Nanobacteria: controversial pathogens in nephrolithiasis and polycystic kidney disease

Citation
Eo. Kajander et al., Nanobacteria: controversial pathogens in nephrolithiasis and polycystic kidney disease, CURR OP NEP, 10(3), 2001, pp. 445-452
Citations number
81
Categorie Soggetti
Urology & Nephrology
Journal title
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
ISSN journal
10624821 → ACNP
Volume
10
Issue
3
Year of publication
2001
Pages
445 - 452
Database
ISI
SICI code
1062-4821(200105)10:3<445:NCPINA>2.0.ZU;2-9
Abstract
Nanobacteria are unconventional agents 100-fold smaller than common bacteri a that can replicate apatite-forming units. Nanobacteria are powerful media tors of biogenic apatite nucleation (crystal form of calcium phosphate) and crystal growth under conditions simulating blood and urine. Apatite is fou nd in the central nidus of most kidney stones and in mineral plaques (Randa ll's plaques) in renal papilla. The direct injection of nanobacteria into r at kidneys resulted in stone formation in the nanobacteria-injected kidney during one month follow-up, but not in the control kidney injected with veh icle. After intravenous administration in rats and rabbits, nanobacteria ar e rapidly excreted from the blood into the urine, as a major elimination ro ute, and damage renal collecting tubuli. Nanobacteria are cytotoxic to fibr oblasts in vitro. Human kidney cyst fluids contain nanobacteria. Nanobacter ia thus appear to be potential provocateurs and initiators of kidney stones , tubular damage, and kidney cyst formation. It is hypothesized that nanoba cteria are the initial nidi on which kidney stone is built up. at a rate de pendent on the supersaturation status of the urine. Those individuals havin g both nanobacteria and diminished defences against stone formation (i.e. g enetic factors, diet and drinking habits) could be at high risk. Kidney cys t formation is hypothesized to involve nanobacteria-induced tubular damage and defective tissue regeneration yielding cyst formation, the extent of wh ich is dependent on genetic vulnerability. Curr Opin Nephrol Hypertens 10:4 45-452. (C) 2001 Lippincott Williams & Wilkins.