Reduced urinary magnesium levels after ileocolic resection in patients with Crohn’s disease
Authors:
V. Navrátil 1
; Lumír Kunovský 1-3
; B. Pipek 1,4
; Jan Křivinka 1
; J. Zapletalová 5; Přemysl Falt 1
Authors place of work:
II. interní klinika – gastroenterologická a geriatrická LF UP a FN Olomouc
1; Chirurgická klinika LF MU a FN Brno
2; Gastroenterologické oddělení a digestivní endoskopie, Masarykův onkologický ústav, Brno
3; Centrum péče o zažívací trakt, Nemocnice AGEL Ostrava-Vítkovice a. s.
4; Ústav lékařské biofyziky LF UP v Olomouci
5
Published in the journal:
Gastroent Hepatol 2024; 78(1): 19-26
Category:
IBD
doi:
https://doi.org/10.48096/ccgh202419
Summary
: Introduction: Urinary excretion of magnesium is an important preventive factor against nephrolithiasis by inhibiting several key processes in its pathogenesis. Patients with Crohn’s disease (CD) have an approximately 2-fold higher risk of lithiasis, especially those after ileocolic (IC) resection. The aim is to determine the magnesuria level in these patients and compare it with patients with CD and IC involvement without resection and then both groups with healthy controls. The secondary objective was to assess calciuria and other modifying factors. Methods: CD patients aged 18 years or older with IC resection (group 1) and terminal ileal involvement without resection (group 2) were enrolled in the study, with subjects without known bowel disease as controls (group 3). Exclusion criteria were citrate therapy, severe renal insufficiency (GFR < 30 ml/ min/ 1.73 m2), more than two bowel resections, ileostomy, colectomy, short bowel syndrome, acute urinary tract infection and evidence of CD relapse. Anamnestic data were collected by questionnaire, blood and fresh urine samples were collected, renal and gallbladder ultrasound was performed for the presence of lithiasis, and patients underwent 24-hour urine collection to determine oxaluria, citraturia, magnesuria and calciuria. Results: 107 subjects were included in the study, including 34 patients with IC resection, 42 with CD without resection and 31 healthy controls. 43% were women, mean age was 38 ± 11.5 years. There was a significant difference in magnesuria values between the resection and non-resection group (median 2.28 vs. 3.97 mmol/ l; P = 0.047) and especially between the resection group and healthy controls (median 2.28 vs. 4.31 mmol/ l; P = 0.0003). The group without resection vs. healthy controls did not reach a significant difference (median 3.97 vs. 4.31 mmol/ l; P = 0.455). Calciuria values did not differ significantly between groups (median 3.75 vs. 4.6 vs. 4.3 mmol/ l; P = 0.293). Conclusion: Magnesuria values of CD patients after IC resection were significantly lower compared to the group of CD patients with IC involvement without resection and healthy controls. The group without resection achieved results comparable to controls. Calciuria values were not significantly different between groups in our study. We hypothesize that patients with CD after IC resection at higher risk of urolithiasis might benefit from Mg supplementation to prevent concretion formation. However, confirmation of this thesis will require verification by further research.
Zdroje
1. Torres J, Mehandru S, Colombel JF et al. Crohn’s disease. Lancet 2017; 389(10080): 1741–1755. doi: 10.1016/ S0140-6736(16)31711-1.
2. Ferreira SD, Oliveira BB, Morsoletto AM et al. Extraintestinal manifestations of inflammatory bowel disease: Clinical aspects and pathogenesis. J Gastroenterol Dig Dis 2018; 3(1): 4–11.
3. Lukáš M. Možnosti medikamentózní léčby u Crohnovy nemoci a ulcerózní kolitidy. Med praxi 2011; 8(9): 360–363.
4. Bortlík M, Ďuricová D, Douda T et al. Doporučení pro po dávání biologické léčby pacientům s idiopatickými střevní mi záněty: čtvrté, aktualizované vydání. Gastroent Hepatol 2019; 73(1): 11–24.
5. Vavricka SR, Schoepfer A, Scharl M et al. Extraintestinal Manifestations of Inflammatory Bowel Disease. Inflamm Bowel Dis 2015; 21(8): 1982–1992. doi: 10.1097/ MIB.0000000 000000392.
