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Gastrointestinal Disease and Stone Risk: Nutritional Management

  • Desiree de WaalEmail author
Chapter
Part of the Nutrition and Health book series (NH)

Abstract

Gastrointestinal (GI) health and function may contribute to the development of kidney stones. The GI tract provides nutrients via the multiphasic process of digestion. The gut and its resident microbes also modulate immune function and produce several vitamins and nutrients. Oxalate transport carriers have been identified throughout the digestive system. The bacteria in the intestinal tract perform a number of crucial functions, including digesting otherwise indigestible carbohydrates, stimulating the immune system, fending off colonization of pathogens, and directing the body to store fats. The composition of food that passes through the gut changes the microbiome which can affect the health of the host. Inflammatory diseases of the digestive system or surgical changes to the length of the gastrointestinal system have been shown to increase the risk for kidney stone formation. Generally a diet that protects against cardiovascular disease (less meat, salt, and processed foods plus more fruits, vegetables, and whole grains) promotes an improved microflora and also prevents kidney stone formation.

Keywords

Digestion Gastrointestinal health Probiotics Prebiotics Microbiome Hyperoxaluria Bowel disease 

References

  1. 1.
    Slavin J. Fiber and prebiotics: mechanisms and health benefits. Nutrients. 2013;5:1417–35.PubMedPubMedCentralCrossRefGoogle Scholar
  2. 2.
    Belkaid Y, et al. Role of the microbiota in immunity and inflammation. Cell. 2014;157(1):121–41.PubMedPubMedCentralCrossRefGoogle Scholar
  3. 3.
    Mehta M, Goldfarb D, Nazzal L. The role of the microbiome in kidney stone formation. Int J of Surg. 2016;36:607–12.CrossRefGoogle Scholar
  4. 4.
    Sekirov I, et al. Gut microbiota in health and disease. Physiol Rev. 2010;90:859–904.PubMedCrossRefGoogle Scholar
  5. 5.
    Marchesi JR, Adams DH, Fava F, et al. The gut microbiota and host health: a new clinical frontier. Gut. 2016;65:330–9.PubMedCrossRefGoogle Scholar
  6. 6.
    Montoliu I, et al. Current status on genome-metabolome-wide associations: an opportunity in nutrition research. Genes Nutr. 2013;8:19–27.PubMedCrossRefGoogle Scholar
  7. 7.
    Rossi M, et al. The kidney-gut axis: implications for nutrition care. J Ren Nutr. 2015;25:399.PubMedCrossRefGoogle Scholar
  8. 8.
    Robinson CJ, et al. From structure to function: the ecology of host-associated microbial communities. Microbiol Mol Biol Rev. 2010;74:453–76.PubMedPubMedCentralCrossRefGoogle Scholar
  9. 9.
    David LA, Maurice CF, Carmody RN, et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature. 2014;505(7484):559–63.CrossRefGoogle Scholar
  10. 10.
    Suryavanshi MV, et al. Hyperoxaluria leads to dysbiosis and drives selective enrichment of oxalate metabolizing bacterial species in recurrent kidney stone endures. Sci Rep. 2016;6:34712. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5052600/.PubMedPubMedCentralCrossRefGoogle Scholar
  11. 11.
    Seiner R, et al. The role of Oxalobacter formigenes colonization in calcium oxalate stone disease. Kid Int. 2013;83:1144–9.CrossRefGoogle Scholar
  12. 12.
    Parselis Kelly J, et al. Factors related to colonization with Oxalobacter formigenes in US adults. J Endourol. 2011;25(4):673–9.PubMedCrossRefGoogle Scholar
