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Excerpt from:

KIDNEYS (p. 153-154)

One of the most striking features in the early stage of fluorosis is the craving for fluids, accompanied by excess production of urine. Indeed, the more water the patient drinks the thirstier he or she becomes. (26) Polyuric nephropathy (a kidney disease characterized by excess urination) has been established as a major manifestation of fluoride toxicity in its early stage. (27) This fact and the important role of the kidneys in the elimination of fluoride from the body have led to extensive studies of the action of fluoride on kidneys.

Experimental Data. For instance, the presence of 500 ppm of sodium fluoride in the diet of rats for 21 to 28 days produced damage to the kidney tubules which regulate homeostasis (the equilibrium of ions) in the blood. (28) Similar levels of fluoride intake resulted in impaired kidney function and accounted for retention of non-protein nitrogen and of creatinine in the blood. (29) Such high intakes of fluoride also affect the glomeruli, the filtering units of the kidneys. (30) Fluoride in amounts of 2 to 7.5 mg given daily to rats for 18 to 48 weeks induced excessive thirst, frequent urination, and increased elimination of nitrogen through the urine. It also lowered the kidney threshold for sugar. Histologic examination showed vascular, glomerular, and tubular degeneration leading finally to interstitial fibrosis. (31)

In contrast to these short-term, relatively large-dose experiments, three Cornell University scientists more closely approached conditions of fluoridation by giving 0, 1, 5, and 10 ppm of fluoride in drinking water to 86 albino rats throughout 520 days or their approximate lifetime. (32) In these prolonged experiments with small amounts of fluoride corresponding to the daily human intake from fluoridated water, they found changes in the tubules which were similar to those from larger doses in short-term experiments; the kidneys of the control rats drinking nonfluoridated water remained normal. In a follow-up study, the same abnormalities were observed, but this time the authors concluded that the changes were due to "old age." (33,34) Such a difference in interpretation of the same results could have been easily resolved had the affected kidneys been analyzed for their fluoride content and compared with those of the control animals. Since no analyses were made, these studies did not rule out the possibility that consuming fluoridated water at the 1 ppm concentration throughout a person's lifetime can damage the kidneys. In fact, electron microscopic examination of the kidneys of monkeys drinking fluoridated water at a concentration of 1 and 5 ppm for 18 months reveals definite cytochemical abnormalities compared to controls on fluoride-free water. (19)

Observations on Humans. Related observations are also available on humans with skeletal fluorosis, where kidney disease is not uncommon. In persons drinking water containing 5 to 16.2 ppm fluoride (about 7 to 25 mg per day), kidney function was impaired, as indicated by depressed clearance of urea, lowered rate of filtration, and enhanced elimination of amino acids-products of protein metabolism. (35-37)

Unfortunately, it can rarely be determined whether a coexisting kidney dysfunction is actually the result of long-term fluoride intake or whether, on the other hand, the skeletal changes are precipitated by excessive fluoride storage in the body, because of a pre-existing kidney disorder.

References

19.  Manocha, S.L., Warner, H., and Olkowski, Z.: Cytochemical Response of Kidney, Liver, and Nervous System to Fluoride Ions in Drinking Water. Histochem. J. 7: 343-355, 1975. (See abstract)

26. Waldbott, G.L.: Incipient Chronic Fluorine Intoxication from Drinking Water. Acta Med. Scand., 156: 157-168, 1956.

27. Whitford, G.M., and Taves, D.R.: Fluoride-Induced Diuresis: Plasma Concentrations in the Rat. Proc. Soc. Exp. Biol. Med., 137:458-460, 1971; Fluoride-Induced Diuresis: Renal Tissue Solute Concentrations, Functional, Hemodynamic, and Histologic Correlates in the Rat. Anesthesiology, 39:416-427,1973.

28. Pindborg, J.J.: The Effect of 0.05 Per Cent Dietary Sodium Fluoride on the Rat Kidney. Acta Pharmacol. Toxicol., 13:36-45, 1957.

29. Kawahara, H.: Influence of Sodium Fluoride on the Urine Changes and Non-Protein Nitrogen, Creatinine and Sodium Chloride in Serum of Rabbits. Shikoku Acta Med., 8:266-272, 1956. (Abstracted in Fluoride, 5:46-48, 1972.)

30. Kawahara, H.: Experimental Studies on the Changes of the Kidney Due to Fluorosis. Part 3. Morphological Studies on the Changes of the Kidney of Rabbits and Growing Albino Rats Due to Sodium Fluoride. Shikoku Acta Med., 8:283-288, 1956. (Abstracted in Fluoride, 5:50-53, 1972.)

31. Bond, A.M., and Murray, M.M.: Kidney Function and Structure in Chronic Fluorosis. Br. J. Exp. Pathol., 33:168-176, 1952.

32. Ramseyer, W.F., Smith, C.A.H., and McCay, C.M.: Effect of Sodium Fluoride Administration on Body Changes in Old Rats. J. Gerontol., 12:14-19, 1957.

33. Bosworth, E.B., and McCay, C.M.: Pathologic Studies of Rat Kidneys: Absence of Effects Ascribed to Fluoride Following Long-Term Ingestion of Drinking Water Containing Fluoride. J. Dent. Res., 41:949-960, 1962.

34. Lovelace, F., Black, R.E., Kunz, Y., Smith, C.A.H., Bosworth, E.B., Wang, C.N., Austria, L., Park, R.L., and McCay, C.M.: Metabolism of Fluoride in Old Rats and Hamsters. J. Appl. Nutr., 12:142-151, 1959.

35. Shortt, H.E., McRobert, G.R., Barnard, T.W., and Mannadi Nayar, A.S.: Endemic Fluorosis in the Madras Presidency. Indian J. Med. Res., 25: 553-568, 1937.

36. Siddiqui, A.H.: Fluorosis in Nalgonda District, Hyderabad-Deccan. Br. Med. J., 2:1408-1413, 1955.

37. Singh, A., Jolly, S.S., Bansal, B.C., and Mathur, C.C.: Endemic Fluorosis. Epidemiological, Clinical and Biochemical Study of Chronic Fluorine Intoxication in Punjab (India). Medicine, 42:229-246, 1963; 44:97, 1965.

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