6. Navrátil V, Cveková S, Slodička P et al. Extraintestinal complications of inflammatory bowel diseases. Mimostřevní komplikace idiopatických střevních zánětů. Vnitr Lek 2021; 67(2): 92–96.
7. Gaspar SR da S, Mendonça T, Oliveira P et al. Urolithiasis and crohn’s disease. Urol Ann 2016; 8(3): 297–304. doi: 10.4103/ 0974-7796.184879.
8. Miyajima S, Ishii T, Watanabe M et al. Risk factors for urolithiasis in patients with Crohn’s disease. Int J Urol 2021; 28(2): 220–224. doi: 10.1111/ iju.14442.
9. Teplan V, Netušil R, Lukáš M. Urolitiáza u pacientů s idiopatickými střevními záněty – možnosti prevence a metabolického ovlivnění. Gastroent Hepatol 2023; 77(5): 437–446. doi: 10.48095/ ccgh2023446.
10. Thakore P, Liang TH. Urolithiasis. In: StatPearls. Treasure Island (FL): StatPearls Publishing 2023. Dostupné z: https:/ / www.ncbi.nlm.nih.gov/ books/ NBK559101/ .
11. Scales CD Jr, Smith AC, Hanley JM et al. Urologic Diseases in America Project. Prevalence of kidney stones in the United States. Eur Urol 2012; 62(1): 160–165. doi:10.1016/ j.eururo. 2012.03.052.
12. Khan SR, Pearle MS, Robertson WG et al. Kidney stones. Nat Rev Dis Primers 2016; 2: 16008. doi: 10.1038/ nrdp.2016.8.
13. Sobotka R, Hanuš T. Příčiny a rizikové faktory vzniku urolitiázy. Urol praxi 2012; 13(1): 11–15.
14. Dimke H, Winther-Jensen M, Allin KH et al. Risk of Urolithiasis in Patients With Inflammatory Bowel Disease: A Nationwide Danish Cohort Study 1977–2018. Clin Gastroenterol Hepatol 2021; 19(12): 2532–2540. doi: 10.1016/ j.cgh.2020.09.049.
15. Corica D, Romano C. Renal Involvement in Inflammatory Bowel Diseases. J Crohns Colitis 2016; 10(2): 226–235. doi: 10.1093/ ecco-jcc/ jjv138.
16. Katsanos K, Tsianos EV. The kidneys in inflammatory bowel disease. Ann Gastroenterol 2002; 15(1): 41–52.
17. Rokyta R et al. Fyziologie a Patologická Fyziologie: Pro Klinickou Praxi. Praha: Grada Publishing 2015.
18. Chung MJ. Urolithiasis and nephrolithiasis. JAAPA 2017; 30(9): 49–50. doi: 10.1097/ 01.JAA.0000522145.52305.aa.
19. Gajendran M, Loganathan P, Catinella AP et al. A comprehensive review and update on Crohn’s disease. Dis Mon 2018; 64(2): 20–57. doi: 10.1016/ j.disamonth.2017.07.001.
20. Šerclová Z, Ryska O, Bortlík M et al. Doporučené postupy chirurgické léčby pacientů s nespecifickými střevními záněty – 2. část: Crohnova nemoc. Gastroent Hepatol 2015; 69(3): 223–238. doi: 10.14735/ amgh2015223.
21. 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.
22. Bianchi L, Gaiani F, Bizzarri B et al. Renal lithiasis and inflammatory bowel diseases, an update on pediatric population. Acta Biomed 2018; 89(9-S): 76–80. doi: 10.23750/ abm.v89i9-S.7908.
23. Worcester EM. Stones from bowel disease. Endocrinol Metab Clin North Am 2002; 31(4): 979–999. doi: 10.1016/ s0889-8529(02)000 35-x.
24. Teplan V, Lukáš M. Urolithiasis in patients with inflammatory bowel diseases. Gastroent Hepatol 2015; 69(6): 561–569. doi: 10.14735/ amgh2015561.
25. Shringi S, Raker CA, Tang J. Dietary Magnesium Intake and Kidney Stone: The National Health and Nutrition Examination Survey 2011–2018. R I Med J (2013) 2023; 106(11): 20–25.
