肠道菌群与肾脏疾病相关性研究进展
|
摘要
人体是一个有机的整体,不同系统之间存在着相互影响。近年来,随着科学的不断发展,肠道菌群与人体健康的关系也逐渐受到重视。肠道菌群虽然居住于肠道,但其作用已经不仅仅局限于消化系统。通过对人体代谢和免疫功能的影响,肠道菌群对人体产生的作用是全身性的。肾脏是体内代谢产物排泄的主要器官,也是免疫复合物沉积的重要部位。因此,肠道菌群在肾脏疾病发展和治疗中都起着至关重要的作用。现如今,两者的关系已经成为科学研究的热点话题。本文总结了近5年的文献,从中西医的角度,针对肠道菌群与肾脏疾病之间的相互关系作一综述。
The human body is an organic whole, with different systems interacting with each other. In recent years, with the development of science, the relationship between gut microbiome and human health has been paid more and more attention. Although gut microbiome lives in the gut, its influence is no longer limited to the digestive system. The effect of gut microbiome on human body is systemic. Kidney is the main organ of excretion of metabolic products in the body, and also the important site of immune complex depositions. Therefore, gut microbiome plays an important role in the development and treatment of kidney diseases. Nowadays, the relationship between the two has become a hot topic in scientific research. This paper summarizes the literatures published during the past five years, and reviews the relationship between gut microbiome and renal diseases from the perspective of traditional Chinese medicine and western medicine.
The human body is an organic whole, with different systems interacting with each other. In recent years, with the development of science, the relationship between gut microbiome and human health has been paid more and more attention. Although gut microbiome lives in the gut, its influence is no longer limited to the digestive system. The effect of gut microbiome on human body is systemic. Kidney is the main organ of excretion of metabolic products in the body, and also the important site of immune complex depositions. Therefore, gut microbiome plays an important role in the development and treatment of kidney diseases. Nowadays, the relationship between the two has become a hot topic in scientific research. This paper summarizes the literatures published during the past five years, and reviews the relationship between gut microbiome and renal diseases from the perspective of traditional Chinese medicine and western medicine.
引文
[1] 武庆斌,郑跃杰,黄永坤.儿童肠道菌群[M].北京:科学出版社,2012:13-14.
[2] Clemente JC,Ursell LK,Parfrey LW.The impact of the gut microbiota on human health:An integrative view[J].Cell,2012,148(6):1258-1270.
[3] Al Khodor S.Gut microbiome and kidney disease:A bidirectional relationship[J].Pediatr Nephrol,2017,32(6):921-931.
[4] Evenepoel P,Poesen R,Meijers B.The gut-kidney axis[J].Pediatr Nephrol,2017,32(11):2005-2014.
[5] O′Hara AM,Shanahan F.The gut flora as a forgotten organ[J].EMBO Rep,2006,7(7):688-693.
[6] SHAO Xiaojiao,CHENG Zedong.Discussion on intestinal flora based on theories of Yin-Yang and Five Elements in TCM[J].J Liaoning Univ TCM,2013,15(7):136-137.(in Chinese) 邵晓姣,成泽东.从中医阴阳五行理论谈肠道菌群[J].辽宁中医药大学学报,2013,15(7):136-137.
[7] WU Guolin,YU Guoyou,LU Wenwen.Discussion on TCM essence of intestinal microecology[J].Chin Arch Trad Chin Med,2015,33(11):2586-2588.(in Chinese) 吴国琳,余国友,卢雯雯.肠道微生态的中医本质探讨[J].中华中医药学刊,2015,33(11):2586-2588.
[8] KONG Fanhua,CHENG Zedong.Discussion on the intestinal flora disorder of TCM pathogenesis[J].J Jiangxi Univ of TCM,2016,28(6):6-7.(in Chinese) 孔凡华,成泽东.肠道菌群失调的中医病机探讨[J].江西中医药大学学报,2016,28(6):6-7.
[9] Mair RD,Sirich TL,Meyer TW.Uremic toxin clearance and cardiovascular toxicities[J].Toxins(Basel),2018,10(6).pii:E226.
