Renal illness in patients with inflammatory bowel disease

Czech version

Authors: V. Teplan ^{1 4}; Honsová E. ⁵; Lukáš M. ^1,2
Authors‘ workplace: Klinické a výzkumné centrum pro idiopatické střevní záněty ISCARE I. V. F. a. s., Praha ¹; 1. LF UK, Praha ²; Subkatedra nefrologie, Institut postgraduálního vzdělávání ve zdravotnictví, Praha ³; Katedra interních oborů LF OU, Ostrava ⁴; Pracoviště klinické a transplantační patologie, Transplantcentrum, IKEM, Praha ⁵
Published in: Gastroent Hepatol 2020; 74(3): 256-266
Category: Chapters from internal medicine: Review Article
doi: https://doi.org/10.14735/amgh2020256

Overview

Gastrointestinal and renal diseases may occur simultaneously. Inflammatory bowel diseases (IBD) are typically accompanied with diarrhea and malabsorption, both of which are predisposing factors for the formation of renal calculi. Enteric hyperoxaluria is a frequent complication of IBD with ileal resection and is well known to cause nephrolithiasis and nephrocalcinosis. 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. Urinary complications in IBD patients with urolithiasis are infection of urinary tract, ureteral obstruction and fistulas. Potential nephrotoxic effect of long-term mesalasine (5-ASA) administration (toxoalergic or chronic nephrotoxic effect) is very important and can lead to tubulointerstitial nephritis, serious damage of renal function and, exceptionally, to renal failure. Therefore, it is recommended to control renal function and urine analysis in the beginning every 3 months, following by a 6-month control. Renal AA amyloidosis is also relatively frequent due to chronic bowel inflammation. Recently, great interest is focused on concomitant immunologic illnesses, mainly glomerulonephritides. The most frequent is mesangioproliferative glomerulopathy with IgA deposits (IgA nephropathy Berger). Acute glomerulonephritis accompanied with bowel inflammation can also occur. Renal damage is associated with decreased renal function (glomerulal filtration rate, concentration and acidification ability) and frequently also with proteinuria, sometimes even nephrotic. Specific situation occurs in IBD patients on biologic therapy and in those with simultaneous renal disease indicated for immunosuppresive treatment with corticosteroids and azathioprine.

Keywords:

inflammatory bowel disease – tubulointerstitial nephritis – glomerulopathy – urolithiasis

Sources

1. Bortlík M. Vývoj léčby idiopatických střevních zánětů v posledních 20. letech. Gastroent Hepatol 2015; 69 (4): 341–350.

2. Magro F, Langner C, Driessen A et al. European consensus on the histopathology of inflammatory bowel disease. J Crohns Colitis 2013; 7 (10): 827–851. doi: 10.1016/j.crohns.2013.06.001.

3. Lukáš M et al. Pokroky v diagnostice a léčbě idiopatických střevních zánětů. Praha: Galen 2019.

4. Krebs CF, Paust HJ, Krohn S et al. Autoimmune renal disease is exacerbated by S1P-receptor-1-dependent intestinal TH17 cell migration to the kidney. Immunity 2016; 45 (5): 1078–1092. doi: 10.1016/j.immuni.2016.10.020.

5. Oikonomou K, Kapsoritakis A, Eleftheriadis T et al. Renal manifestations and complications of inflammatory bowel disease. Inflamm Bowel Dis 2011; 17 (4): 1034–1045. doi: 10.1002/ibd.21468.

6. Ridder RM, Kreth HW, Kiss E et al. Membranous nephropathy associated with familial chronic ulcerative colitis in a 12-year-old girl. Pediatr Nephrol 2005; 20 (9): 1349–1351. doi: 10.1007/s00467-005-1986-6.

7. Van Staa TP, Travis S, Leufkens HG et al. 5-aminosalicylic acids and the risk of renal disease: a large British epidemiologic study. Gastroenterology 2004; 126 (7): 1733–1739. doi: 10.1053/j.gastro.2004.03.016.

8. Riley SA, Lloyd DR, Mani V. Tests of renal function in patients with quiscent colitis: effect of drug treatment. Gut 1992; 33 (10): 1348–1352. doi: 10.1136/gut.33.10.1348.

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

10. Teplan V. Nefrologické minimum pro klinickou praxi. 3. přepracované a doplněné vyd. Praha: Maxdorf 2020.

11. Teplan V, Marečková O, Lukáš M. Onemocnění gastrointestinálního traktu a choroby ledvin. Gastroent Hepatol 2018; 72 (1): 50–57. doi: 10.14735/amgh201850.

12. Teplan V, Ševela K. Toxické a lékové poškození jater a ledvin. Gastroent Hepatol 2019; 73 (1): 66–74. doi: 10.14735/amgh201966.

