Abstract

Nanobacteria are unconventional agents 100-fold smaller than common bacteria that can replicate apatite-forming units. Nanobacteria are powerful mediators of biogenic apatite nucleation (crystal form of calcium phosphate) and crystal growth under conditions simulating blood and urine. Apatite is found in the central nidus of most kidney stones and in mineral plaques (Randall's plaques) in renal papilla. The direct injection of nanobacteria into rat kidneys resulted in stone formation in the nanobacteria-injected kidney during one month follow-up, but not in the control kidney injected with vehicle. After intravenous administration in rats and rabbits, nanobacteria are rapidly excreted from the blood into the urine, as a major elimination route, and damage renal collecting tubuli. Nanobacteria are cytotoxic to fibroblasts in vitro. Human kidney cyst fluids contain nanobacteria. Nanobacteria thus appear to be potential provocateurs and initiators of kidney stones, tubular damage, and kidney cyst formation. It is hypothesized that nanobacteria are the initial nidi on which kidney stone is built up, at a rate dependent on the supersaturation status of the urine. Those individuals having both nanobacteria and diminished defences against stone formation (i.e. genetic factors, diet and drinking habits) could be at high risk. Kidney cyst formation is hypothesized to involve nanobacteria-induced tubular damage and defective tissue regeneration yielding cyst formation, the extent of which is dependent on genetic vulnerability.

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