Key Findings - Fluoride & Renal Osteodystrophy:

1) Individuals with kidney disease have a diminished ability to excrete fluoride in their urine. As a result, kidney disease results in an elevated accumulation of fluoride in the bones.

2) The spectrum of bone disorders (e.g. osteomalacia, osteoporosis, osteosclerosis, and secondary hyperparathyroidism), collectively known as renal osteodystrophy, which are found in people with advanced kidney disease can all be individually produced, or exacerbated, by elevated fluoride exposure.

3) Aluminum's impact on bone is amplified in the presence of fluoride, and vice versa. Both elements accumulate to high levels in the bones of kidney patients, and it is quite plausible that the deterimental effect of aluminum in renal-osteodystrophy is enhanced by the presence of fluoride and/or the presence of aluminum-fluoride complexes.

4) No systematic studies have ever been conducted to investigate the relationship between fluoride exposure and severity of bone changes in individuals with kidney disease.

Excerpts from the Scientific Literature - Kidney Patients at Increased Risk of Fluorosis: (back to top)

"[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... The National Kidney Foundation in its ‘Position Paper on Fluoride—1980’ as well as the Kidney Health Australia express concern about fluoride retention in kidney patients. They caution physicians to monitor the fluoride intake of patients with advanced stages of kidney diseases. However, a number of reasons will account for the failure to monitor fluoride intake in patients with stages 4 and 5 of chronic kidney diseases and to detect early effects of fluoride retention on kidneys and bone. The safety margin for exposure to fluoride by renal patients is unknown, measurements of fluoride levels are not routine, the onset of skeletal fluorosis is slow and insidious, clinical symptoms of this skeletal disorder are vague, progression of renal functional decline is multifactorial and physicians are unaware of side effects of fluoride on kidneys or bone."
SOURCE: Schiffl H. (2008). Fluoridation of drinking water and chronic kidney disease: absence of evidence is not evidence of absence. Nephrology Dialysis Transplantation 23:411.

"Individuals with kidney disease have decreased ability to excrete fluoride in urine and are at risk of developing fluorosis even at normal recommended limit of 0.7 to 1.2 mg/l."
SOURCE: Bansal R, Tiwari SC. (2006). Back pain in chronic renal failure. Nephrology Dialysis Transplantation 21:2331-2332.

"In patients with reduced renal function, the potential for fluoride accumulation in the skeleton is increased. It has been known for many years that people with renal insufficiency have elevated plasma fluoride concentrations compared with normal healthy persons and are at a higher risk of developing skeletal fluorosis."
SOURCE: National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press, Washington D.C. p140.

"Persons with renal failure can have a four fold increase in skeletal fluoride content, are at more risk of spontaneous bone fractures, and akin to skeletal fluorosis even at 1.0 ppm fluoride in drinking water."
SOURCE: Ayoob S, Gupta AK. (2006). Fluoride in Drinking Water: A Review on the Status and Stress Effects. Critical Reviews in Environmental Science and Technology 36:433–487

"Skeletal fluorosis seems possible, especially in hot climates or with renal compromise, from drinking excessive quantities of instant or bottled teas. Our observations support the need for better understanding of the amounts and systemic effects of fluoride in teas."
SOURCE: Whyte M. (2006). Fluoride levels in bottled teas. American Journal of Medicine 119:189-190.

"We hypothesize that elevated serum F levels might contribute to the disturbances in mineral ion homeostasis that are observed in patients with CRI [Chronic Renal Insufficiency]. This is of particular concern since the incidence of dental fluorosis has increased due to increased F– uptake from multiple fluoridated sources. The ubiquitous presence of F in food and beverage products regardless of the degree of water fluoridation suggests that the overall F exposure in individuals with CRI may need to be more closely monitored."
SOURCE: Mathias RS, et al. (2000). Increased fluoride content in the femur growth plate and cortical bone of uremic rats. Pediatric Nephrology 14:935–939

"Though (skeletal) fluorosis is prevalent in certain geographic parts of the world, it is likely to occur... in people with latent kidney disease even when they consume relatively lower amounts of fluoride than in endemic regions."
SOURCE: Reddy DR, et al. (1993). Neuro-radiology of skeletal fluorosis. Annals of the Academy of Medicine, Singapore 22(3 Suppl):493-500.

"It would not be surprising if there were some undetected cases of skeletal fluorosis in the Australian population in individuals with pathological thirst disorders and/or impaired renal function. However, the matter has not been systematically examined. This matter should be the subject of careful and systematic review."
SOURCE: National Health and Medical Research Council. (1991). The effectiveness of water fluoridation. Canberra, Australia: Australian Government Publishing Service.

