
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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Exposure Pathways Linked to Skeletal Fluorosis
Excessive fluoride exposure from any source -- and from all sources combined -- can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include: Fluoridated Water for Kidney Patients Excessive Tea Consumption High-Fluoride Well Water Industrial Fluoride Exposure Fluorinated Pharmaceuticals (Voriconazole
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