[10] Vaziri ND,Wong J,Pahl M,et al.Chronic kidney disease alters intestinal microbial flora[J].Kidney Int,2013,83(2):308-315.
[11] Wong J,Piceno YM,DeSantis TZ,et al.Expansion of urease- and uricase-containing,indole- and p-cresol-forming and contraction of short-chain fatty acid-producing intestinal microbiota in ESRD[J].Am J Nephrol,2014,39(3):230-237.
[12] Barrios C,Beaumont M,Pallister T,et al.Gut-microbiota-metabolite axis in early renal function decline[J].PLoS One,2015,10(8):e0134311.
[13] 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[J].Circ Res,2015,116(3):448-455.
[14] Sun G,Yin Z,Liu N,et al.Gut microbial metabolite TMAO contributes to renal dysfunction in a mouse model of diet-induced obesity[J].Biochem Biophys Res Commun,2017,493(2):964-970.
[15] Li T,Gua C,Wu B,et al.Increased circulating trimethylamine N-oxide contributes to endothelial dysfunction in a rat model of chronic kidney disease[J].Biochem Biophys Res Commun,2018,495(2):2071-2077.
[16] Kim RB,Morse BL,Djurdjev O,et al.Advanced chronic kidney disease populations have elevated trimethylamine N-oxide levels associated with increased cardiovascular events[J].Kidney Int,2016,89(5):1144-1152.
[17] Poesen R,Claes K,Evenepoel P,et al.Microbiota-derived phenylacetylglutamine associates with overall mortality and cardiovascular disease in patients with CKD[J].J Am Soc Nephrol,2016,27(11):3479-3487.
[18] Lau WL,Kalantar-Zadeh K,Vaziri ND.The gut as a source of inflammation in chronic kidney disease[J].Nephron,2015,130(2):92-98.
[19] Hu J,Luo H,Wang J,et al.Enteric dysbiosis-linked gut barrier disruption triggers early renal injury induced by chronic high salt feeding in mice[J].Exp Mol Med,2017,49(8):e370.
[20] Wang F,Zhang P,Jiang H,et al.Gut bacterial translocation contributes to microinflammation in experimental uremia[J].Dig Dis Sci,2012,57(11):2856-2862.
[21] Wang F,Jiang H,Shi K,et al.Gut bacterial translocation is associated with microinflammation in end-stage renal disease patients[J].Nephrology(Carlton),2012,17(8):733-738.
[22] Missailidis C,H?llqvist J,Qureshi AR,et al.Serum trimethylamine-N-oxide is strongly related to renal function and predicts outcome in chronic kidney disease[J].PLoS One,2016,11(1):e0141738.
[23] Sun L,Liu H,Jiang H,et al.Macrophages are involved in gut bacterial translocation and reversed by Lactobacillus in experimental uremia[J].Dig Dis Sci,2016,61(6):1534-1544.
[24] Adesso S,Popolo A,Bianco G,et al.The uremic toxin indoxyl sulphate enhances macrophage response to LPS[J].PLoS One,2013,8(9):e76778.
[25] Azevedo ML,Bonan NB,Dias G,et al.p-Cresyl sulfate affects the oxidative burst,phagocytosis process,and antigen presentation of monocyte-derived macrophages[J].Toxicol Lett,2016,263:1-5.
[26] Rossi M,Campbell KL,Johnson DW,et al.Protein-bound uremic toxins,inflammation and oxidative stress:A cross-sectional study in stage 3-4 chronic kidney disease[J].Arch Med Res,2014,45(4):309-317.
[27] Ranganathan N,Ranganathan P,Friedman EA,et al.Pilot study of probiotic dietary supplementation for promoting healthy kidney function in patients with chronic kidney disease[J].Adv Ther,2010,27(9):634-647.
[28] Nazzal L,Roberts J,Singh P,et al.Microbiome perturbation by oral vancomycin reduces plasma concentration of two gut-derived uremic solutes,indoxyl sulfate and p-cresyl sulfate,in end-stage renal disease[J].Nephrol Dial Transplant,2017,32(11):1809-1817.