26. Levey AS, Eckardt KU, Tsukamoto Y et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2005; 67(6): 2089–2100. doi: 10.1111/ j.1523-1755.2005.00365.x.
27. Israr B, Frazier RA, Gordon MH. Effects of phytate and minerals on the bioavailability of oxalate from food. Food Chem 2013; 141(3): 1690–1693. doi: 10.1016/ j.foodchem.2013.04. 130.
28. Hsu YC, Lin YH, Shiau LD. Effects of Various Inhibitors on the Nucleation of Calcium Oxalate in Synthetic Urine. Crystals 2020; 10(4): 333. doi: 10.3390/ cryst10040333.
29. Lieske JC, Farell G, Deganello S. The effect of ions at the surface of calcium oxalate monohydrate crystals on cell-crystal interactions. Urol Res 2004; 32(2): 117–123. doi: 10.1007/ s00240-003-0391-5.
30. Jaeger P, Robertson WG. Role of dietary intake and intestinal absorption of oxalate in calcium stone formation. Nephron Physiol 2004; 98(2): 64–71. doi: 10.1159/ 000080266.
31. Allie S, Rodgers A. Effects of calcium carbonate, magnesium oxide and sodium citrate bicarbonate health supplements on the urinary risk factors for kidney stone formation. Clin Chem Lab Med 2003; 41(1): 39–45. doi: 10.1515/ CCLM.2003.008.
32. Guillen B, Atherton NS. Short Bowel Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing 2023.
33. Jabłońska B, Mrowiec S. Nutritional Status and Its Detection in Patients with Inflammatory Bowel Diseases. Nutrients 2023; 15(8): 1991. doi: 10.3390/ nu15081991.
34. Parks JH, Worcester EM, O’Connor RC 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.15 23-1755.2003.00725.x.
35. 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.
36. Kumar R, Ghoshal UC, Singh G et al. Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: possible role in renal stone formation. J Gastroenterol Hepatol 2004; 19(12): 1403–1409. doi:10.1111/ j.1440-1746.2004.03510.x.
37. Caudarella R, Rizzoli E, Pironi L et al. Renal stone formation in patients with inflammatory bowel disease. Scanning Microsc 1993; 7(1): 371–380.
38. Geerling BJ, Badart-Smook A, Stockbrügger RW et al. Comprehensive nutritional status in recently diagnosed patients with inflammatory bowel disease compared with population controls. Eur J Clin Nutr 2000; 54(6): 514–521. doi: 10.1038/ sj.ejcn.1601049.
39. McIntosh HW, Seraglia M. Urinary Excretion of Calcium and Citrate in Normal Individuals and Stone Formers with Variation in Calcium Intake. Can Med Assoc J 1963; 89(24): 1242–1243.
ORCID autorů
V. Navrátil 0000-0002-9323-1996,
L. Kunovský 0000-0003-2985-8759,
B. Pipek 0000-0002-0315-8845,
J. Křivinka 0009-0008-2705-1357,
P. Falt 0000-0001-8843-4716.
Doručeno/ Submitted: 21. 12. 2023
Přijato/ Accepted: 15. 1. 2024
MU Dr. Vít Navrátil
II. interní klinika – gastroenterologická a geriatrická
LF UP a FN Olomouc
Zdravotníku 248/ 7
779 00 Olomouc
vit.navratil@fnol.cz
Štítky
Paediatric gastroenterology Gastroenterology and hepatology SurgeryČlánok vyšiel v časopise
Gastroenterology and Hepatology
2024 Číslo 1
- Metamizole at a Glance and in Practice – Effective Non-Opioid Analgesic for All Ages
- Metamizole vs. Tramadol in Postoperative Analgesia
- Spasmolytic Effect of Metamizole
- Possibilities of Using Metamizole in the Treatment of Acute Primary Headaches
- Current Insights into the Antispasmodic and Analgesic Effects of Metamizole on the Gastrointestinal Tract
Najčítanejšie v tomto čísle
- Mirikizumab – the first anti-IL23 p19 antibody in ulcerative colitis therapy
- Idiopathic hypereosinophilic syndrome with gastrointestinal involvement
- Hidradenitis suppurativa, intestinal microbiome and SIBO – a comprehensive overview of the issue
- Methotrexate is the re-discovered drug for Crohn’s disease