Tom 18, Nr 1 (2021)
Artykuł przeglądowy
Opublikowany online: 2021-05-27
Dieta a metabolity mikrobioty jelitowej i ryzyko sercowo-naczyniowe wśród pacjentów z przewlekłą chorobą nerek
Choroby Serca i Naczyń 2021;18(1):31-38.
Streszczenie
Pacjenci z przewlekłą chorobą nerek (CKD) charakteryzują się wyższą śmiertelnością w porównaniu z populacją ogólną. Główną przyczyną zgonów są powikłania sercowo-naczyniowe. Ogromne zainteresowanie tematyką mikrobioty jelitowej sprawia, że powstaje coraz więcej badań wskazujących na wpływ mikroorganizmów i ich metabolitów na ryzyko sercowo-naczyniowe. Niektóre metabolity mikrobioty jelitowej są zaliczane do toksyn mocznicowych. Do najlepiej poznanych metabolitów należy N-tlenek trimetyloaminy, siarczan p-krezolu oraz siarczan indoksylu. Zaobserwowano, że wymienione toksyny mocznicowe promują rozwój miażdżycy oraz przyczyniają się do występowania przewlekłego stanu zapalnego. Jednym z czynników wpływających na skład mikrobioty jelitowej jest dieta. Celem pracy jest przedstawienie na podstawie najnowszych badań związku pomiędzy metabolitami mikrobioty, dietą a zwiększonym ryzykiem sercowo naczyniowym w grupie osób z CKD.
Słowa kluczowe: przewlekła choroba nerekryzyko sercowo-naczyniowemetabolity mikrobioty jelitowejN-tlenek trimetyloaminysiarczan p-krezolusiarczan indoksylu
Referencje
- Hill NR, Fatoba ST, Oke JL, et al. Global prevalence of chronic kidney disease - a systematic review and meta-analysis. PLoS One. 2016; 11(7): e0158765.
- Eckardt KU, Coresh J, Devuyst O, et al. Evolving importance of kidney disease: from subspecialty to global health burden. Lancet. 2013; 382(9887): 158–169.
- Lainščak M. 10. Cardiovascular Risk in Chronic Kidney Disease. EJIFCC. 2009; 20(1): 73–76.
- Schunk SJ, Speer T, Fliser D, et al. Chronic kidney disease-a cardiovascular high-risk constellation. Internist (Berl). 2020; 61(4): 340–348.
- Sarnak MJ, Amann K, Bangalore S, et al. Conference Participants. Chronic kidney disease and coronary artery disease: JACC state-of-the-art review. J Am Coll Cardiol. 2019; 74(14): 1823–1838.
- Knauf F, Brewer JR, Flavell RA. Immunity, microbiota and kidney disease. Nat Rev Nephrol. 2019; 15(5): 263–274.
- Berg G, Rybakova D, Fischer D, et al. Microbiome definition re-visited: old concepts and new challenges. Microbiome. 2020; 8(1): 103.
- Rinninella E, Raoul P, Cintoni M, et al. What is the healthy gut microbiota composition? A changing ecosystem across age, environment, diet, and diseases. Microorganisms. 2019; 7(1).
- Sender R, Fuchs S, Milo R. Revised estimates for the number of human and bacteria cells in the body. PLoS Biol. 2016; 14(8): e1002533.
- Arumugam M, Raes J, Pelletier E, et al. MetaHIT Consortium. Enterotypes of the human gut microbiome. Nature. 2011; 473(7346): 174–180.
- Castillo-Rodríguez E, Pizarro-Sánchez S, Sanz AB, et al. Inflammatory cytokines as uremic toxins: "ni son todos los que estan, ni estan todos los que son". Toxins (Basel). 2017; 9(4).
- Vaziri ND, Yuan J, Norris K. Role of urea in intestinal barrier dysfunction and disruption of epithelial tight junction in chronic kidney disease. Am J Nephrol. 2013; 37(1): 1–6.
- Chang M, Kistler EB, Schmid-Schönbein GW. Disruption of the mucosal barrier during gut ischemia allows entry of digestive enzymes into the intestinal wall. Shock. 2012; 37(3): 297–305.
- Ikee R, Sasaki N, Yasuda T, et al. Chronic kidney disease, gut dysbiosis, and constipation: a burdensome triplet. Microorganisms. 2020; 8(12).
- Vaziri ND, Zhao YY, Pahl MV. Altered intestinal microbial flora and impaired epithelial barrier structure and function in CKD: the nature, mechanisms, consequences and potential treatment. Nephrol Dial Transplant. 2016; 31(5): 737–746.
- Lee SH. Intestinal permeability regulation by tight junction: implication on inflammatory bowel diseases. Intest Res. 2015; 13(1): 11–18.