[29] Vaziri ND,Liu SM,Lau WL,et al.High amylose resistant starch diet ameliorates oxidative stress,inflammation,and progression of chronic kidney disease[J].PLoS One,2014,9(12):e114881.
[30] Kieffer DA,Piccolo BD,Vaziri ND,et al.Resistant starch alters gut microbiome and metabolomic profiles concurrent with amelioration of chronic kidney disease in rats[J].Am J Physiol Renal Physiol,2016,310(9):F857-871.
[31] Andrade-Oliveira V,Amano MT,Correa-Costa M,et al.Gut bacteria products prevent AKI induced by ischemia-reperfusion[J].J Am Society Nephrol,2015,26(8):1877-1888.
[32] Huang W,Guo HL,Deng X,et al.Short-chain fatty acids inhibit oxidative stress and inflammation in mesangial cells induced by high glucose and lipopolysaccharide[J].Exp Clin Endocrinol Diabetes,2017,125(2):98-105.
[33] Sato E,Saigusa D,Mishima E,et al.Impact of the oral adsorbent AST-120 on organ-specific accumulation of uremic toxins:LC-MS/MS and MS imaging techniques[J].Toxins(Basel),2017,10(1).pii:E19.
[34] Yoshifuji A,Wakino S,Irie J,et al.Oral adsorbent AST-120 ameliorates gut environment and protects against the progression of renal impairment in CKD rats[J].Clin Exp Nephrol,2018,22(5):1069-1078.
[35] Wu CJ,Chen CY,Lai TS,et al.The role of indoxyl sulfate in renal anemia in patients with chronic kidney disease[J].Oncotarget,2017,8(47):83030-83037.
[36] Yamamoto S,Fukagawa M.Uremic toxicity and bone in CKD[J].J Nephrol,2017,30(5):623-627.
[37] JIANG Dongjing,ZHANG Li,CAO Yudan,et al.Application of gut microbiota in research of Chinese medicines[J].China J Chin Mater Med,2016,41(17):3218-3225.(in Chinese) 姜东京,张丽,曹雨诞,等.肠道菌群在中药研究中的应用[J].中国中药杂志,2016,41(17):3218-3225.
[38] Zeng YQ,Dai Z,Lu F,et al.Emodin via colonic irrigation modulates gut microbiota and reduces uremic toxins in rats with chronic kidney disease[J].Oncotarget,2016,7(14):17468-17478.
[39] Du LY,Tao JH,Jiang S,et al.Metabolic profiles of the Flos Abelmoschus manihot extract by intestinal bacteria from the normal and CKD model rats based on UPLC-Q-TOF/MS[J].Biomed Chromatogr,2017,31(2).doi:10.1002/bmc.
[40] Tao JH,Zhao M,Jiang S,et al.Comparative metabolism of two major compounds in Fructus Corni extracts by gut microflora from normal and chronic nephropathy rats in vitro by UPLC-Q-TOF/MS[J].J Chromatogr B Analyt Technol Biomed Life Sci,2018,1073:170-176.
[41] Alelign T,Petros B.Kidney stone disease:An update on current concepts[J].Adv Urol,2018,2018:3068365
[42] Stern JM,Moazami S,Qiu Y,et al.Evidence for a distinct gut microbiome in kidney stone formers compared to non-stone formers[J].Urolithiasis,2016,44(5):399-407.
[43] Gnanandarajah JS,Abrahante JE,Lulich JP.Presence of Oxalobacter formigenes in the intestinal tract is associated with the absence of calcium oxalate urolith formation in dogs[J].Urol Res,2012,40(5):467-473.
[44] Sadaf H,Raza SI,Hassan SW.Role of gut microbiota against calcium oxalate[J].Microb Pathog,2017,109:287-291.
[45] XIAN Xiaoying,XIE Yuanliang,YE Juan,et al.Quantification of oxalate-degrading bacteria in the gut of kidney stone patients using real-time PCR[J].Genom Appl Biol,2016,35(9):2222-2228.(in Chinese) 咸晓莹,谢远亮,叶娟,等.肾结石患者肠道内草酸降解细菌的定量检测[J].基因组学与应用生物学,2016,35(9):2222-2228.
