NANOBACTERIUM SANGUINEUM & THE GU SYSTEM

 A.  Kidney stones: 

Nanobacteremia and Nanobacteriuria are not uncommon, and renal excretion appears to be the primary mechanism by which N. sanguineum is cleared from the blood.  The kidney does not clear Nanobacteria through glomerular filtration (they are too large) but by active transport across the tubular cells, into the urine.  The relative concentration of Nanobacteria will thus be highest in the renal papillae, into which the collecting tubules converge, and from which urine percolates into the renal pelvis. 

Papillary stones, a common type of kidney stones, look like buckeyes.  Their concave surface, which fits over the convex surface of the renal papillae, always contains carbonate apatite – this region is known as Randall’s plaque.  Regardless of the mineral composition of the papillary stone proper, Randall’s plaque is always composed of carbonate apatite.  Electron microscopic analysis shows that Randall’s plaque material (fig. 1) is actually dead, calcified, papillary tissue; basically dead, calcified, urine collecting tubules, blood vessels, and interstitial cells.  Thus papillary stones form over a nucleus of dead papillary cells.  Some agent, present in the urine and thus concentrated in the renal papillae, is taken up by or invades the renal cells, and this agent then kills the cells and calcifies them. 

        What causes kidney stones?  We didn’t learn the answer in medical school – they just “happen”.  It certainly doesn’t have to do with dietary calcium (and neither does atherosclerotic calcification), but the presence of kidney stones is associated with an increased risk of hypertension and renal dysfunction – and they hurt, just ask the 12% of American men and 4% of American women who will be troubled by stone disease.  Sure, 15% of kidney stones can be explained as “infectious” from regular bacteria.  Urease secreting, common bacteria raise the pH of the urine, favoring the precipitation of urine minerals into stone – an interaction between infection and physical chemistry.  High uric acid and cystine levels can precipitate stones of the same composition, but the majority of stones, “mineral stones”, form without an obvious etiology, and thus without an obvious medical treatment.  Of note, all mineral stones contain significant amounts of carbonate apatite, and infectious stones contain detectable amounts.

Dr. Neva Ciftcioglu analyzed stones obtained from 72 consecutive patients presenting to a stone clinic in Finland.  The electron microscopic appearance of the pulverized stones, before and after stone demineralization with HCL, was identical to that of lab stock Nanobacterium sanguineum isolated from fetal bovine serum (fig. 2 – calcified nanobacterial colonies; fig. 3 – ground up kidney stone).  Monoclonal antibodies to N. sanguineum reacted to the demineralized stones.  From these ground up, HCL dissolved kidney stones, which had been passed by humans weeks to months earlier, Nanobacterium sanguineum could be cultured in 93%.  The cultured Nanobacteria remained virulent, able to invade and destroy mammalian cells in tissue culture, and 92% could still fix calcium – they were trying to form new stones.

Cuerpo injected N. sanguineum, isolated from fetal bovine serum, directly into the kidneys of rats, using a translumbar skinny needle approach.  Rats receiving low doses of N. sanguineum did fine, while those inoculated with higher doses developed obstructive stones.

Akerman administered radioisotope labeled N. sanguineum, and as a control, same-sized radioisotope labeled nanocolloid, IV into rabbits, and then measured their distribution in blood, urine, and tissue.

    In the circulation, Nanobacteria were found in the red blood cells (RBCs), with less in the plasma.  Relatively little Nanobacteria was present in bone and liver, while Nanobacteria were taken up by the kidney, and 10-15 minutes later, viable and still cytotoxic Nanobacteria could be detected in the urine.  Histological study (fig. 4) shows Nanobacteria within the renal parenchymal cells, “lining up” to be transported into a urine collecting tubule.  Thus Nanobacteria access the urine not through glomerular filtration (they are too large), but via the tubular cells, which demonstrate Nanobacteria in their cytoplasm and tubular surfaces.  Presumably, blood-borne Nanobacteria bind to the renal tubular cells, directly enter the cells (or trick the tubular cells into endocytosing them), and then cross the tubular epithelial surface into the urine.

 Aho intravenously administered radioisotope labeled Nanobacteria into rabbits and rats.  Tissue distribution was similar to that observed in the Akerman study.  Nanobacteria were excreted in the urine more effectively than the control substances, radioisotope labeled hydroxyapatite and nanocolloid.  Toxicity of Nanobacteria was studied in mice, rats, and rabbits.  Mouse strains showed no symptoms of toxicity, while rats and rabbits developed tubular cell dilatation and apoptotic changes of the renal cells were observed.    

 Hjelle was able to randomly recover Nanobacteria from the urine of 30% of male and 10% of female young, healthy, control subjects.  Kajander and Ciftcioglu cultured N. sanguineum from the blood of 5% of Finnish medical students and 15% of blood donors.  Thus Nanobacteremia and Nanobacteriuria are not uncommon.  The kidney clears Nanobacteria from the blood and actively transports the still virulent organisms into the urine (urine is infectious, not sterile as we have previously presumed), where they are progressively concentrated in the urine collecting tubules as the tubules converge upon the renal papillae.  Intravenously administered N. sanguineum concentrates in the urine, and N. sanguineum injected into the kidney produces obstructive stones.  N. sanguineum can be cultured from 93% of human stones.  Thus Koch’s postulates have been filled – renal infection with N. sanguineum is the cause of most kidney stones in humans.

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