The Gut as a Source of Inflammation in Chronic Kidney Disease.
The Gut as a Source of Inflammation in Chronic Kidney Disease.
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作者：
Lau WL;Kalantar-Zadeh K;Vaziri ND
慢性炎症是慢性肾脏病(CKD)人群心血管死亡的非传统危险因素。近年来，胃肠道已成为慢性肾脏病全身炎症的主要诱因。此前的尸检研究发现，慢性透析患者的整个消化道都存在肠壁炎症。在CKD动物中，结肠壁炎症与上皮紧密连接屏障(“漏肠”)的破坏以及细菌DNA和内毒素的移位进入血液有关。CKD和透析患者的血清中也检测到肠道细菌DNA和内毒素，内毒素水平随着CKD分期的增加而增加，并与透析人群全身炎症的严重程度相关。低植物纤维和共生生物(同时低钾、低磷摄入量)的CKD饮食会改变正常的肠道微生物群，导致产生尿毒症毒素的细菌过度生长，如甲苯和吲哚分子。这些毒素从“渗漏的肠道”转移到血液中，进一步促进全身炎症、不利的心血管后果和慢性肾脏病的进展。在CKD中，缺乏最优纤维和酸奶消费的数据，这些数据将有利于更多共生微生物的生长，同时避免钾和磷超载。益生菌和益生菌制剂在小型临床试验中显示出了降低尿毒症毒素水平和改善生活质量的前景。证据表明，肠道炎症和慢性肾脏病的不良结局之间存在很强的相关性，需要进行更多的肠道靶向治疗试验。
Chronic inflammation is a non-traditional risk factor for cardiovascular mortality in the chronic kidney disease (CKD) population. In recent years the gastrointestinal tract has emerged as a major instigator of systemic inflammation in CKD. Post-mortem studies previously discovered gut wall inflammation present throughout the digestive tract in chronic dialysis patients. In CKD animals, colon wall inflammation is associated with breakdown of the epithelial tight junction barrier (“leaky gut”) and translocation of bacterial DNA and endotoxin into the bloodstream. Gut bacterial DNA and endotoxin have also been detected in the serum from CKD and dialysis patients, whereby endotoxin levels increase with CKD stage and correlate with severity of systemic inflammation in the dialysis population. The CKD diet that is low in plant fiber and symbiotic organisms (in adherence with low potassium, low phosphorus intake) can alter the normal gut microbiome, leading to overgrowth of bacteria that produce uremic toxins such as cresyl and indoxyl molecules. The translocation of these toxins from the “leaky gut” into the bloodstream further promotes systemic inflammation, adverse cardiovascular outcomes and CKD progression. Data is lacking on optimal fiber and yogurt consumption in CKD that would favor growth of a more symbiotic microbiome while avoiding potassium and phosphorus overload. Prebiotic and probiotic formulations have shown promise in small clinical trials, in terms of lowering serum levels of uremic toxins and improving quality of life. The evidence points to a strong relationship between intestinal inflammation and adverse outcomes in CKD, and more trials investigating gut-targeted therapeutics are needed.
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影响因子：
64.8
作者：
Arumugam, Manimozhiyan;Raes, Jeroen;Pelletier, Eric;Le Paslier, Denis;Yamada, Takuji;Mende, Daniel R.;Fernandes, Gabriel R.;Tap, Julien;Bruls, Thomas;Batto, Jean-Michel;Bertalan, Marcelo;Borruel, Natalia;Casellas, Francesc;Fernandez, Leyden;Gautier, Laurent;Hansen, Torben;Hattori, Masahira;Hayashi, Tetsuya;Kleerebezem, Michiel;Kurokawa, Ken;Leclerc, Marion;Levenez, Florence;Manichanh, Chaysavanh;Nielsen, H. Bjorn;Nielsen, Trine;Pons, Nicolas;Poulain, Julie;Qin, Junjie;Sicheritz-Ponten, Thomas;Tims, Sebastian;Torrents, David;Ugarte, Edgardo;Zoetendal, Erwin G.;Wang, Jun;Guarner, Francisco;Pedersen, Oluf;de Vos, Willem M.;Brunak, Soren;Dore, Joel;Weissenbach, Jean;Ehrlich, S. Dusko;Bork, Peer
通讯作者：
Bork, Peer
DOI：
10.2215/cjn.02720409
发表时间：
2009-12-01
影响因子：
9.8
作者：
Carrero, Juan Jesus;Stenvinkel, Peter
通讯作者：
Stenvinkel, Peter
影响因子：
13.2
作者：
Akizawa, Tadao;Asano, Yasushi;Kurokawa, Kiyoshi
通讯作者：
Kurokawa, Kiyoshi
影响因子：
2.5
作者：
Laukoetter, MG;Bruewer, M;Nusrat, A
通讯作者：
Nusrat, A
影响因子：
3.2
作者：
Lee, Hyun Ji (Julie);Pahl, Madeleine V.;Blake, Donald R.
通讯作者：
Blake, Donald R.