[46] Ticinesi A,Milani C,Guerra A,et al.Understanding the gut-kidney axis in nephrolithiasis:An analysis of the gut microbiota composition and functionality of stone formers[J].Gut,2018,67(12):2097-2106.
[47] Batagello CA,Monga M,Miller AW.Response to lange re:Calcium oxalate urolithiasis:A case of missing microbes?[J].J Endourol,2018,32(11):1007.
[48] Zheng X,Zhao A,Xie G,et al.Melamine-induced renal toxicity is mediated by the gut microbiota[J].Sci Transl Med,2013,5(172):172ra22.
[49] Jokiranta TS.HUS and atypical HUS[J].Blood,2017,129(21):2847-2856.
[50] SUN Changqi,LI Shiguo,LIU Zongzheng,et al.Escherichia coli O157∶H7 infection not decreasing the diversity of mice intestinal microflora[J].Chin J Microecol,2015,27(1):19-23.(in Chinese) 孙长奇,李世国,刘宗正,等.小鼠肠道菌群的多样性不因大肠埃希菌O157:H7感染而降低[J].中国微生态学杂志,2015,27(1):19-23.
[51] Fukuda S,Toh H,Hase K,et al.Bifidobacteria can protect from enteropathogenic infection through production of acetate[J].Nature,2011,469(7331):543-547.
[52] Almaani S,Meara A,Rovin BH.Update on lupus nephritis[J].Clin J Am Soc Nephrol,2017,12(5):825-835.
[53] Johnson BM,Gaudreau MC,Al-Gadban MM,et al.Impact of dietary deviation on disease progression and gut microbiome composition in lupus-prone SNF1 mice[J].Clin Exp Immunol,2015,181(2):323-337.
[54] Mu Q,Zhang H,Liao X,et al.Control of lupus nephritis by changes of gut microbiota[J].Microbiome,2017,5(1):73.
[55] Penfold RS,Prendecki M,McAdoo S.Primary IgA nephropathy:Current challenges and future prospects[J].Int J Nephrol Renovasc Dis,2018,11:137-148.
[56] McCarthy DD,Kujawa J,Wilson C,et al.Mice overexpressing BAFF develop a commensal flora-dependent,IgA-associated nephropathy[J].J Clin Invest,2011,121(10):3991-4002.
[57] Xin G,Shi W,Xu LX,et al.Serum BAFF is elevated in patients with IgA nephropathy and associated with clinical and histopathological features[J].J Nephrol,2013,26(4):683-690.
[58] De Angelis M,Montemurno E,Piccolo M,et al.Microbiota and metabolome associated with immunoglobulin A nephropathy(IgAN)[J].PLoS One,2014,9(6):e99006.
[59] Jennette JC,Nachman PH.ANCA glomerulonephritis and vasculitis[J].Clin J Am Soc Nephrol,2017,12(10):1680-1691.
[60] 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[J].Immunity,2016,45(5):1078-1092.
[2] Clemente JC,Ursell LK,Parfrey LW.The impact of the gut microbiota on human health:An integrative view[J].Cell,2012,148(6):1258-1270.
[3] Al Khodor S.Gut microbiome and kidney disease:A bidirectional relationship[J].Pediatr Nephrol,2017,32(6):921-931.
[4] Evenepoel P,Poesen R,Meijers B.The gut-kidney axis[J].Pediatr Nephrol,2017,32(11):2005-2014.
[5] O′Hara AM,Shanahan F.The gut flora as a forgotten organ[J].EMBO Rep,2006,7(7):688-693.
[6] SHAO Xiaojiao,CHENG Zedong.Discussion on intestinal flora based on theories of Yin-Yang and Five Elements in TCM[J].J Liaoning Univ TCM,2013,15(7):136-137.(in Chinese) 邵晓姣,成泽东.从中医阴阳五行理论谈肠道菌群[J].辽宁中医药大学学报,2013,15(7):136-137.
