Abstract
Although sevoflurane is used in clinical anesthesia, its effects on renal function and inorganic fluoride (F-) kinetics in patients with chronic renal failure (CRF) have not been determined. We investigated F- kinetics and renal tubular function in sevoflurane anesthesia in CRF patients having hemodialysis. Five patients dialyzed and five with normal renal function undergoing parathyroidectomy or thyroidectomy were anesthetized with sevoflurane (1.0%-2.5%) and nitrous oxide in oxygen. Serum and urine levels of F-, blood urea nitrogen (BUN), serum creatinine (Cr), serum and urine beta 2-microglobulin (BMG) levels, and urine N-acetyl-beta-D-glucosaminidase (NAG) level were measured. BUN, Cr, and serum and urine BMG levels were significantly higher in the CRF patients than in the controls. There were no differences in serum F- level, rate of elimination, and area under the curve of serum F- levels between the two groups. However, the CRF patients had a significantly lower level of urine F- than control subjects. These data suggest that the F- kinetics in the CRF patients is different from that in normal renal function subjects. This clinical study with a limited number of patients may facilitate further studies to define the mechanisms of differences in the F- kinetics between normal subjects and CRF patients having hemodialysis after sevoflurane anesthesia.
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Long-term follow up of ionic plasma fluoride level in patients receiving hemodialysis treatment
The elimination half-life of fluoride is significantly increased in patients with chronic renal failure. This led us to conduct a study of variations of its plasma levels in 35 patients receiving dialysis treatment. In this population, there is a gaussian distribution of the values before and after the hemodialysis session,
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Exposure to excessive fluoride during hemodialysis.
The safety of fluoridated community water supplies for dialysate and long-term intermittent hemodialysis has been questioned since 1965 [1]. The only significant means of clearing fluoride from body fluids are renal excretion and incorporation into bone [2]. When dialysate is prepared with fluoridated water, fluoride ion moves along a concentration
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Studies on serum fluoride and bone metabolism in patients with long term hemodialysis
With growing experience of the long-term treatment of patients with end stage renal disease by hemodialysis, the safety of fluoridated water supply for dialysate and the effect on the bone metabolism has been discussed. In this study, concentrations of fluoride (F), calcium (Ga). aluminum (AI) and biochemical indices of bone metabolism,
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Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water
Serum and bone fluoride concentrations of ten patients maintained on long-term hemodialysis with fluoridated water (1 ppm, i.e., 50uM) were correlated with duration of treatment and the occurrence of clinical, radiological, and histological manifestations of bone disease. Two patients had symptomatic renal osteodystrophy when accepted on the program, whereas six
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Effects of fluoride on bone metabolism in patients with hemodialysis
The maior pathway of fluoride elimination from the human body is the kidney. The discharge of fluoride into urine depends on the clearance of the kidney. Fluoride in serum of hemodialysis patients is higher than that of healthy subjects. Fluoride is not reduced sufficiently with hemodialysis. Those patients are in
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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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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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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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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