肠源性高草酸尿症的发病机制与治疗进展

杨顺航; 李炯明; 刘建和; 王光; 李沛

doi:10.12259/j.issn.2095-610X.S20220734

肠源性高草酸尿症的发病机制与治疗进展

doi: 10.12259/j.issn.2095-610X.S20220734

昆明医科大学第二附属医院泌尿外科三病区，云南昆明　650032

基金项目: 国家自然科学基金资助项目（82060137）

详细信息

作者简介:
杨顺航（1991～），男，云南临沧人，在读硕士研究生，主要从事泌尿系结石相关工作

通讯作者:
李炯明，E-mail：jiongmingli@aliyun.com

中图分类号: R692.4
计量
- 文章访问数: 2926
- HTML全文浏览量: 826
- PDF下载量: 152
- 被引次数: 0
出版历程
- 收稿日期: 2022-01-01
- 刊出日期: 2022-07-14

Progress in Pathogenesis and Treatment of Enteric Hyperoxaluria

Dept. of Urology，The 2nd Affiliated Hospital of Kunming Medical University，Kunming Yunnan 650032，China

摘要

摘要: 肠源性高草酸尿症是由多种原因引起的以肠道草酸盐过量吸收和尿草酸盐排泄增加为特点的继发性高草酸尿症。肠源性高草酸尿症与尿路草酸钙结石的发生密切相关，有效减少肠道草酸盐的吸收，降低尿草酸盐的排泄，对预防尿路草酸钙结石的发生具有重要意义。回顾了近年来有关肠源性高草酸尿症的发病机制与治疗方面的相关文献，综述如下。
- 肠源性高草酸尿症 /
- 继发性高草酸尿症 /
- 草酸钙结石 /
- 尿草酸盐 /
- 肠道菌群
Abstract: Enteric hyperoxaluria is a secondary hyperoxaluria characterized by excessive absorption of intestinal oxalate and increased urinary oxalate. Enteric hyperoxaluria is closely related to the occurrence of urinary calcium oxalate stones. It is of great significance to effectively reduce the absorption of intestinal oxalate and urinary oxalate to prevent the occurrence of urinary calcium oxalate stones. This article reviews the pathogenesis and treatment of enteric hyperoxaluria.
- Enteric hyperoxaluria /
- Secondary hyperoxaluria /
- Calcium oxalate stone /
- Urinary oxalate /
- Intestinal flora

HTML全文

参考文献(30)

