Urolithiasis in patients with inflammatory bowel disease – possibilities of prevention and metabolic influence

Česká verzia

Authors: V. Teplan ^1-3 ; R. Netušil ⁴ ; M. Lukáš ¹
Authors place of work: Klinické a výzkumné centrum pro střevní záněty, Klinické centrum ISCARE a. s. a 1. LF UK v Praze ¹; Interní a kardiologická klinika a Katedra interních oborů LF OU a FN Ostrava ²; Subkatedra nefrologie, IPVZ, Praha ³; Oddělení vědy a výzkumu, Medi Pharma Vision s. r. o., Brno ⁴
Published in the journal: Gastroent Hepatol 2023; 77(5): 437-446
Category: IBD: Review Article
doi: https://doi.org/10.48095/ccgh2023437

Summary

Inflammatory bowel diseases (IBD) are typically accompanied by diarrhoea and frequently by malabsorption, both of which are predisposing factors for the formation of renal calculi. In patients who have not undergone bowel surgery the prevalence of urolithiasis has ranged from 1.5 to 5%, but after surgery, stone prevalence can increase to up to 16%. Enteric hyperoxaluria is a frequent complication of inflammatory bowel diseases after ileal-coecal resection, ileostomy, colostomy resection and bariatric surgery. The excess of oxalate is primarily excreted by the kidneys. Increased urinary excretion of oxalate results in urinary calcium oxalate supersaturation, leading to crystal aggregation, urolithiasis, and/or nephrocalcinosis. Prevention of oxalate lithiasis includes high fluid intake, nutritionally balanced low-oxalate, low-fat, low-salt diet, prescription of oral citrate and magnesium, calcium supplement, and also biological manipulation of intestinal flora (microbiota). In IBD patients, urolithiasis can be associated with serious urinary tract infection – in some cases asymptomatic – which can lead to chronic renal insufficiency and failure. New therapeutic approaches to patients with inflammatory bowel diseases have completely changed the natural history of these diseases with reduced number of bowel surgery. Whether this has changed the prevalence and risk factors for urinary calculi in patients with inflammatory bowel diseases is still unknown.

Keywords:

prevention – hyperoxaluria – urolithiasis – inflammatory bowel diseases – intestinal flora

Zdroje

1. Lukáš M et al. Idiopatické střevní záněty II. Nové trendy a mezioborové souvislosti. Praha: Grada Publishing 2021.

2. Manganiotis AN, Banner MP, Malkowicz SB. Urologic complications of Crohn’s disease. Surg Clin North Am 2001; 81 (1): 197–215. doi: 10.1016/s0039-6109 (05) 70281-4.

3.Teplan V, Lukaš M. Urolithiasis in patients with inflammatory bowel disease. Gastroent Hepatol 2015; 69 (6): 561–569. doi: 10.14735/amgh 2015561.

4. McLeod RS, Churchill DN. Urolithiasis complicating inflammatory bowel disease. J Urol 1993; 148 (2): 974–978. doi: 10.1016/s0022-5347 (17) 36794-0.

5. Maratka Z, Nedbal J. Urolithiasis as a complication of the surgical treatment of ulcerative colitis. Gut 1964; 5 (3): 214–217. doi: 10.1136/gut. 5.3.214.

6. Worcester EM. Stones due to bowel disease. In: Coe FL, Favus MJ, Pak CYC et al. Kidney stones: medical and surgical management. Philadelphia: Lippincott-Raven 1996: 883–904.

7. Curhan GC, Rimm EB, Willett WC et al. Regional variation in nephrolithiasis incidence and prevalence among United States men. J Urol 1994; 151 (4): 838–841. doi: 10.1016/s0022-53 47 (17) 35101-7.

8. Soucie JM, Thun MJ, Coates RJ. Demographic and geographic variability of kidney stones in the United States. Kidney Int 1994; 46 (3): 893–899. doi: 10.1038/ki.1994.347.

