Fluoride Action Network

Fluoride Gels & Kidney Function

May 1st, 2012

Scientists have found that the application of “Fluoride Gels” at the dental office causes very high spikes in the blood fluoride level. The high spikes in blood fluoride levels are a result of three factors: the high concentration of fluoride in the gel (= 12.3 mg of fluoride in each milliliter of gel), the gel’s high acidity (which prompts excess salivation and ingestion), and the creation of hydrofluoric acid in the mouth (which allows fluoride to cross directly through the gum membrane).

One consequence from introducing high levels of fluoride into the blood is that kidney function can be impaired.  Specifically, fluoride impairs the kidney’s ability to concentrate, thus producing a diabetes insipidus-type condition marked by excessive urination. (Mazze 1977). The concentration of fluoride that causes this effect (570 ppb) is lower than the concentration that children (up to 1,450 ppb) and adults (up to 950 ppb) can receive in their blood following fluoride-gel treatment. While the kidney defect is believed to be reversible (i.e., it ends when the fluoride clears from the blood), no research has yet been conducted to determine the long-term kidney health of those who have repeatedly experienced short-term toxic exposures to fluoride.

Here is a summary of the issue from Gary Whitford:

“The kidney is one of the target organs in acute fluoride toxicity. This is due in part to the fact that, at any given plasma fluoride level and  compared with other organs, the cells of the kidney are exposed to relatively high fluoride concentrations. Moreover, like sodium and chloride, fluoride shows a progressive cortex-to-medulla concentration gradient, so that the inner medulla cortex concentration ratio is between three and four. Thus, those portions of the nephron which are responsible for the kidney’s ability to concentrate urine and conserve water for the organism (the loops of Henle, collecting ducts, and vasa recta) are exposed to the highest fluoride concentrations within the kidney. In the 1960s, it was first reported that a high-output renal failure was experienced by some patients who had been anesthetized with methoxylflurane, a volatile fluorinated anesthetic. The syndrome, which resembles diabetes insipidus, was characterized by an ADH-resistant diuresis, a low urinary osmolarity, and, in some seriously affected patients, hemoconcentration and electrolyte imbalances. . . . It has since been determined that the renal concentrating defect can be produced in rats, dogs, and humans and that the plasma fluoride level threshold for the problem is approximately 30 umol/L. . . . As noted above plasma fluoride concentrations of some patients who have been treated with 1.23% APF gels reach levels of 30 umol/L or more for several hours. It is likely that some of these patients would experience the renal concentrating defect during these periods and perhaps for several hours thereafter. Research with human subjects is needed to evaluate this possibility. Although the renal concentrating defect is reversible and without known long-term sequelae, it represents a physiologic disturbance that can be avoided, mainly by reducing the amounts of fluoride available for systemic absorption during APF gel applications.”
SOURCE: Whitford GM, et al. (1987). Topical fluorides: effects on physiologic and biochemical processes. J Dent Res. 66(5):1072-8.