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

14. Magalhães-Costa P, Matos L, Chagas C. Chronic tubulointerstitial nephritis induced by 5-aminosalicylate in an ulcerative colitis patient: a rare but serious adverse event. BMJ Case Rep 2015; bcr2014207928. doi: 10.1136/bcr-2014-207928.

15. World MJ, Stevens PE, Ashton M et al. Mesalasine-associated interstitial nephritis. Nephrol Dial Transpl 1996; 11 (4): 614–621. doi: 10.1093/oxfordjournals.ndt.a027349.

16. Calviño J, Romero R, Pintos E et al. Mesalasine-associated tubulo-interstitial nephritis in inflammatory bowel disease. Clin Nephrol 1998; 49 (4): 265–267.

17. Pohjonen J, Nurmi R, Metso M et al. Inflammatory bowel disease in patients undergoing renal biopsies. Clin Kidney J 2019; 12 (5): 645–651. doi: 10.1093/ckj/sfz004.

18. De Jong DJ, Tielen J, Habraken CM et al. 5-aminosalicylates and effect on renal function in patients with Crohn’s diseases. Inflamm Bowel Dis 2005; 11 (11): 972–976. doi: 10.1097/01.mib.0000185402.65288.19.

19. Mahmud N, McDonald GS, Kelleher D et al. Microalbuminuria correlates with intestinal histopathological grading in patients with inflammatory bowel disease. Gut 1996; 38 (1): 99–103. doi: 10.1136/gut.38.1.99.

20. Barbour VM, Williams PF. Nephrotic syndrome associated with sulphasalazine. BMJ 1990; 301 (6755): 818–822. doi: 10.1136/bmj.301.6755.818-b.

21. Mahmud N, O’Toole D, O’Hare N et al. Evaluation of renal function following treatment with 5-aminosalicylic acid derivatives in patients with ulcerative colitis. Aliment Phamacol Ther 2002; 16 (2): 207–215. doi: 10.1046/j.1365-2036.2002.01155.x.

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

23. Oikonomou KA, Kapsoritakis AN, Stefanidis Iet al. Drug-induced nephrotoxicity in inflammatory bowel disease. Nephron Clin Pract 2011; 119 (2): 89–94. doi: 10.1159/000326682.

24. Hämling J, Raeder A, Helmchen U et al. 5-aminosalicylic acid-associated renal tubular acidosis with decreased renal function in Crohn’s disease. Digestion 1997; 58 (3): 304–307. doi: 10.1159/000201459.

25. Kiryluk K, Li Y, Scolari F et al. Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens. Nat Genet 2014; 46 (11): 1187–1196. doi: 10.1038/ng.3118.

26. Honkanen T, Mustonen J, Kainulainen H et al. Small bowel cyclooxygenase 2 (COX-2) expression in patients with IgA nephropathy. Kidney Int 2005; 67 (6): 2187–2195. doi: 10.1111/ j.1523-1755.2005.00324.x.

27. Ritz E. Gastrointestinal disease and the kidney. In: Davison AM, Cameron JS, Grunfeld JP et al (eds). Oxford Textbook of Clinical Nephrology. Oxford University Press 1998: 2733–2735.

28. Ramos-Casals M, Brito-Zerón P, Muñoz S et al. Autoimmune diseases induced by TNF-targeted therapies: analysis of 233 cases. Medicine (Baltimore) 2007; 86 (4): 242–251. doi: 10.1097/MD.0b013e3181441a68.

29. Haake H, Köneke J, Amann K et al. Development of systemic lupus erythematosus with focal proliferative lupus nephritis during anti-TNF-alpha therapy for psoriatic arthritis. Med Klin (Munich) 2007; 102 (10): 852–857. doi: 10.1007/s00063-007-1104-6.

30. Saint Marcoux B, De Bandt M, CRI (Club Rhumatismes et Inflammation). Vasculitides induced by TNF alpha antagonists: a study in 39 patients in France. Joint Bone Spine 2006; 73 (6): 710–713. doi: 10.1016/j.jbspin.2006.02.010.

31. Teplan V, Honsová E, Lukáš M. Glomerulopatie u pacientů s idiopatickými střevními záněty. Gastroent Hepatol 2020; 74 (1): 62–67. doi: 10.14735/amgh202062.

32. Cuquerella JT, Bosca-Watts MM, Ausejo RA et al. Amyloidosis in inflammatory bowel disease: a systematic review of epidemiology, clinical features, and treatment. J Crohns Colitis 2016; 10 (10): 1245–1253. doi: 10.1093/ecco-jcc/jjw080.

33. Ryšavá R. Postižení gastroinstestinálního traktu amyloidózou – kdy na ni myslet a jak diagnostikovat. Gastroent Hepatol 2019; 73 (2): 154–162. doi: 10.14735/amgh2019154.

34. Teplan V, Lukáš M. Urolithiasis in patients with inflammatory bowel disease. Gastroent Hepatol 2015; 69 (6): 561–569. doi: 10.14735/ amgh2015561.