9. Parks JH, Worcester EM, O’ConnorRC et al. Urine stone risk factors in nephrolithiasis patients with and without bowel disease. Kidney Int 2003; 63 (1): 255–265. doi: 10.1046/j.1523- 1755.2003.00725.x.

10. McConnell N, Campbell S, Gillanders I et al. Risk factors for developing renal stones in Inflammatory bowel disease. BJU Int 2002; 89 (9): 835–841. doi: 10.1046/j.1464-410x.2002.02739.x.

11. Ishii G, Nakajima K, Tanaka N et al. Clinical evaluation of urolithiasis in Crohn’s disease. Int J Urol 2009; 16 (5): 477–480. doi: 10.1111/ j.1442-2042.2009.02285.x.

12. Gustavsson A, Halfvarson J, Magnuson A et al. Long-term colectomy rate after intensive intravenous corticosteroid therapy for ulcerative colitis prior tothe immunosuppressive treatment era. Am J Gastroenterol 2007; 102 (11): 2513–2519. doi: 10.1111/j.1572-0241.2007.01435.x.

13. Filippi J, Allen PB, Hebuterne X et al. Does anti-TNF therapy reduce the requirement for surgery in ulcerative colitis? A systematic review. Curr Drug Targets 2011; 12 (10): 1440–1447. doi: 10.2174/138945011796818153.

14. Shen B, Remzi FH, Oikonomou IK et al. Risk factors for low bone mass in patients with ulcerative colitis following ileal pouch – anal anastomosis. Am J Gastroenterol 2009; 104 (3): 639– 646. doi: 10.1038/ ajg.2008.78.

15. Oikonomou IK, Fazio VW, Remzi FH et al. Risk factors for anemia in patients with ileal pouch-anal anastomosis. Dis Colon Rectum 2007; 50 (1): 69–74. doi: 10.1007/s10350-006-0752-6.

16. Kuisma J, Luukkonen P, Jarvinen H et al. Risk of osteopenia after proctocolectomy and ileal pouch-anal anastomosis for ulcerative colitis. Scand J Gastroenterol 2002; 37 (2): 171–176. doi: 10.1080/0036552027534 16830.

17. Knudsen L, Marcussen H, Fleckenstein P et al. Urolithiasis in chronic inflammatory bowel disease. Scand J Gastroenterol 1978; 13 (4): 433–436. doi: 10.3109/00365527809181917.

18. Kennedy HJ, Al-Dujaili EA, Edwards CR et al. Water and electrolyte balance in subjects with a permanent ileostomy. Gut 1983; 24 (8): 702–705. doi: 10.1136/gut.24.8.702.

19. Watts RW. Primary hyperoxaluria type I. QJM 1994; 87 (10): 593–600.

20. Robijn S, Hoppe B, Vervat BA et al. Hyperoxaluria: a gut-kidney axis? Kidney Int 2011; 80 (11): 1146–1158. doi: 10.1038/ ki.2011. 287.

21. Streit J, Tran-Ho L, Konigsberger E. Solubility of the three calcium oxalate hydrates in sodium chloride solutions and urine-like liquors. Monatsh Chem Chem Mon 1998; 129: 1225–1236. doi: 10.1007/PL00010134.

22. Asplin JR. Hyperoxaluric calcium nephrolithiasis. Endocrinol Metab Clin North Am 2002; 31 (4): 927–949. doi: 10.1016/s0889-8529 (02) 00030-0.

23. Earnest DL. Enteric hyperoxaluria. Adv Intern Med 1979; 24: 407–427.

24. Williams HE. Oxalic acid and the hyperoxaluricsyndromes. Kidney Int 1978; 13 (5): 410–417. doi: 10.1038/ki.1978.59.

25. Molodecky NA, Soon IS, Rabi DM et al. Increasing incidence and prevalence of the Inflammatory bowel diseases with time, based on systematic review. Gastroenterology 2012; 142 (1): 46–54. doi: 10.1053/ j.gastro.2011.10.001.