"Persons with chronic renal failures constitute a possible group at-risk with respect to the occurrence of skeletal fluorosis, because of an increased fluoride retention after oral intake. Based on the results of one study, in which the difference in retention between nephritic patients and healthy persons was quantified (average retention: 65% and 20%, respectively), a total daily intake of about 1.5 mg appears to be the maximum acceptable intake for nephritic patients. In view of the limitations of this comparative study and of the individual differences in retention and sensitivity, this figure must only be regarded as an indication."
SOURCE: National Institute for Public Health and Environmental Protection. (1989). Integrated criteria document fluorides. Report No 758474010. The Netherlands.

"The skeletal complication of fluoride is more common in renal disease. Because of the impairment in renal excretion of fluoride, high circulating concentrations of fluoride may be achieved in renal disease."
SOURCE: Pak CY. (1989). Fluoride and osteoporosis. Proceedings of the Society for Experimental Biology and Medicine 191: 278-86.

"Fluoridation of drinking water up to 1.2 ppm apparently does not pose a potential risk to bone provided the renal function is normal... We should, however, recognize that it is difficult to give a strict value for a safe fluoride concentration in drinking water, because individual susceptibility to fluoride varies."
SOURCE: Arnala I, et al. (1985). Effects of fluoride on bone in Finland. Histomorphometry of cadaver bone from low and high fluoride areas. Acta Orthop Scand. 56(2):161-6.

"Because the kidney is the main pathway of fluoride excretion, patients with chronic renal failure are especially vulnerable to osseous accumulation of ingested fluoride and to potentially deleterious effects."
SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38: 833-5.

"The finding of adverse effects (skeletal fluorosis) in (kidney) 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."
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.

"In the United States, there have been no reported cases of skeletal fluorosis in persons who drink water containing only one part per million (ppm) of fluoride. However, since no systematic studies have been carried out in patients with renal insufficiency, this possibility cannot be excluded with certainty."
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.

"It seems probable that some people with severe or long-term renal disease, which might not be advanced enough to require hemodialysis, can still experience reduced fluoride excretion to an extent that can lead to fluorosis, or aggravate skeletal complications associated with kidney disease... It has been estimated that one in every 25 Americans may have some form of kidney disease; it would seem imperative that the magnitude of risk to such a large sub-segment of the population be determined through extensive and careful study. To date, however, no studies of this sort have been carried out, and none is planned."
SOURCE: Groth, E. (1973), Two Issues of Science and Public Policy: Air Pollution Control in the San Francisco Bay Area, and Fluoridation of Community Water Supplies. Ph.D. Dissertation, Department of Biological Sciences, Stanford University, May 1973.

"It is generally agreed that water fluoridation is safe for persons with normal kidneys. Systemic fluorosis in patients with diminished renal function, however, seems a reasonable possibility. In such patients, fluoride may be retained with resulting higher tissue fluoride levels than in persons with normal renal function."
SOURCE: Juncos LI, Donadio JV. (1972). Renal failure and fluorosis. Journal of the American Medical Association 222:783-5.

"Prolonged polydipsia (excessive thirst) may be hazardous to persons who live in areas where the levels of fluoride in drinking water are not those usually associated with significant fluorosis."
SOURCE: Sauerbrunn BJ, et al. (1965). Chronic fluoride intoxication with fluorotic radiculomyelopathy. Annals of Internal Medicine 63: 1074-1078.

"The question of the effect of water containing 1 p.p.m. upon patients with severe impairment of kidney function requires special consideration in view of the fact that radiologic evidence of chronic fluorosis has been found in two persons with severe kidney disease who died at the early ages of 22 and 23 years, respectively..."
SOURCE: Heyroth F. (1952). Hearings Before the House Select Committee to Investigate the Use of Chemicals in Foods and Cosmetics, House of Representatives, 82nd Congress, Part 3, Washington D.C., Government Printing Office, p. 28.

"All patients with dental fluorosis and anemia and/or signs of renal impairment should have radiographic examinations of the skeletal system to rule out the existence of fluoride osteosclerosis... It is likely that the reason our patient retained fluorine in his bones was that he had renal damage of long standing; without this the osteosclerosis might not have developed."
SOURCE: Linsman JF, McMurray CA. (1943). Fluoride osteosclerosis from drinking water. Radiology 40: 474-484.

Excerpts from the Scientific Literature - Similarities between Fluorosis & Renal Osteodystrophy: (back to top)

"Fluoride is bone-seeking due to its high affinity for calcium phosphate and therefore accumulates in bone. Radiological changes can be quite similar to changes of renal osteodystrophy, and therefore the diagnosis may be missed unless specifically investigated."
SOURCE: Bansal R, Tiwari SC. (2006). Back pain in chronic renal failure. Nephrology Dialysis Transplantation 21:2331-2332.

"[R]enal disease and fluoride cause similar changes. This overlap makes it very difficult to assess the effect of fluoride per se in these patients."
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.