[7] WU Guolin,YU Guoyou,LU Wenwen.Discussion on TCM essence of intestinal microecology[J].Chin Arch Trad Chin Med,2015,33(11):2586-2588.(in Chinese) 吴国琳,余国友,卢雯雯.肠道微生态的中医本质探讨[J].中华中医药学刊,2015,33(11):2586-2588.
[8] KONG Fanhua,CHENG Zedong.Discussion on the intestinal flora disorder of TCM pathogenesis[J].J Jiangxi Univ of TCM,2016,28(6):6-7.(in Chinese) 孔凡华,成泽东.肠道菌群失调的中医病机探讨[J].江西中医药大学学报,2016,28(6):6-7.
[9] Mair RD,Sirich TL,Meyer TW.Uremic toxin clearance and cardiovascular toxicities[J].Toxins(Basel),2018,10(6).pii:E226.
[10] Vaziri ND,Wong J,Pahl M,et al.Chronic kidney disease alters intestinal microbial flora[J].Kidney Int,2013,83(2):308-315.
[11] Wong J,Piceno YM,DeSantis TZ,et al.Expansion of urease- and uricase-containing,indole- and p-cresol-forming and contraction of short-chain fatty acid-producing intestinal microbiota in ESRD[J].Am J Nephrol,2014,39(3):230-237.
[12] Barrios C,Beaumont M,Pallister T,et al.Gut-microbiota-metabolite axis in early renal function decline[J].PLoS One,2015,10(8):e0134311.
[13] 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[J].Circ Res,2015,116(3):448-455.
[14] Sun G,Yin Z,Liu N,et al.Gut microbial metabolite TMAO contributes to renal dysfunction in a mouse model of diet-induced obesity[J].Biochem Biophys Res Commun,2017,493(2):964-970.
[15] Li T,Gua C,Wu B,et al.Increased circulating trimethylamine N-oxide contributes to endothelial dysfunction in a rat model of chronic kidney disease[J].Biochem Biophys Res Commun,2018,495(2):2071-2077.
[16] Kim RB,Morse BL,Djurdjev O,et al.Advanced chronic kidney disease populations have elevated trimethylamine N-oxide levels associated with increased cardiovascular events[J].Kidney Int,2016,89(5):1144-1152.
[17] Poesen R,Claes K,Evenepoel P,et al.Microbiota-derived phenylacetylglutamine associates with overall mortality and cardiovascular disease in patients with CKD[J].J Am Soc Nephrol,2016,27(11):3479-3487.
[18] Lau WL,Kalantar-Zadeh K,Vaziri ND.The gut as a source of inflammation in chronic kidney disease[J].Nephron,2015,130(2):92-98.
[19] Hu J,Luo H,Wang J,et al.Enteric dysbiosis-linked gut barrier disruption triggers early renal injury induced by chronic high salt feeding in mice[J].Exp Mol Med,2017,49(8):e370.
[20] Wang F,Zhang P,Jiang H,et al.Gut bacterial translocation contributes to microinflammation in experimental uremia[J].Dig Dis Sci,2012,57(11):2856-2862.
[21] Wang F,Jiang H,Shi K,et al.Gut bacterial translocation is associated with microinflammation in end-stage renal disease patients[J].Nephrology(Carlton),2012,17(8):733-738.
[22] Missailidis C,H?llqvist J,Qureshi AR,et al.Serum trimethylamine-N-oxide is strongly related to renal function and predicts outcome in chronic kidney disease[J].PLoS One,2016,11(1):e0141738.
[23] Sun L,Liu H,Jiang H,et al.Macrophages are involved in gut bacterial translocation and reversed by Lactobacillus in experimental uremia[J].Dig Dis Sci,2016,61(6):1534-1544.
[24] Adesso S,Popolo A,Bianco G,et al.The uremic toxin indoxyl sulphate enhances macrophage response to LPS[J].PLoS One,2013,8(9):e76778.