26. Lichtenstein GR, Feagan BG, Cohen RD et al. Serious infection and mortality in patients with crohn’s disease: more than 5 years of follow-up in the TREAT registry. Am J Gastroenterol 2012; 107 (9): 1409–1422. doi: 10.1038/ ajg.2012.218.

27. AberraFN, Lichtenstein GR. Methods to avoid infections in doi: 10.1097/01.mib.0000160742. 91602.b7.

28. Nguyen GC, Munsell M, Harris ML. Nationwide prevalence and prognostic signifikance of clinically diagnosable protein calorie malnutrition in hospitalized inflammatory bowel disease patients. Inflamm Bowel Dis 2008; 14 (8): 1105–1111. doi: 10.1002/ ibd.20429.

29. Ananthakrishnan AN, McGinley EL. Infection-related hospitalizations are associated with increased mortality in patients with inflammatory bowel diseases. J Crohn Colitis 2013; 7 (2): 107–112. doi: 10.1016/ j. crohns.2012.02.015.

30. Naganuma M, Kunisaki R, Yoshimura N et al. A prospective analysis of the incidence of and risk factors for opportunistic infections in patients with inflammatory bowel disease. J Gastroenterol 2012; 48 (5): 595–600. doi: 10.1007/ s00535-012-0686-9.

31. Peyrin-Biroulet L, Pillot C, Oussalah A et al. Urinary tract infections in hospitalized Inflammatory bowel disease patients: a 10-year experience. Inflamm Bowel Dis 2012; 18 (4): 697–702. doi: 10.1002/ ibd.21777.

32. Pardi DS, Tremaine WJ, Sandborn WJ et al. Renal and urologic complications of Inflammatory bowel disease. Am J Gastroenterol 1998; 93 (4): 504–514. doi: 10.1111/j.1572-02 41.1998.156_b.x.

33. Primas C, Novacek G, Schweiger K et al. Renal insufficiency in IBD – prevalence and Possible pathogenetic aspects. J Crohn Colitis 2013; 7 (12): 630–634. doi: 10.1016/ j.crohns.2013.05.001.

34. Cury D, Moss A, Schor N. Nephrolithiasis in patients with inflammatory bowel disease in the community. Int J Nephrol Renovasc Dis 2013; 6: 139–142. doi: 10.2147/IJNRD.S45466.

35. Huang V, Mishra R, Thanabalan R et al. Patient awareness of extraintestinal manifestations of inflammatory bowel disease. J Crohn Colitis 2013; 7 (8): 318–324. doi: 10.1016/ j.crohns.2012.11.008.

36. Sammon JD, Ghani KR, Karakiewicz PI et al. Temporal trends, practice patterns, and treatment outcomes for infected upper urinary tract stones in the United States. Eur Urol 2013; 64 (1): 85–92. doi: 10.1016/j.eururo.2012.09.035.

37. Larsen S, Bendtzen K, Nielsen OH. Extraintestinal manifestations of inflammatory bowel disease: epidemiology, diagnosis, and management. Ann Med Mar 2010; 42 (2): 97–114. doi: 10.3109/ 07853890903559724.

38. Danese S, Semeraro S, Papa A et al. Extraintestinal manifestations in inflammatory bowel disease. World J Gastroenterol 2005; 11 (46): 7227–7236. doi: 10.3748/wjg.v11.i46.7227.

39. Rothfuss KS, Stange EF, Herrlinger KR. Extraintestinal manifestations and complicationsin inflammatory bowel diseases. World J Gastroenterol 2006; 14 (30): 4819–4831. doi: 10.3748/wjg.v12.i30.4819.

40. Bernstein CN, Blanchard JF, Rawsthorne P et al. The prevalence of extraintestinal diseases in inflammatory bowel disease: a population-based study. Am J Gastroenterol 1996; 96 (4): 1116–1122. doi: 10.1111/j.1572-0241.2001.037 56.x.