"The findings of osteosclerosis, osteomalacia and increased bone resorption have been confirmed in experimental fluorosis in animals. It can be seen, therefore, that fluoride bone disease could mimic renal osteodystrophy."
SOURCE: Cordy PE, et al. (1974). Bone disease in hemodialysis patients with particular reference to the effect of fluoride. Transactions of the American Society of Artifical Internal Organs 20: 197-202.

"[T]he observed changes (osteomalacia, osteitis fibrosa and osteoporosis) were similar to those induced by high doses of fluoride in humans and experimental animals, in which widened osteoid seams have been observed, and where increased areas of resorption due to secondary hyperparathyroidism may be seen."
SOURCE: Posen GA, et al. (1971). Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water. Fluoride 4: 114- 128.

"Osteosclerosis from chronic renal disease associated with secondary hyperparathyroidism may produce similar changes (as fluorosis), and indeed may have intensified the findings (of fluorosis) in one of our patients."
SOURCE: Morris JW. (1965). Skeletal fluorosis among indians of the American Southwest. American Journal of Roentgenology, Radium Therapy & Nuclear Medicine 94: 608-615.

In the fluoride-treated patients, "we observed osteoclasts resorbing bone beneath osteoid seams, and fragments of osteoid isolated in the bone marrow. This type of resorption beneath unmineralized bone matrix is often observed in osteomalacia, particularly that caused by renal abnormalities and associated secondary hyperparathyroidism."
SOURCE: Lundy MW, et al. (1995). Histomophometric analysis of iliac crest bone biopsies in placebo-treated versus fluoride-treated subjects. Osteoporosis International 5:115-129.

"During our field studies our attention was drawn to the high incidence of bone disease and bony leg deformities with clinical invalidism in children exposed to high intake of endemic fluoride in drinking water. Due to variable and unusual clinical features, these children (with fluorosis) had often been mistaken for rickets, renal osteodystrophy, osteosclerosis and hereditary osteopathies etc."
SOURCE: Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. Indian Journal of Pediatrics 65:371-81.

"A 40-year-old American Indian woman with chronic pyelonephritis and renal failure complained of progressive muscular weakness, fatigue, and increasingly severe pain in her ribs, low back, and left hip. X-ray study of these areas showed evidence of osteosclerosis, compatible with either renal osteodystrophy or skeletal fluorosis... No other pathologic changes were apparent in the bones or ligaments..."
SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38: 833-5.

Excerpts from the Scientific Literature - Fluoride as a Contributing Factor to Renal Osteodystrophy: (back to top)

"Additional studies should be carried out to determine the incidence, prevalence, and severity of renal osteodystrophy in patients with renal impairments in areas where there is fluoride at up to 4 mg/L in the drinking water."
SOURCE: National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press, Washington D.C. p258.

"Fluoride interfered with bone mineralization and increased osteoid content, which was most evident in osteomalacia and the mixed bone disorder. In addition, fluoride may interact with aluminum to worsen the osteomalacic lesion."
SOURCE: Ng AHM, et al. (2004). Association between fluoride, magnesium, aluminum and bone quality in renal osteodystrophy. Bone 34: 216-224.

"fluoride-treated, aluminum-loaded rats accumulated a sevenfold larger amount of osteoid volume as compared to (the aluminum-only group) and exhibited an increase in osteoid surface of a corresponding degree...The results of our study confirm that pretreatment and concurrent administration of fluoride during aluminum loading does have a profound impact on the evolution of aluminum-induced osteodystrophy."
SOURCE: Ittel TH, et al. (1992). Effect of fluoride on aluminum-induced bone disease in rats with renal failure. Kidney International 41: 1340-1348.

"It is possible that deposition of aluminum-fluoride complexes at the mineralized bone-osteoid interface disturb mineralization more effectively than aluminum itself... Exposure to fluoride will have to be considered when evaluating aluminum-related bone disease in clinical cases or in experimental models."
SOURCE: Ittel TH, et al. (1992). Effect of fluoride on aluminum-induced bone disease in rats with renal failure. Kidney International 41: 1340-1348.

"Renal failure augmented skeletal retention of excessive fluoride intake which, in turn, appears to have intensified symptomatic renal osteodystrophy."
SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38: 833-5.

"In the present case, elimination of dietary fluoride and treatment with calcitrol was associated with improvement in the symptoms and biochemical findings of osteodystrophy, perhaps as a result of a decrease in unmineralized osteoid."
SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38: 833-5.

Excerpts from the Scientific Literature - No Systematic Studies Investigating Relationship between Fluoride/Renal Osteodystrophy: (back to top)

"a fairly substantial body of research indicates that people with kidney dysfunction are at increased risk of developing some degree of skeletal fluorosis... However, there has been no systematic survey of people with impaired kidney function to determine how many actually suffer a degree of skeletal fluorosis that is clearly detrimental to their health."
SOURCE: Hileman B. (1988). Fluoridation of water.Questions about health risks and benefits remain after more than 40 years. Chemical and Engineering News August 1, 1988, 26-42.