[25] Azevedo ML,Bonan NB,Dias G,et al.p-Cresyl sulfate affects the oxidative burst,phagocytosis process,and antigen presentation of monocyte-derived macrophages[J].Toxicol Lett,2016,263:1-5.
[26] Rossi M,Campbell KL,Johnson DW,et al.Protein-bound uremic toxins,inflammation and oxidative stress:A cross-sectional study in stage 3-4 chronic kidney disease[J].Arch Med Res,2014,45(4):309-317.
[27] Ranganathan N,Ranganathan P,Friedman EA,et al.Pilot study of probiotic dietary supplementation for promoting healthy kidney function in patients with chronic kidney disease[J].Adv Ther,2010,27(9):634-647.
[28] Nazzal L,Roberts J,Singh P,et al.Microbiome perturbation by oral vancomycin reduces plasma concentration of two gut-derived uremic solutes,indoxyl sulfate and p-cresyl sulfate,in end-stage renal disease[J].Nephrol Dial Transplant,2017,32(11):1809-1817.
[29] Vaziri ND,Liu SM,Lau WL,et al.High amylose resistant starch diet ameliorates oxidative stress,inflammation,and progression of chronic kidney disease[J].PLoS One,2014,9(12):e114881.
[30] Kieffer DA,Piccolo BD,Vaziri ND,et al.Resistant starch alters gut microbiome and metabolomic profiles concurrent with amelioration of chronic kidney disease in rats[J].Am J Physiol Renal Physiol,2016,310(9):F857-871.
[31] Andrade-Oliveira V,Amano MT,Correa-Costa M,et al.Gut bacteria products prevent AKI induced by ischemia-reperfusion[J].J Am Society Nephrol,2015,26(8):1877-1888.
[32] Huang W,Guo HL,Deng X,et al.Short-chain fatty acids inhibit oxidative stress and inflammation in mesangial cells induced by high glucose and lipopolysaccharide[J].Exp Clin Endocrinol Diabetes,2017,125(2):98-105.
[33] Sato E,Saigusa D,Mishima E,et al.Impact of the oral adsorbent AST-120 on organ-specific accumulation of uremic toxins:LC-MS/MS and MS imaging techniques[J].Toxins(Basel),2017,10(1).pii:E19.
[34] Yoshifuji A,Wakino S,Irie J,et al.Oral adsorbent AST-120 ameliorates gut environment and protects against the progression of renal impairment in CKD rats[J].Clin Exp Nephrol,2018,22(5):1069-1078.
[35] Wu CJ,Chen CY,Lai TS,et al.The role of indoxyl sulfate in renal anemia in patients with chronic kidney disease[J].Oncotarget,2017,8(47):83030-83037.
[36] Yamamoto S,Fukagawa M.Uremic toxicity and bone in CKD[J].J Nephrol,2017,30(5):623-627.
[37] JIANG Dongjing,ZHANG Li,CAO Yudan,et al.Application of gut microbiota in research of Chinese medicines[J].China J Chin Mater Med,2016,41(17):3218-3225.(in Chinese) 姜东京,张丽,曹雨诞,等.肠道菌群在中药研究中的应用[J].中国中药杂志,2016,41(17):3218-3225.
[38] Zeng YQ,Dai Z,Lu F,et al.Emodin via colonic irrigation modulates gut microbiota and reduces uremic toxins in rats with chronic kidney disease[J].Oncotarget,2016,7(14):17468-17478.
[39] Du LY,Tao JH,Jiang S,et al.Metabolic profiles of the Flos Abelmoschus manihot extract by intestinal bacteria from the normal and CKD model rats based on UPLC-Q-TOF/MS[J].Biomed Chromatogr,2017,31(2).doi:10.1002/bmc.
[40] Tao JH,Zhao M,Jiang S,et al.Comparative metabolism of two major compounds in Fructus Corni extracts by gut microflora from normal and chronic nephropathy rats in vitro by UPLC-Q-TOF/MS[J].J Chromatogr B Analyt Technol Biomed Life Sci,2018,1073:170-176.