41. Ricart E, Panaccione R, Loftus EV Jr et al. Autoimmune disorders and extraintestinal manifestations in first-degree familial and sporadic inflammatory bowel disease: a case-control study. Inflamm Bowel Dis 2004; 10 (3): 207–214. doi: 10.1097/00054725-200405000-00005.

42. Mendoza JL, Lana R, Taxonera C et al. Extraintestinal manifestations in inflammatory bowel disease: differences between Crohn’s disease and ulcerative colitis. Med Clin (Barc) 2005; 125 (8): 297–300. doi: 10.1157/13078423.

43. Pardi DS, Tremaine WJ, Sandborn WJ et al. Renal and urologic complications of Inflammatory bowel disease. Am J Gastroenterol 1998; 93 (4): 504–514. doi: 10.1111/j.1572-02 41.1998.156_b.x.

44. Serra I, Oller B, Mañosa M et al. Systemic amyloidosis in inflammatory bowel disease: retrospective study on its prevalence, clinical presentation and outcome. J Crohns Colitis 2010; 4 (3): 269–274. doi: 10.1016/ j. crohns.2009.11.009.

45. Basturk T, Ozagari A, Ozturk T et al. Crohn’s disease and secondary amyloidosis: early complication? A case report and review of the literature. J Ren Care 2009; 35 (3): 147–150. doi: 10.1111/ j.1755-6686.2009.00106.x.

46. Peeters AJ, van den Wall Bake AW, Daha MR et al. Inflammatory bowel disease and Ankylosing spondylitis associated with cutaneous vasculitis, glomerulonephritis, and Circulating IgA immune complexes. Ann Rheum Dis 1990; 49 (8): 638–640. doi: 10.1136/ard.49.8.638.

47. Shaer AJ, Stewart LR, Cheek DE et al. IgA antiglomerular basement membrane nephritis Associated with Crohn‘s disease: a case report and review of glomerulonephritis in Inflammatory bowel disease. Am J Kidney Dis 2003; 41 (5): 1097–1109. doi: 10.1016/s0272-6386 (03) 00208-7.

48. Kreisel W, Wolf LM, Grotz W et al. Renal tubular damage: an extraintestinal manifestation of chronic inflammatory bowel disease. Eur J Gastroenterol Hepatol 1996; 8 (5): 461–468.

49. Lukáš M, Bortlík M, Novotný A et al. Nefrotoxicita mesalazinu při dlouhodobé léčbě ulcerózní kolitidy a Crohnovy nemoci. Čes a Slov Gastroent 1999; 53 (5): 135–139.

50.Teplan V. Nefrologické komplikace idiopatických střevních zánětů. In Lukáš M et al. Idiopatické střevní záněty. Nové trendy a mezioborové sopuvislosti. Praha: Grada Publishing 2020: 117–135.

51. Kato Y, Yamaguchi S, Yachiku S et al. Changes in urinary parameters after oral administration of potassium- sodium citrate and magnesium oxide to prevent urolithiasis. Urology 2004; 63 (1): 7–11. doi: 10.1016/j.urology.2003.09.057.

52. Massey L. Magnesium therapy for nephrolithiasis. Magnes Res 2005; 18 (2): 123–126.

53. Siener R, Schade N, Nocolay C et al. The efficacy of dietary intervention on urinary risk factors for stone formation in recurrent calcium oxalate stone patients. J Urol 2005; 173 (5): 1601–1605. doi: 10.1097/01.ju.0000154626.163 49.d3.

54. Stewart CS, Duncan SH, Cave DR. Oxalobacter formigenes and its role in oxalate metabolism in the human gut. FEMS Microbiol Lett 2004; 230 (1): 1–7. doi: 10.1016/S0378-1097 (03) 00864-4.

