TOPLINE:
Gut and urinary microbiota alterations appear to play key roles in the development of kidney stones, suggesting that
Kidney stones are commonly formed by calcium oxalate produced by the body, but the findings suggest that in efforts to better understand the formation and prevention of the stones, focus should shift away from the long-held focus on specific gut bacterium, such as Oxalobacter formigenesm,to apparent systems-level microbial imbalances.
METHODOLOGY:
- The authors evaluated the gut, urinary, and oral microbiota of 83 patients having kidney stones surgically removed at St. Joseph’s Hospital in London, Ontario, and compared them to 30 healthy controls recruited between August 2015 and January 2019.
- Analysis using measures including shotgun metagenomic sequencing were used to identify specific gut bacteria and the genetic capabilities of the bacteria, and simpler sequencing was conducted using oral and urinary microbiota samples.
- Patients had no antibiotic exposure within the previous 90 days.
TAKEAWAY:
- Significant differences were observed in disturbances in microbiota in all three microbiomes among those who did and did not form kidney stones.
- Patients who formed kidney stones also showed more antibiotic-resistant genes, suggesting greater exposure to antimicrobials.
- Those who had formed kidney stones had reduced taxonomic and functional diversity compared with healthy controls.
- Core functional bioenergetic pathways had been replaced with virulence-associated gene markers in gut and urinary microbiota in those with kidney stones.
- And community network microbiota had collapsed among those with kidney stones.
- “These multisite microbial community shifts may be the result of deleterious environmental factors including antibiotic exposure,” the authors speculated.
- However, no differences were observed between the cohorts in terms of oxalate metabolism — commonly considered a culprit in kidney stone formation.
IN PRACTICE:
- “We found not only that those who got kidney stones had an unhealthy microbiome, including a gut microbiome that was more likely to excrete toxins to the kidneys, but also that they were antibiotic resistant,” explains senior author Jeremy Burton, PhD, the Lawson Scientist and Research Chair of Human Microbiome and Probiotics at St. Joseph’s Health Care London, in a press statement.
- “We conclude that multisite microbiota alteration is a hallmark of stone formation, and kidney stone disease treatment should consider microbial functional restoration and the avoidance of aberrant modulators such as poor diet and antibiotics, where applicable, to prevent stone recurrence,” the authors further wrote in the study.
- “Based on these findings, we suggest that the historic emphasis put on O formigenes and other direct oxalate-handling taxa should be discontinued in favor of mechanistic study into the apparent systems-level microbial imbalances in kidney stone formers,” they said.
SOURCE:
The study was published in Microbiome.
It was conducted by the first author Kait F. Al, PhD, of the department of microbiology and immunology, The University of Western Ontario, London, and colleagues.
LIMITATIONS:
The sampling techniques used in the study provide relative compositional but not absolute abundance information, and the sequencing methods do not provide taxonomic annotation to the species level in all cases.
“For this reason, as well as the problematic nature of comparison across sequencing methodologies, caution should be taken when comparing these data and taxonomic annotations in future studies,” the authors noted.
Furthermore, as the study was observational, causality of stone disease cannot be established to the differences detected between the microbiota of healthy control individuals and those with kidney stones.
DISCLOSURES:
The authors had no disclosures to report.
A version of this article appeared on Medscape.com.