- Suzuki T. Regulation of the intestinal barrier by nutrients: The role of tight junctions. Anim Sci J. 2020; 91(1): e13357.
- Tripathi A, Lammers KM, Goldblum S, et al. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009; 106(39): 16799–16804.
- McIntyre CW, Harrison LEA, Eldehni MT, et al. Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease. Clin J Am Soc Nephrol. 2011; 6(1): 133–141.
- Meijers B, Farré R, Dejongh S, et al. Intestinal barrier function in chronic kidney disease. Toxins (Basel). 2018; 10(7).
- Moraes C, Fouque D, Amaral AC, et al. Trimethylamine N-oxide from gut microbiota in chronic kidney disease patients: focus on diet. J Ren Nutr. 2015; 25(6): 459–465.
- Cho CE, Taesuwan S, Malysheva OV, et al. Trimethylamine-N-oxide (TMAO) response to animal source foods varies among healthy young men and is influenced by their gut microbiota composition: A randomized controlled trial. Mol Nutr Food Res. 2017; 61(1).
- Baza danych składników odżywczych USDA. https://ndb.nal.usda.gov/ndb/ (January 18, 2021).
- Zeisel SH, Mar MH, Howe JC, et al. Concentrations of choline-containing compounds and betaine in common foods. J Nutr. 2003; 133(5): 1302–1307.
- Przygoda B, Wierzejska R, Matczuk E, Kłys W, Jarosz M. Witaminy. In: Jarosz M, Rychlik E, Stoś K, Charzewska J. ed. Normy żywienia dla populacji Polski i ich zastosowanie. Narodowy Instytut Zdrowia Publicznego — Państwowy Zakład Higieny, Warszawa 2020: 236–240.
- Rospond B, Chłopicka J. Funkcje biologiczne L-karnityny i jej zawartość w wybranych produktach spożywczych. Przegl Lek. 2013; 70(2): 85–91.
- Ślęczka A, Krzywonos M, Wilk M, et al. Występowanie i rola betainy w organizmach żywych. Nauka Przyroda Technologie. 2015; 9(2): 43.
- Koeth RA, Wang Z, Levison BS, et al. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atheroscleros. Nat Med. 2013; 19(5): 576–585.
- Flores-Guerrero JL, Osté MCJ, Baraldi PB, et al. Association of circulating trimethylamine -oxide and its dietary determinants with the risk of kidney graft failure: results of the transplantlines cohort study. Nutrients. 2021; 13(1): 262.
- Guo F, Dai Q, Zeng X, et al. Renal function is associated with plasma trimethylamine-N-oxide, choline, L-carnitine and betaine: a pilot study. Int Urol Nephrol. 2021; 53(3): 539–551.
- Gryp T, Vanholder R, Vaneechoutte M, et al. p-Cresyl Sulfate. Toxins (Basel). 2017; 9(2): 52.
- Kunachowicz H, Przygoda B, Nadolna I, Iwanow K. Tabele składu i wartości odżywczej żywności. PZWL, Warszawa 2017: Warszawa.
- Jongkees BJ, Hommel B, Kühn S, et al. Effect of tyrosine supplementation on clinical and healthy populations under stress or cognitive demands--A review. J Psychiatr Res. 2015; 70: 50–57.
- National Academies Press (NAP) Food and nutrition board. Dietary reference intakes (DRI): the essential guide to nutrient requirements [Internet] Washington, DC: NAP; 2006. https://www.nal.usda.gov/sites/default/files/fnic_uploads/DRIEssentialGuideNutReq.pdf (January 18, 2021).
- Fernandes AL, Borges NA, Black AP, et al. Dietary intake of tyrosine and phenylalanine, and p-cresyl sulfate plasma levels in non-dialyzed patients with chronic kidney disease. J Bras Nefrol. 2020; 42(3): 307–314.
- Gryp T, De Paepe K, Vanholder R, et al. Gut microbiota generation of protein-bound uremic toxins and related metabolites is not altered at different stages of chronic kidney disease. Kidney Int. 2020; 97(6): 1230–1242.
- Ellis RJ, Small DM, Vesey DA, et al. Indoxyl sulphate and kidney disease: Causes, consequences and interventions. Nephrology (Carlton). 2016; 21(3): 170–177.
- Zhang LS, Davies SS. Microbial metabolism of dietary components to bioactive metabolites: opportunities for new therapeutic interventions. Genome Med. 2016; 8(1): 46.
- Ravindran AV, da Silva TL. Complementary and alternative therapies as add-on to pharmacotherapy for mood and anxiety disorders: a systematic review. J Affect Disord. 2013; 150(3): 707–719.
- Poesen R, Mutsaers HAM, Windey K, et al. The influence of dietary protein intake on mammalian tryptophan and phenolic metabolites. PLoS One. 2015; 10(10): e0140820.