55. Delvecchio FC, Preminger GM. Medical management of stone disease. Curr Opin Urol 2003; 13 (3): 229–233. doi: 10.1097/00042307-2003 05000-00011.

56. Duncan SH, Richardson AJ, Kaul P et al. Oxalobacter formigenes and its potential role in human health. Appl Environ Microbiol 2002; 68 (8): 3841–3847. doi: 10.1128/AEM.68. 8.3841-3847.2002.

57. Hoppe B, von Unruh G, Laube N et al. Oxalate degrading bacteria: new treatment option for patients with primary and secondary hyperoxaluria? Urol Res 2005; 33 (5): 372–375. doi: 10.1007/s00240-005-0497-z.

58. Campieri C, Campieri M, Bertuzzi V et al. Reduction of oxaluria after an oral course of lactic acid bacteria at high concentration. Kidney Int 2001; 60 (3): 1097–1105. doi: 10.1046/j.15 23-1755.2001.0600031097.x.

59. Lieske JC, Goldfarb DS, De Simone C et al. Use of a probiotic to decrease enteric hyperoxaluria. Kidney Int 2005; 68 (3): 1244–1249. doi: 10.1111/j.1523-1755.2005.00520.x.

60. Mittal RD, Kumar R, Bid HK et al. Effect of antibiotics on Oxalobacter formigenes colonization of human gastrointestinal tract. J Endourol 2005; 19 (1): 102–106. doi: 10.1089/end.2005.19.102.

61. Sidhu H, Hoppe B, Hesse A et al. Absence of Oxalobacter formigenes in cystic fibrosis patients: a risk factor for hyperoxaluria. Lancet 1998; 352 (9133): 1026–1029. doi: 10.1016/S0140-6736 (98) 03038-4.

62.Troxel SA, Sidhu H, Kaul P et al. Intestinal Oxalobater formigenes colonisation in calcium oxalate stone formers and its relation to urinary oxalate. J Endourol 2003; 17 (3): 173–1767. doi: 10.1089/089277903321618743.

63. Hoppe B, Leumann E, von Unruh G et al. Diagnostic and therapeutic approaches in patients with secondary hyperoxaluria. Front Biosci 2003; 8: e437–e443. doi: 10.2741/1135.

64. Cannon JP, Lee TA, Bolanos JT et al. Pathogenic relevance of Lactobacillus: a retrospective review of over 200 cases. Eur J Clin. Microbiol Infect Dis 2005; 24 (1): 31–40. doi: 10.1007/s10096-004-1253-y.

65.Vaidyanathan S, von Unruh GE, Watson ID et al. Hyperoxaluria, hypocitraturia, hypomagnesiuria, and lack of intestinal colonisation by Oxalobacter formigenes in a cervical spinal cor injury patients with suprapublic cystostomy,short bowel,and nephrolithiasis. Scienfific World J 2006; 6 (6): 2403–2410. doi: 10.1100/tsw.2006.373.

66. Kolektiv řešitelů Oddělení vědy a výzkumu společnosti Medi Pharma Vision v Brně. Grant TAČR: Vývoj probiotického přípravku pro pacienty s poruchou funkcí ledvin. Evidenční číslo projektu: FV40254.

67. Wigner P, Bijak M, Saluk-Bijak J. Probiotics in the Prevention of the Calcium Oxalate Urolithiasis. Cells 2022; 11 (2): 284. doi: 10.3390/cells 11020284.

68. Prezioso D, Strazzullo P, Lotti T et al. Dietary tratment of urinary risk factors for renal stone formation.A review of CLU Working Group. Arch Ital Urol Androl 2015; 87 (2): 105–120. doi: 10.4081/aiua.2015.2.105.

69. Nazzal L, Puri S, Goldfarb DS. Enteric hyperoxaluria: an important cause of end-stage kidney disease. Nephrol Dial Transplant 2016; 31 (3): 375–382. doi: 10.1093/ndt/gfv005.