  13. 13.
    Moe OW. Kidney stones: pathophysiology and medical management. Lancet. 2006;367:333–44.PubMedPubMedCentralCrossRefGoogle Scholar
  14. 14.
    Robijn S, et al. Hyperoxaluria: a gut-kidney axis? Kidney Int. 2011;80:1146–58. This reference has some great pictures of oxalate handling in the GI tract.PubMedCrossRefGoogle Scholar
  15. 15.
    Fink HA, et al. Diet, fluid, or supplements for secondary prevention of nephrolithiasis: a systematic review and meta-analysis of randomized trials. Eur Urol. 2009;56:72–80.PubMedPubMedCentralCrossRefGoogle Scholar
  16. 16.
    Tappenden KA. Pathophysiology of short bowel syndrome: considerations of resected and residual anatomy. JPEN J Parenter Enteral Nutr. 2014;38(1 Suppl):14S–22S.PubMedCrossRefGoogle Scholar
  17. 17.
    Noori N, et al. Urinary lithogenic risk profile in recurrent stone formers with hyperoxaluria: a randomized trial comparing DASH (Dietary Approaches to Stop Hypertension)-style diets. Am J Kidney Dis. 2014;63(3):456–63.CrossRefGoogle Scholar
  18. 18.
    Erdem E, et al. Is there a relation between irritable bowel syndrome and urinary stone disease. Dig Dis Sci. 2005;50(3):605–8.PubMedCrossRefGoogle Scholar
  19. 19.
    Da Silva GSR, et al. Urolithiasis and crohn’s disease. Urol Ann. 2016;8(3):297–304.CrossRefGoogle Scholar
  20. 20.
    Bleicher MB, Wasserstein AG. Nephrolithiasis in bowel disease. Gastroenterol Hepatol. 2009;5(2):131–6.Google Scholar
  21. 21.
    Lomer MCE. Symposium 7: nutrition in inflammatory bowel disease dietary and nutritional considerations for inflammatory bowel disease. Proc Nutr Soc. 2011;70:329–35.PubMedCrossRefGoogle Scholar
  22. 22.
    Lieske JC, et al. Use of a probiotic to decrease enteric hyperoxaluria. Kidney Int. 2005;68:1244–9.CrossRefGoogle Scholar
  23. 23.
    Boynton W, Floch M. New strategies for the management of diverticular disease: insights for the clinician. Ther Adv Gastroenterol. 2013;6(3):205–13.CrossRefGoogle Scholar
  24. 24.
    Wong YV, et al. The association of metabolic syndrome and urolithiasis. Int J Endocrinol. 2015, Article ID 570674, 9 pages.Google Scholar
  25. 25.
    Nasr SH, et al. Oxalate nephropathy comlicating Roux-en-Y Gastric Bypass: an underrecognized cause of irreversible renal failure. Clin J Am Soc Nephrol. 2008;3:1676–83.PubMedPubMedCentralCrossRefGoogle Scholar
  26. 26.
    Lieske JC, et al. Nephrolithiasis after bariatric surgery for obesity. Semin Nephrol. 2008;28(2):163–73.PubMedPubMedCentralCrossRefGoogle Scholar
  27. 27.
    Canales BK. Kidney stone risk following Roux-en-Y gastric bypass surgery. Transl Androl Urol. 2014;3(3):242–9.PubMedPubMedCentralGoogle Scholar
  28. 28.
    Roberfroid M. Prebiotics: the concept revisited. J Nutr. 2007;137(3):830S–7S. http://jn.nutrition.org/content/137/3/830S.full.PubMedCrossRefGoogle Scholar
  29. 29.
    Jardine M. The role of the microbiota in obesity and diabetes. OTCE. 2015;35(6):10–4.Google Scholar
  30. 30.
    Bermudez-Brito M, et al. Probiotic mechanisms of action. Ann Nutr Metab. 2012;61:160–74.CrossRefGoogle Scholar
  31. 31.
    Cresci G. Probiotics: are they really “good little bugs?”. Support Line. 2005;27(1):20–8.Google Scholar
  32. 32.
    Sanders ME. Probiotics: definition, sources, selection, and uses. Clin Infect Dis. 2008;46(Suppl 2):S58–61.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.University of Vermont Medical Center, NephrologyBurlingtonUSA

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