It has long been suspected that fluoride may contribute to the formation of kidney stones. This suspicion has recently gained support from a study of an American man with skeletal fluorosis. According to the authors:
“A new, important, medical problem (that seemed temporally related to cessation of fluoride exposure and subsequent negative calcium balance) was renal calculus formation, with stones composed of calcium oxalate. The first episode occurred 9 months following diagnosis. He experienced numerous occurrences of nephrolithiasis over the past 7 years, requiring lithotripsy on multiple occasions. Frank hematuria occurs almost monthly. . . Unloading the skeleton of excess mineral appears to increase urinary calcium excretion causing nephrolithiasis and increments in serum creatinine levels. It is unclear what further morbidity will ensue if the latter problem continues, unabated.”
SOURCE: Kurland ES, et al. (2007). Recovery from skeletal fluorosis (an enigmatic, American case). J Bone Miner Res. 22(1):163-70.
The following are excerpts from two previous studies that also found connections between fluoride exposure and kidney stones:
“The present study was designed to evaluate the role of fluoride in urolithiasis in humans. Two areas were selected for this purpose, a fluoride endemic area (EA) and a fluoride non-endemic area (NEA). The prevalence of urolithiasis was 4.6 times higher in EA than in NEA. Furthermore, the prevalence was almost double in subjects with fluorosis than without fluorosis in the endemic area. No relationship was observed between urolithiasis and the duration of fluorosis. The fluoride levels in drinking water ranged from 3.5 to 4.9 ppm in EA and subjects from this area excreted more fluoride. A comparison of normal subjects (NS) from EA and NEA revealed that endemic subjects tend to have slightly higher mean serum thiobarbituric acid reactive substance (TBAR) levels and excrete more oxalate and fluoride than their non-endemic counterparts. The urinary stone formers (SF) from the two areas showed a similar tendency, though again the difference was not significant. Citrate excretion in SF was almost normal in the EA, but NEA SF had significantly lower excretion levels. Urinary stones from endemic patients had higher fluoride, oxalate and calcium levels than those from non-endemic patients. In vitro studies suggested that fluoride did not influence the heterogonous mineralization of calcium oxalate. In conclusion, the data suggest that fluoride in vivo may behave as a mild promoter of urinary stone formation by (a) excretion of insoluble calcium fluoride, (b) increasing oxalate excretion and (c) mildly increasing the oxidative burden.”
SOURCE: Singh PP, et al. (2001). Evidence suggesting that high intake of fluoride provokes nephrolithiasis in tribal populations. Urological Research 29(4):238-44.
“In our previous experiment using rats, fluoride was reported to cause renal calcification, whose mechanism was deduced to be due to an increase in parathyroid hormone (PTH) secretion. However fluoride-induced renal calcification that was independent of PTH has not been understood well in the nephron of fluoride-treated animals. Thus, we examined the effect of sodium fluoride on intracellular calcium mobilization in a normal rat kidney epithelial cell line (NRK-52E cells). The calcium accumulation was found to be remarkably increased by the addition of sodium fluoride (NaF). The elevation of [Ca2+]i was demonstrated to be due to calcium entry through nifedipine-sensitive calcium channels.”
SOURCE: Murao H, et al. (2000). Sodium fluoride increases intracellular calcium in rat renal epithelial cell line NRK-52E.Biol Pharm Bull. 23(5):581-4.