You may already be aware that some kidney stones can result from urinary tract infections. These are the so-called “struvite” stones, which can form large staghorn type stones. What you may not know is that researchers have suggested that bacteria may also contribute to the formation of the more common “calcium oxalate” and “calcium phosphate” type stones.
Below, we discuss the three ways that bacteria may be the cause of kidney stones.
Typical infection stones are mainly composed of magnesium ammonium phosphate. The substance was named “struvite” by a Swedish geologist and this name is commonly used to refer to this type of kidney stone. In 1901, Brown first theorized that bacteria could split a substance known as urea, which would set up the necessary conditions for struvite stone formation in urine. These conditions include alkaline urine, sufficient concentrations of carbonate, and sufficient concentrations of ammonia. Later researchers were able to isolate the enzyme “urease”, which allowed the bacteria to split urea.
Struvite stones comprise 5% to 15% of all stones. It is now accepted that struvite stones only occur when urea splitting bacterial infections are present. The most common urease-producing bacteria include Proteus, Klebsiella, Pseudomonas, and Staphylococcus.
Treatment of these stones involves removing all fragments if possible because the culprit bacteria are usually harbored within the stone. Antibiotics are then used to reduce the change of reinfection.
Nanobacteria were first described by Kajander and colleagues in 1992. They are felt to be extremely small particles that can self-replicate and may contain protein, features consistent with being a life form. They appear to be very hardy and have been found widely in geological samples and in humans. An important feature of nanobacteria appears to be their involvement with biomineralization. Because of this mineralization, some research has suggested nanobacteria may play a role in kidney stone development.
Kajander and colleagues found that nanobacteria were present in kidney stones and that giving rats nanobacteria can lead to the development of stones. They propose that the small particles can act as “seeds” for the formation of larger calcium phosphate crystals, which in turn can lead to calcium oxalate crystals.
However, other researchers have not been able to consistently find these particles in kidney stones or in the urine of kidney stone patients. Other researchers have suggested that nanobacteria may actually represent smaller subunits of known bacteria, and not independent life forms on their own. Nanobacteria’s existence and its role in the development of diseases have been controversial ever since its discovery and it is still unclear whether it truly is a cause of kidney stones.
Unlike in the two preceding examples where having too much bacteria is a problem, in the case of Oxalobacter formigenes, it’s not having enough of these bacteria that may be the cause of stones.
Oxalobacter formigenes are bacteria that normally live in the gut of humans and other animals. It is present in nearly all children and is found in about 75% of adults. Oxalobacter are unique in getting its energy only from breaking down oxalate in the colon. This breakdown process can lower oxalate levels in the urine by decreasing the amount available to be absorbed in the gut.
High oxalate levels in the urine are a risk factor for stones, as oxalate can combine with calcium to form calcium-oxalate stones, the most common stone type. Intriguingly, several researchers have found that stone formers were less likely to be colonized by oxalobacter (26-46%) than non-stone formers (60-77%). However, other researchers have suggested that the chronic use of antibiotics leads to a decrease in oxalobacter, not stone status. They instead found that while kidney stone patients on antibiotics did have decreased oxalobacter levels, kidney stone patients not on antibiotics had the same colonization rates as non-stone formers.
Researchers have proposed that kidney stone formers with high levels of oxalate in their urine may benefit from being given either oxalobacter in the form of concentrate or other bacteria that can degrade oxalate in the form of probiotics containing lactic acid bacilli. So far, the research has been mixed, with some studies suggesting a difference while others showed that the addition of probiotics was not useful.
Further work needs to be done in this area to definitively determine the true role of oxalobacter formigenes in stone disease and its potential as a treatment to reduce stone rates.
Lieske et al, “Diet, but not oral probiotics, effectively reduces urinary oxalate excretion and calcium oxalate supersaturation” Kidney International 2010.
Wood and Shoskes, “The role of nanobacteria in urologic disease” World Journal Urology 2006.
Siva et al, “A critical analysis of the role of gut Oxalobacter formigenes in oxalate stone disease” BJU International, 2008.