"In the United States, there have been no reported cases of skeletal fluorosis in persons who drink water containing only one part per million (ppm) of fluoride. However, since no systematic studies have been carried out in patients with renal insufficiency, this possibility cannot be excluded with certainty."
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.

"It seems probable that some people with severe or long-term renal disease, which might not be advanced enough to require hemodialysis, can still experience reduced fluoride excretion to an extent that can lead to fluorosis, or aggravate skeletal complications associated with kidney disease... It has been estimated that one in every 25 Americans may have some form of kidney disease; it would seem imperative that the magnitude of risk to such a large sub-segment of the population be determined through extensive and careful study. To date, however, no studies of this sort have been carried out, and none is planned."
SOURCE: Groth, E. (1973). Two Issues of Science and Public Policy: Air Pollution Control in the San Francisco Bay Area, and Fluoridation of Community Water Supplies. Ph.D. Dissertation, Department of Biological Sciences, Stanford University, May 1973.

"Information is particularly needed on fluoride plasma and bone concentrations in people with small-to-moderate changes in renal function as well as in those with serious renal deficiency."
SOURCE: National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press, Washington D.C. p 9.

General Info - Renal Osteodystrophy: (back to top)

"The medical term 'renal' describes things related to the kidneys. Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain the proper levels of calcium and phosphorus in your blood. It's a common problem in people with kidney disease and affects 90 percent of dialysis patients."
SOURCE: National Institute of Diabetes and Digestive and Kidney Diseases (UK)

“Osteodystrophy is a combination of bone disorders that is usually caused by chronic kidney failure (renal disease). The bone disorders affecting patients with osteodystrophy include varying combinations and degrees of osteoporosis, osteomalacia, osteitis fibrosa, and osteosclerosis.”
SOURCE: MedicineNet.com

"The most common presentation of renal osteodystrophy is a combination of osteomalacia, secondary hyperparathyroidism, and a varying degree of osteosclerosis."
SOURCE: eMedicine.com

"Renal osteodystrophy may cause osteosclerosis, soft tissue calcification, and bone resorption... Soft tissue calcifications may take the form of the large, cloudlike collections in a periarticular distribution known as tumoral calcinosis."
SOURCE: AmershamHealth.com

"The changes in bone seen in patients with chronic renal insufficiency are complex in that there is a spectrum of findings. At one extreme is pure osteotis fibrosis, which shows a pattern of excessive bone resorption... At the other extreme is osteomalacic bone disease that is due to a deficiency of the active vitamin D metabolites normally produced by the kidneys. Osteomalacia is recognized histologically by excessive amounts of osteoid (that is, unmineralized bone matrix)... In addition, the patients occasionally have sclerosis. Histologically, the sclerosed bone exhibits an increase in the thickness of the trabeculae, and roentgenographically, there is a coarsening of the trabecular pattern with increased opacity of the mineralized tissues. Sclerosis and increased amounts of osteoid are also features of fluorosis."
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.

Symptoms - Renal Osteodystrophy: (back to top)

"Renal osteodystrophy, if not treated, can lead to severe disability.  Patients suffering from severe cases are often unable to walk or get out of bed without help."
SOURCE: iKidney.com

"The most common complication of renal osteodystrophy is fracture, which may be insufficiency fractures through osteomalacic bone or pathologic fractures through brown tumors or amyloid deposits."
SOURCE: eMedicine.com

"The bone changes from renal osteodystrophy can begin many years before symptoms appear in adults with kidney disease. For this reason, it's called the "silent crippler." The symptoms of renal osteodystrophy aren't usually seen in adults until they have been on dialysis for several years. Older patients and women who have gone through menopause are at greater risk for this disease because they're already vulnerable to osteoporosis, even without kidney disease. If left untreated, the bones gradually become thin and weak, and a person with renal osteodystrophy may begin to feel bone and joint pain. There's also an increased risk of bone fractures."
SOURCE: National Institute of Diabetes and Digestive and Kidney Diseases (UK)

"Renal osteodystrophy is most serious in children because their bones are still growing. The condition slows growth and causes deformities. One such deformity occurs when the legs bend inward or outward (toward or away from the body); this deformity is referred to as "renal rickets." Another important consequence is short stature."
SOURCE: National Institute of Diabetes and Digestive and Kidney Diseases (UK)

Frequency - Renal Osteodystrophy: (back to top)

"In the US: Statistics from the Health Care Financing Administration report that more than 230,000 Americans are under treatment for end-stage renal disease (ESRD). Renal osteodystrophy rarely is seen prior to the laboratory and clinical diagnosis of renal failure."
SOURCE: eMedicine.com