- Di Iorio BR, Rocchetti MT, De Angelis M, et al. Nutritional therapy modulates intestinal microbiota and reduces serum levels of total and free indoxyl sulfate and p-cresyl sulfate in chronic kidney disease (medika study). J Clin Med. 2019; 8(9).
- Tang WH, Wang Z, Kennedy DJ, et al. Gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway contributes to both development of renal insufficiency and mortality risk in chronic kidney disease. Circ Res. 2015; 116(3): 448–455.
- Hai X, Landeras V, Dobre MA, et al. Mechanism of prominent trimethylamine oxide (TMAO) accumulation in hemodialysis patients. PLoS One. 2015; 10(12): e0143731.
- Bain MA, Faull R, Fornasini G, et al. Accumulation of trimethylamine and trimethylamine-N-oxide in end-stage renal disease patients undergoing haemodialysis. Nephrol Dial Transplant. 2006; 21(5): 1300–1304.
- Qi J, You T, Li J, et al. Circulating trimethylamine N-oxide and the risk of cardiovascular diseases: a systematic review and meta-analysis of 11 prospective cohort studies. J Cell Mol Med. 2018; 22(1): 185–194.
- Schiattarella GG, Sannino A, Toscano E, et al. Gut microbe-generated metabolite trimethylamine-N-oxide as cardiovascular risk biomarker: a systematic review and dose-response meta-analysis. Eur Heart J. 2017; 38(39): 2948–2956.
- Ma G, Pan B, Chen Y, et al. Trimethylamine N-oxide in atherogenesis: impairing endothelial self-repair capacity and enhancing monocyte adhesion. Biosci Rep. 2017; 37(2).
- Zhang X, Li Y, Yang P, et al. Trimethylamine-N-oxide promotes vascular calcification through activation of NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome and nf-κb (nuclear factor κB) signals. Arterioscler Thromb Vasc Biol. 2020; 40(3): 751–765.
- Neirynck N, Glorieux G, Schepers E, et al. Review of protein-bound toxins, possibility for blood purification therapy. Blood Purif. 2013; 35(Suppl 1): 45–50.
- Lin CJ, Wu V, Wu PC, et al. Meta-Analysis of the associations of p-Cresyl sulfate (PCS) and indoxyl sulfate (IS) with cardiovascular events and all-cause mortality in patients with chronic renal failure. PLoS One. 2015; 10(7): e0132589.
- Poveda J, Sanchez-Niño MD, Glorieux G, et al. p-Cresyl sulphate has pro-inflammatory and cytotoxic actions on human proximal tubular epithelial cells. Nephrol Dial Transplant. 2014; 29(1): 56–64.
- Han H, Zhu J, Zhu Z, et al. p-Cresyl sulfate aggravates cardiac dysfunction associated with chronic kidney disease by enhancing apoptosis of cardiomyocytes. J Am Heart Assoc. 2015; 4(6): e001852.
- Koppe L, Pillon NJ, Vella RE, et al. p-Cresyl sulfate promotes insulin resistance associated with CKD. J Am Soc Nephrol. 2013; 24(1): 88–99.
- Tanaka S, Watanabe H, Nakano T, et al. Indoxyl sulfate contributes to adipose tissue inflammation through the activation of NADPH oxidase. Toxins (Basel). 2020; 12(8).
- Plata C, Cruz C, Cervantes LG, et al. The gut microbiota and its relationship with chronic kidney disease. Int Urol Nephrol. 2019; 51(12): 2209–2226.
- Vanholder R, Schepers E, Pletinck A, et al. The uremic toxicity of indoxyl sulfate and p-Cresyl sulfate: a systematic review. J Am Soc Nephrol. 2014; 25(9): 1897–1907.
- Sun CY, Hsu HH, Wu MS. p-Cresol sulfate and indoxyl sulfate induce similar cellular inflammatory gene expressions in cultured proximal renal tubular cells. Nephrol Dial Transplant. 2013; 28(1): 70–78.
- Castillo-Rodriguez E, Fernandez-Prado R, Esteras R, et al. Impact of altered intestinal microbiota on chronic kidney disease progression. Toxins (Basel). 2018; 10(7): 300.
- Yang K, Du C, Wang X, et al. Indoxyl sulfate induces platelet hyperactivity and contributes to chronic kidney disease-associated thrombosis in mice. Blood. 2017; 129(19): 2667–2679.
- Nangaku M, Mimura I, Yamaguchi J, et al. Role of uremic toxins in erythropoiesis-stimulating agent resistance in chronic kidney disease and dialysis patients. J Ren Nutr. 2015; 25(2): 160–163.
- Liu WC, Tomino Y, Lu KC. Impacts of indoxyl sulfate and p-Cresol sulfate on chronic kidney disease and mitigating effects of AST-120. Toxins (Basel). 2018; 10(9): 367.