Роль микробиоты кишечника в развитии мочекаменной болезни

Основной целью данной работы стал обзор мировой литературы по вопросам оценки влияния микробиоты кишечника на образование камней в почках. Авторами была поставлена задача определить, указано ли в данных публикациях на несколько конкретных кишечных бактерий или за эту взаимосвязь несет ответственность более широкое число представителей микробиоты кишечника. Проведен обширный поиск литературы в PubMed, Cochrane central и Web of Science Core CollectionScience на предмет роли микробиоты кишечника в образовании камней в почках (2013–2023 гг.). Большое количество более ранних исследований камней в почках было сосредоточено на физико-химических свойствах кристаллов, образуемых камнями. Но в последние годы с улучшением диагностических технологий прослеживается тенденция к изучению связи микробиоты кишечника с развитием других, не связанных заболеваний. Появились работы, где показано влияние микробиоты кишечника на развитие мочекаменной болезни, что дает основание полагать, что образование камней можно предотвратить или вызвать путем изменения структуры микробиома кишечника. Однако необходимы дальнейшие исследования по изучению вопросов родов или видов кишечной микробиоты, влияющих на расщепление оксалатов, а также снижение риска образования камней в почках. 

1. Российское общество урологов. Клинические рекомендации «Мочекаменная болезнь». Российское общество урологов; 2020.

2. Sorokin I, Mamoulakis C, Miyazawa K, Rodgers A, Talati J, Lotan Y. Epidemiology of stone disease across the world. World J Urol. 2017;35(9):1301–1320. PMID: 28213860. https://doi.org/10.1007/s00345-017-2008-6

3. Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006;367(9507):333–344. PMID: 16443041. https://doi.org/10.1016/S0140-6736(06)68071-9

4. Buttó LF, Haller D. Dysbiosis in Crohn’s disease - joint action of stochastic injuries and focal inflammation in the gut. Gut Microbes. 2017;8(1):53–58. PMID: 28102757. PMCID: PMC5341912. https://doi.org/10.1080/19490976.2016.1270810

5. Miller AW, Choy D, Penniston KL, Lange D. Inhibition of urinary stone disease by a multi-species bacterial network ensures healthy oxalate homeostasis. Kidney Int. 2019;96(1):180– 188. PMID: 31130222. PMCID: PMC6826259. https://doi.org/10.1016/j.kint.2019.02.012

6. Singh P, Enders FT, Vaughan LE, et al. Stone composition among first-time symptomatic kidney stone formers in the community. Mayo Clin Proc. 2015;90(10):1356–1365. PMID: 26349951. PMCID: PMC4593754. https://doi.org/10.1016/j.mayocp.2015.07.016

7. Dhondup T, Kittanamongkolchai W, Vaughan LE, et al. Risk of ESRD and mortality in kidney and bladder stone formers. Am J Kidney Dis. 2018;72(6):790–797. PMID: 30146423. PMCID: PMC6252145. https://doi.org/10.1053/j.ajkd.2018.06.012

8. Shoag J, Halpern J, Goldfarb DS, Eisner BH. Risk of chronic and end stage kidney disease in patients with nephrolithiasis. J Urol. 2014;192(5):1440–1445. PMID: 24929140. https://doi.org/10.1016/j.juro.2014.05.117

9. Brzica H, Breljak D, Burckhardt BC, Burckhardt G, Sabolić I. Oxalate: from the environment to kidney stones. Arh Hig Rada Toksikol. 2013;64(4):609–630. PMID: 24384768. https://doi.org/10.2478/10004-1254-64-2013-2428

10. Ferraro PM, Bargagli M, Trinchieri A, Gambaro G. Risk of kidney stones: influence of dietary factors, dietary patterns, and vegetarian-vegan diets. Nutrients. 2020;12(3):779. PMID: 32183500. PMCID: PMC7146511. https://doi.org/10.3390/nu12030779

11. Howles SA, Thakker RV. Genetics of kidney stone disease. Nat Rev Urol. 2020;17(7):407–421. PMID: 32533118. https://doi.org/10.1038/s41585-020-0332-x

12. Khan SR, Pearle MS, Robertson WG, et al. Kidney stones. Nat Rev Dis Primers. 2016;2:16008. PMID: 27188687. PMCID: PMC5685519. https://doi.org/10.1038/nrdp.2016.8

13. Xiang L, Jin X, Liu Y, et al. Prediction of the occurrence of calcium oxalate kidney stones based on clinical and gut microbiota characteristics. World J Urol. 2022;40(1):221–227. PMID: 34427737. PMCID: PMC8813786. https://doi.org/10.1007/s00345-021-03801-7

14. Yuan T, Xia Y, Li B, et al. Gut microbiota in patients with kidney stones: a systematic review and meta-analysis. BMC Microbiol. 2023;23(1):143. PMID: 37208622. PMCID: PMC10197343. https://doi.org/10.1186/s12866-023-02891-0

15. Siva S, Barrack ER, Reddy GP, et al. A critical analysis of the role of gut Oxalobacter formigenes in oxalate stone disease. BJU Int. 2009;103(1):18–21. PMID: 19021605. https://doi.org/10.1111/j.1464-410X.2008.08122.x

16. Siener R, Bangen U, Sidhu H, Hönow R, von Unruh G, Hesse A. The role of Oxalobacter formigenes colonization in calcium oxalate stone disease. Kidney Int. 2013;83(6):1144–1149. PMID: 23536130. https://doi.org/10.1038/ki.2013.104