[41] Alelign T,Petros B.Kidney stone disease:An update on current concepts[J].Adv Urol,2018,2018:3068365
[42] Stern JM,Moazami S,Qiu Y,et al.Evidence for a distinct gut microbiome in kidney stone formers compared to non-stone formers[J].Urolithiasis,2016,44(5):399-407.
[43] Gnanandarajah JS,Abrahante JE,Lulich JP.Presence of Oxalobacter formigenes in the intestinal tract is associated with the absence of calcium oxalate urolith formation in dogs[J].Urol Res,2012,40(5):467-473.
[44] Sadaf H,Raza SI,Hassan SW.Role of gut microbiota against calcium oxalate[J].Microb Pathog,2017,109:287-291.
[45] XIAN Xiaoying,XIE Yuanliang,YE Juan,et al.Quantification of oxalate-degrading bacteria in the gut of kidney stone patients using real-time PCR[J].Genom Appl Biol,2016,35(9):2222-2228.(in Chinese) 咸晓莹,谢远亮,叶娟,等.肾结石患者肠道内草酸降解细菌的定量检测[J].基因组学与应用生物学,2016,35(9):2222-2228.
[46] Ticinesi A,Milani C,Guerra A,et al.Understanding the gut-kidney axis in nephrolithiasis:An analysis of the gut microbiota composition and functionality of stone formers[J].Gut,2018,67(12):2097-2106.
[47] Batagello CA,Monga M,Miller AW.Response to lange re:Calcium oxalate urolithiasis:A case of missing microbes?[J].J Endourol,2018,32(11):1007.
[48] Zheng X,Zhao A,Xie G,et al.Melamine-induced renal toxicity is mediated by the gut microbiota[J].Sci Transl Med,2013,5(172):172ra22.
[49] Jokiranta TS.HUS and atypical HUS[J].Blood,2017,129(21):2847-2856.
[50] SUN Changqi,LI Shiguo,LIU Zongzheng,et al.Escherichia coli O157∶H7 infection not decreasing the diversity of mice intestinal microflora[J].Chin J Microecol,2015,27(1):19-23.(in Chinese) 孙长奇,李世国,刘宗正,等.小鼠肠道菌群的多样性不因大肠埃希菌O157:H7感染而降低[J].中国微生态学杂志,2015,27(1):19-23.
[51] Fukuda S,Toh H,Hase K,et al.Bifidobacteria can protect from enteropathogenic infection through production of acetate[J].Nature,2011,469(7331):543-547.
[52] Almaani S,Meara A,Rovin BH.Update on lupus nephritis[J].Clin J Am Soc Nephrol,2017,12(5):825-835.
[53] Johnson BM,Gaudreau MC,Al-Gadban MM,et al.Impact of dietary deviation on disease progression and gut microbiome composition in lupus-prone SNF1 mice[J].Clin Exp Immunol,2015,181(2):323-337.
[54] Mu Q,Zhang H,Liao X,et al.Control of lupus nephritis by changes of gut microbiota[J].Microbiome,2017,5(1):73.
[55] Penfold RS,Prendecki M,McAdoo S.Primary IgA nephropathy:Current challenges and future prospects[J].Int J Nephrol Renovasc Dis,2018,11:137-148.
[56] McCarthy DD,Kujawa J,Wilson C,et al.Mice overexpressing BAFF develop a commensal flora-dependent,IgA-associated nephropathy[J].J Clin Invest,2011,121(10):3991-4002.
[57] Xin G,Shi W,Xu LX,et al.Serum BAFF is elevated in patients with IgA nephropathy and associated with clinical and histopathological features[J].J Nephrol,2013,26(4):683-690.
[58] De Angelis M,Montemurno E,Piccolo M,et al.Microbiota and metabolome associated with immunoglobulin A nephropathy(IgAN)[J].PLoS One,2014,9(6):e99006.
[59] Jennette JC,Nachman PH.ANCA glomerulonephritis and vasculitis[J].Clin J Am Soc Nephrol,2017,12(10):1680-1691.
[60] 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[J].Immunity,2016,45(5):1078-1092.