Deficient butyrate metabolism in the intestinal microbiome is a potential risk factor for recurrent kidney stone disease.

Intestinal microbiome dysbiosis is a known risk factor for recurrent kidney stone disease (KSD) with prior data suggesting a role for dysfunctional metabolic pathways other than those directly utilizing oxalate. To identify alternative mechanisms, the current study analyzed differences in the metabolic potential of intestinal microbiomes of patients (n = 17) and live-in controls (n = 17) and determined their relevance to increased risk for KSD using shotgun metagenomic sequencing. We found no differences in the abundance of genes associated with known oxalate degradation pathways, supporting the notion that dysfunction in other metabolic pathways plays a role in KSD. Further analysis showed decreased abundance of key enzymes involved in butyrate biosynthesis in patient intestinal microbiomes. Furthermore, de novo construction of microbial genomes showed that the majority of genes significantly enriched in non-stone formers are affiliated with Faecalibacterium prausnitzii, a major butyrate producer. Specifically pertaining to butyrate metabolism, the majority of abundant genes mapped back to F. prausnitzii, Alistipes spp., and Akkermansia muciniphila. No differences were observed in ascorbate or glyoxylate metabolic pathways. Collectively, these data suggest that impaired bacterial-associated butyrate metabolism may be an oxalate-independent mechanism that contributes to an increased risk for recurrent KSD. This indicates that the role of the intestinal microbiome in recurrent KSD is multi-factorial, which is representative of the highly intertwined metabolic nature of this complex environment. Future bacteria-based treatments must not be restricted to targeting only oxalate metabolism.

Renal struvite stones--pathogenesis, microbiology, and management strategies.

Infection stones-which account for 10-15% of all urinary calculi-are thought to form in the presence of urease-producing bacteria. These calculi can cause significant morbidity and mortality if left untreated or treated inadequately; optimal treatment involves complete stone eradication in conjunction with antibiotic therapy. The three key principles of treating struvite stones are: removal of all stone fragments, the use of antibiotics to treat the infection, and prevention of recurrence. Several methods to remove stone fragments have been described in the literature, including the use of urease inhibitors, acidification therapy, dissolution therapy, extracorporeal shockwave lithotripsy, ureteroscopy, percutaneous nephrolithotomy (PCNL), and anatrophic nephrolithotomy. PCNL is considered to be the gold-standard approach to treating struvite calculi, but adjuncts might be used when deemed necessary. When selecting antibiotics to treat infection, it is necessary to acquire a stone culture or, at the very least, urine culture from the renal pelvis at time of surgery, as midstream urine cultures do not always reflect the causative organism.