17. Tang R, Jiang Y, Tan A, et al. 16S rRNA gene sequencing reveals altered composition of gut microbiota in individuals with kidney stones. Urolithiasis. 2018;46(6):503–514. PMID: 29353409. https://doi.org/10.1007/s00240-018-1037-y

18. Stern JM, Moazami S, Qiu Y, et al. Evidence for a distinct gut microbiome in kidney stone formers compared to non-stone formers. Urolithiasis. 2016;44(5):399–407. PMID: 27115405. PMCID: PMC8887828. https://doi.org/10.1007/s00240-016-0882-9

19. Kim HN, Kim JH, Chang Y, et al. Gut microbiota and the prevalence and incidence of renal stones. Sci Rep. 2022;12(1):3732. PMID: 35260689. PMCID: PMC8904816. https://doi.org/10.1038/s41598-022-07796-y

20. Cao C, Fan B, Zhu J, Zhu N, Cao JY, Yang DR. Association of gut microbiota and biochemical features in a Chinese population with renal uric acid stone. Front Pharmacol. 2022;13:888883. PMID: 35662733. PMCID: PMC9160931. https://doi.org/10.3389/fphar.2022.888883

21. Ticinesi A, Milani C, Guerra A, et al. Understanding the gut-kidney axis in nephrolithiasis: an analysis of the gut microbiota composition and functionality of stone formers. Gut. 2018;67(12):2097–2106. PMID: 29705728. https://doi.org/10.1136/gutjnl-2017-315734

22. Tavasoli S, Alebouyeh M, Naji M, et al. Association of intestinal oxalate-degrading bacteria with recurrent calcium kidney stone formation and hyperoxaluria: a case-control study. BJU Int. 2020;125(1):133–143. PMID: 31145528. https://doi.org/10.1111/bju.14840

23. Lieske JC. Probiotics for prevention of urinary stones. Ann Transl Med. 2017;5(2):29. PMID: 28217694. PMCID: PMC5300857. https://doi.org/10.21037/atm.2016.11.86

24. Denburg MR, Koepsell K, Lee JJ, Gerber J, Bittinger K, Tasian GE. Perturbations of the gut microbiome and metabolome in children with calcium oxalate kidney stone disease. J Am Soc Nephrol. 2020;31(6):1358–1369. PMID: 32381601. PMCID: PMC7269359. https://doi.org/10.1681/ASN.2019101131

25. Suryavanshi MV, Bhute SS, Jadhav SD, Bhatia MS, Gune RP, Shouche YS. Hyperoxaluria leads to dysbiosis and drives selective enrichment of oxalate metabolizing bacterial species in recurrent kidney stone endures. Sci Rep. 2016;6:34712. PMID: 27708409. PMCID: PMC5052600. https://doi.org/10.1038/srep34712

26. Stanford J, Charlton K, Stefoska-Needham A, Ibrahim R, Lambert K. The gut microbiota profile of adults with kidney disease and kidney stones: a systematic review of the literature. BMC Nephrol. 2020;21(1):215. PMID: 32503496. PMCID: PMC7275316. https://doi.org/10.1186/s12882-020-01805-w

27. Chen F, Bao X, Liu S, et al. Gut microbiota affect the formation of calcium oxalate renal calculi caused by high daily tea consumption. Appl Microbiol Biotechnol. 2021;105(2):789–802. PMID: 33404827. https://doi.org/10.1007/s00253-020-11086-w

28. Cabrera C, Artacho R, Giménez R. Beneficial effects of green tea--a review. J Am Coll Nutr. 2006;25(2):79–99. PMID: 16582024. https://doi.org/10.1080/07315724.2006.10719518

29. Yang Y, Zhang X, Weng PF, Wu ZF. In vitro monitoring of the probiotic activity of tea catechins on human intestinal flora. Modern Food Science and Technology. 2015;31(4):128–136.

30. Tasian GE, Jemielita T, Goldfarb DS, et al. Oral antibiotic exposure and kidney stone disease. J Am Soc Nephrol. 2018;29(6):1731–1740. PMID: 29748329. PMCID: PMC6054354. https://doi.org/10.1681/ASN.2017111213

31. Wang Y, Sun J, Xie S, et al. Increased abundance of bacteria of the family Muribaculaceae achieved by fecal microbiome transplantation correlates with the inhibition of kidney calcium oxalate stone deposition in experimental rats. Front Cell Infect Microbiol. 2023;13:1145196. PMID: 37313343. PMCID: PMC10258309. https://doi.org/10.3389/fcimb.2023.1145196

32. Mehra Y, Rajesh NG, Viswanathan P. Analysis and characterization of Lactobacillus paragasseri and Lacticaseibacillus paracasei: two probiotic bacteria that can degrade intestinal oxalate in hyperoxaluric rats. Probiotics Antimicrob Proteins. 2022;14(5):854–872. PMID: 35699895. https://doi.org/10.1007/s12602-022-09958-w

33. Tian L, Liu Y, Xu X, et al. Lactiplantibacillus plantarum J-15 reduced calcium oxalate kidney stones by regulating intestinal microbiota, metabolism, and inflammation in rats. FASEB J. 2022;36(6):e22340. PMID: 35524736. https://doi.org/10.1096/fj.202101972RR

34. Wu F, Cheng Y, Zhou J, et al. Zn2+ regulates human oxalate mtabolism by manipulating oxalate decarboxylase to treat calcium oxalate stones. Int J Biol Macromol. 2023;234:123320. PMID: 36682657. https://doi.org/10.1016/j.ijbiomac.2023.123320