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The concept that osteomalacia becomes progressively worse on chronic dialysis was reinforced by the findings in the repeat bone biopsies in that 6 of the 8 patients showed a significant increase in their osteoid index. . . . Thus, the progression of osteomalacia appears to be the main reason for the increasing incidence of bone pain and pseudofractures which we and others have observed in patients on chronic dialysis for periods longer than 6 months. Jowsey, et al, has reported similar findings. When the patients reported by Kim, et al. are classified in the same manner as ours were, a similar higher incidence of osteomalacia and absence of severe osteitis fibrosa was observed in patients on chronic dialysis for more than 6 months… The reason(s) for the progression of osteomalacia, which we observed in our chronic dialysis patients, remain(s) unclear. Factors which could result in impaired mineralization which must be considered include fluoride, hypermagnesemia, and phosphate depletion.
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Osteomalacia is associated with high bone fluoride content in dialysis patients
Osteomalacia is now rarely observed in hemodialyzed patients since the prevention of aluminum intoxication and vitamin D deficiency. However, this disorder is still present and may be responsible for bone fractures. Fluoride overload is responsible for mineralization defects. We therefore prospectively measured the bone fluoride content in all dialysis osteomalacic
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Comparison of renal osteodystrophy in patients dialyzed with deionized and non-deionized water
Discussion There are 2 major types of osteodystrophy which occur in various combinations in dialysis patients. The first and most commonly predominant is secondary hyperparathyroidism. This appears to be preventable, or at least controllable, with a bath calcium concentration above 6 mg%. The second type is osteomalacia. In certain centers it
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Bone disease in hemodialysis patients with particular reference to the effect of fluoride
Forty-one patients on our chronic hemodialysis program were assessed for the degree of progression of bone disease over an average period of 46 months. Seven patients were using a fluoridated dialysate. Four of these seven patients developed a marked increase in osteoid as judged by bone biopsy, while in the
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Association between fluoride, magnesium, aluminum and bone quality in renal osteodystrophy
INTRODUCTION: Trace elements are known to influence bone metabolism; however, their effects may be exacerbated in renal failure because dialysis patients are unable to excrete excess elements properly. Our study correlated bone quality in dialysis patients with levels of bone fluoride, magnesium, and aluminum. A number of studies have linked
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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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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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Fluoride & Osteomalacia
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid content of bone. Osteoid is unmineralized bone tissue. When bones have too much of it, they become soft and prone to fracture -- a condition known as osteomalacia. As shown below, fluoride has repeatedly been
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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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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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Skeletal Fluorosis in the U.S.
Although there has been a notable absence of systematic studies on skeletal fluorosis in the U.S., the available evidence indicates that the consumption of artificially fluoridated water is likely to cause skeletal fluorosis and other forms of bone disease in people with kidney disease and other vulnerable populations.
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