Abstract

You have accessJournal of UrologyStone Disease: Basic Research & Pathophysiology I (PD04)1 Apr 2020PD04-01 ANTIBIOTICS AFFECT THE GUT MICROBIOME AND ALTER KIDNEY STONE FORMATION IN GENETIC HYPERCALCIURIC STONE-FORMING RATS Joshua Stern*, John Asplin, Nancy Krieger, Sylvia Suadicani, Luojing Chen, Jennifer Becker, Michaela Chan, Justin Lee, Yi Wang, and David Bushinsky Joshua Stern*Joshua Stern* More articles by this author , John AsplinJohn Asplin More articles by this author , Nancy KriegerNancy Krieger More articles by this author , Sylvia SuadicaniSylvia Suadicani More articles by this author , Luojing ChenLuojing Chen More articles by this author , Jennifer BeckerJennifer Becker More articles by this author , Michaela ChanMichaela Chan More articles by this author , Justin LeeJustin Lee More articles by this author , Yi WangYi Wang More articles by this author , and David BushinskyDavid Bushinsky More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000000824.01AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Recent evidence suggests both antibiotic exposure and the gut microbiome (GMB) are associated with stone disease. Antibiotics can cause rapid alterations in the GMB. We utilized genetic hypercalciuric stone-forming (GHS) rats that form calcium phosphate (CaP) stones, to determine the effect of antibiotics on the gut microbiome, urine ion excretion and stone formation. METHODS: 116th generation GHS rats were fed a fixed amount of a normal Ca (1.2%) and P (0.65%) diet, housed in metabolic cages and divided into 3 groups (n=10): control (CTL) diet, or supplemented with ciprofloxacin (Cipro, 5 mg/d) or Bactrim (250 mg/d). Urine and fecal pellets were collected at 6, 12 and 18 wks for analyses. DNA from fecal pellets were amplified on the 16S rRNA V4 region using primers on an Illumina platform. QIIME was used for analysis. At 18 wks kidney stone formation was determined by Faxitron analysis and assessed by 3 blinded reviewers. RESULTS: After 18 wks, urine Ca decreased with Bactrim (CTL=13.7± 0.4, Bactrim=12.1±0.4 mg/d, p<0.05) as did urine oxalate (CTL=1.2±0.04, Bactrim=0.8±0.02 mg/d, p<0.05). CaP supersaturation increased with Bactrim (CTL=6.8±0.4, Bactrim=8.4±0.5, p<0.05) while CaOx supersaturation fell (CTL=16.2± 0.6, Bactrim=12.0±0.4, p<0.05). Calcification was increased with Bactrim (CTL=1.0±0.2, Bactrim=2.98±0.3, p<0.05). Cipro was not different from CTL for any parameter. Principal component analysis of the GMB showed the Bactrim group and controls clustered separately (p=0.001). Microbial diversity negatively correlated with urinary oxalate in all animals (R=-0.46, p=0.006) and positively correlated with urinary pH in the Bactrim group (R=0.76, p=0.01). CONCLUSIONS: Bactrim altered the GMB of GHS rats, decreased urine Ca, increased CaP supersaturation and increased calcification, while Cipro had no effects. Whether the alteration in the GMB is mechanistically related to the changes in urine ion excretion and calcification remains to be determined. Source of Funding: NIDDK © 2020 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 203Issue Supplement 4April 2020Page: e78-e78 Advertisement Copyright & Permissions© 2020 by American Urological Association Education and Research, Inc.MetricsAuthor Information Joshua Stern* More articles by this author John Asplin More articles by this author Nancy Krieger More articles by this author Sylvia Suadicani More articles by this author Luojing Chen More articles by this author Jennifer Becker More articles by this author Michaela Chan More articles by this author Justin Lee More articles by this author Yi Wang More articles by this author David Bushinsky More articles by this author Expand All Advertisement PDF downloadLoading ...

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