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Microbiome: Kidney Stones and Gut Bacteria

Kidney stones are predominantly composed of calcium oxalate (CaOx) derived from both endogenous and exogenous sources affecting 1 in 11 people in the United States. It is a multifactorial disorder with a complex interaction between gut, liver, bone, and kidney that the underlying mechanisms are complex. There are different types of surgical and lithotripsy interventions available for immediate treatment. However, given the chronic nature of the disease with stone recurrence in many patients, novel therapeutic approaches are necessary. One approach to prevent renal stone recurrence is to decrease consumption of oxalate-rich foods. However, the recent concept of reducing oxalate absorption by a microbiological approach has been increasing attention.

 

What is the bacteria that is clinically significant of kidney stones?

Oxalobacter formigenes, a Gram-negative, anaerobic bacterium colonization metabolizing oxalate in the intestinal tract and is present in a large proportion of the normal adult population.

 

How is the bacteria related to kidney stones?

Oxalobacter formigenes colonization has a strong inverse association with CaOx nephrolithiasis, with a 70% reduction in overall risk. O. formigenes induces fecal oxalate excretion by enhancing secretion into colon and thereby to normalize urinate oxalate excretion. Thus, in the absence of O. formigenes, net intestinal oxalate absorption could increase, resulting in higher plasma and urinary oxalate levels and risk of stone development.

 

What are the symptoms of kidney stones?

 

How do you determine the levels of the bacteria?

Our office can provide a stool test to analyze the microbiome of the patient. Indications for the testing include:

 

What are some interventions to consider?

 

References:

  1. UBiome (n.d.). Treat Guide for Physicians: Calcium Kidney Stones [Online handout]. Retrieved from https://ubiome.com/wp-content/uploads/2017/11/SmartGut-Treatment-Guide-Calcium-Kidney-Stones.pdf.
  2. C.D. Scales, A.C. Smith, J.M. Hanley, C.S. Saigal, Urologic Diseases in America Project, Eur. Urol. 62 (2012) 160–165.
  3. M.L. Ellis, A.E. Dowell, X. Li, J. Knight, Arch. Microbiol. 198 (2016) 1019–1026.
  4. O. Ivanovski, T.B. Drüeke, Kidney Int. 83 (2013) 998–1000.
  5. D.W. Kaufman, J.P. Kelly, G.C. Curhan, T.E. Anderson, S.P. Dretler, G.M. Preminger, D.R. Cave, J. Am. Soc. Nephrol. 19 (2008) 1197–1203.
  6. J.N. Lange, K.D. Wood, H. Wong, R. Otto, P.W. Mufarrij, J. Knight, H. Akpinar, R.P. Holmes, D.G. Assimos, Urology 79 (2012) 1286–1289.
  7. J.C. Lieske, W.J. Tremaine, C. De Simone, H.M. O’Con- nor, X. Li, E.J. Bergstralh, D.S. Goldfarb, Kidney Int. 78 (2010) 1178–1185.
  8. E. Hylander, S. Jarnum, K. Nielsen, Scand. J. Gastroen- terol. 15 (1980) 349–352.
  9. D.G. Assimos, Rev Urol 8 (2006) 170–171.
  10. M.L. Ellis, K.J. Shaw, S.B. Jackson, S.L. Daniel, J. Knight, Urology 85 (2015) 517–521.
  11. B. Hoppe, G. von Unruh, N. Laube, A. Hesse, H. Sidhu, Urol. Res. 33 (2005) 372–375.
  12. S. Pence, I. Ikizceli, E. Ozbek, N.O. Tiryakioglu, H. Eren, E.C. Polat, H.H. Pence, CUR 8 (2014) 189–193.
Author
Anna Chung Patient Care Coordinator

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