Nanobacteria: An infectious cause for kidney stone formation

Citation
N. Ciftcioglu et al., Nanobacteria: An infectious cause for kidney stone formation, KIDNEY INT, 56(5), 1999, pp. 1893-1898
Citations number
29
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
56
Issue
5
Year of publication
1999
Pages
1893 - 1898
Database
ISI
SICI code
0085-2538(199911)56:5<1893:NAICFK>2.0.ZU;2-A
Abstract
Background. Nanobacteria are cytotoxic, sterile-filterable, gram-negative, atypical bacteria detected in bovine and human blood. Nanobacteria produce carbonate apatite on their cell walls. Data on Randall's plaques suggest th at apatite may initiate kidney stone formation. We assessed nanobacteria in 72 consecutively collected kidney stones from Finnish patients. Methods. Nanobacteria and kidney stone units were compared using scanning e lectron microscopy (SEM). Demineralized kidney stones were screened for nan obacteria using a double-staining method and a specific culture method. Iso lated nanobacteria were analyzed for mineral formation in vitro with Ca and Sr-85 incorporation tests. Results. SEM highlighted the resemblance in size and morphology of nanobact eria and the smallest apatite units in the kidney stones. Nanobacterial ant igens could be detected after the demineralization of the stones in 1 N HCl . Nanobacteria were surprisingly resistant to this treatment, and cultures could be established from 93.1% of the stones. Only struvite stones had com mon bacteria, in addition to the nanobacteria. When the results of all of t he assays were combined, 70 of the 72 stones (that is, 97.25) were nanobact eria positive. Although apatite stones indicated highest nanobacteria antig en signals, the overall nanobacteria positivity did not depend on the stone type. The isolated nanobacteria produced apatite stones in vitro, measured by Ca and Sr-85 incorporation. Conclusions. We propose that kidney stone formation is a nanobacterial dise ase analogous to Helicobacter pylori infection and peptic ulcer disease. Bo th diseases are initiated by bacterial infection and subsequently endogenou s and dietary factors influence their progression.