[1]	Zeng G,Mai Z,Xia S,et al. Prevalence of kidney stones in China:an ultrasonography based cross-sectional study[J]. BJU International,2017,120(1):109-116. doi: 10.1111/bju.13828
[2]	Witting C,Langman C B,Assimos D,et al. Pathophysiology and treatment of enteric hyperoxaluria[J]. Clinical Journal of the American Society of Nephrology,2020,16(3):487-495.
[3]	于健鹏,谌卫,郭志勇. 继发性高草酸尿症的诊治进展[J]. 肾脏病与透析肾移植杂志,2020,29(6):567-571. doi: 10.3969/j.issn.1006-298X.2020.06.014
[4]	Kinsey L,Burden S. A survey of people with inflammatory bowel disease to investigate their views of food and nutritional issues[J]. European Journal of Clinical Nutrition,2016,70(7):852-854. doi: 10.1038/ejcn.2016.57
[5]	Crivelli J J,Mitchell T,Knight J,et al. Contribution of dietary oxalate and oxalate precursors to urinary oxalate excretion[J]. Nutrients,2021,13(1):62.
[6]	Knauf F,Velazquez H,Pfann V,et al. Characterization of renal NaCl and oxalate transport in Slc26a6−/− mice[J]. American Journal of Physiology-Renal Physiology,2019,316(1):F128-F133. doi: 10.1152/ajprenal.00309.2018
[7]	Lieske J,Mehta R,Milliner D. Kidney stones are common after bariatric surgery[J]. Kidney International,2015,4(87):839-845.
[8]	Canales B K,Gonzalez R D. Kidney stone risk following Roux-en-Y gastric bypass surgery[J]. Translational Andrology and Urology,2014,3(3):242-249.
[9]	Nazzal L,Puri S,Goldfarb D S. Enteric hyperoxaluria:an important cause of end-stage kidney disease[J]. Nephrol Dial Transplant,2016,31(3):375-382. doi: 10.1093/ndt/gfv005
[10]	Liu M,Nazzal L. Enteric hyperoxaluria:role of microbiota and antibiotics[J]. Current Opinion in Nephrology and Hypertension,2019,28(4):352-359. doi: 10.1097/MNH.0000000000000518
[11]	邱瑾,刘剑新,钟薏. 肠道菌群和抗生素与肾结石的形成[J]. 临床泌尿外科杂志,2020,35(12):1011-1014.
[12]	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. doi: 10.1136/gutjnl-2017-315734
[13]	Miller A W,Choy D,Penniston K L,et al. Inhibition of urinary stone disease by a multi-species bacterial network ensures healthy oxalate homeostasis[J]. Kidney Int,2019,96(1):180-188. doi: 10.1016/j.kint.2019.02.012
[14]	Hatch M,Gjymishka A,Salido E C,et al. Enteric oxalate elimination is induced and oxalate is normalized in a mouse model of primary hyperoxaluria following intestinal colonization withOxalobacter[J]. American Journal of Physiology-Gastrointestinal and Liver Physiology,2011,300(3):G461-G469. doi: 10.1152/ajpgi.00434.2010
[15]	Alper S L,Sharma A K. The SLC26 gene family of anion transporters and channels[J]. Molecular Aspects of Medicine,2013,34(2-3):494-515. doi: 10.1016/j.mam.2012.07.009
[16]	Tavasoli S,Alebouyeh M,Naji M,et al. Association of intestinal oxalate-degrading bacteria with recurrent calcium kidney stone formation and hyperoxaluria:a case-control study[J]. BJU International,2020,125(1):133-143. doi: 10.1111/bju.14840
[17]	Borghi L,Schianchi T,Meschi T. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria[J]. N Engl J Med,2002,346(2):77-84. doi: 10.1056/NEJMoa010369
[18]	Canales B,Hatch M. Oxalobacter formigenes colonization normalizes oxalate excretion in a gastric bypass model of hyperoxaluria[J]. Surg Obes Relat Dis,2017,13(7):1152-1157. doi: 10.1016/j.soard.2017.03.014
[19]	Jiang J,Knight J,Easter L H,et al. Impact of dietary calcium and oxalate,and oxalobacter formigenes colonization on urinary oxalate excretion[J]. Journal of Urology,2011,186(1):135-139. doi: 10.1016/j.juro.2011.03.006
[20]	Campieri C,Campieri M,Bertuzzi V,et al. Reduction of oxaluria after an oral course of lactic acid bacteria at high concentration[J]. Kidney International,2001,60(3):1097-1105. doi: 10.1046/j.1523-1755.2001.0600031097.x
[21]	Lieske J C,Goldfarb D S,De Simone C,et al. Use of a probiotic to decrease enteric hyperoxaluria[J]. Kidney Int,2005,68(3):1244-1249. doi: 10.1111/j.1523-1755.2005.00520.x
[22]	Lingeman J E,Pareek G,Easter L,et al. ALLN-177,oral enzyme therapy for hyperoxaluria[J]. International Urology and Nephrology,2019,51(4):601-608. doi: 10.1007/s11255-019-02098-1
[23]	Pfau A,Grujic D,Keddis M T,et al. Pilot study of reloxaliase in patients with severe enteric hyperoxaluria and hyperoxalemia[J]. Nephrology Dialysis Transplantation,2021,36(5):945-948. doi: 10.1093/ndt/gfaa379
[24]	Langman C B,Grujic D,Pease R M,et al. A double-blind,placebo controlled,randomized phase 1 cross-over study with ALLN-177,an orally administered oxalate degrading enzyme[J]. American Journal of Nephrology,2016,44(2):150-158. doi: 10.1159/000448766
[25]	Chung J,Granja I,Taylor M G,et al. Molecular modifiers reveal a mechanism of pathological crystal growth inhibition[J]. Nature,2016,536(7617):446-450. doi: 10.1038/nature19062
[26]	Han S,Zhao C,Pokhrel G,et al. Hydroxycitric acid tripotassium inhibits calcium oxalate crystal formation in the drosophila melanogaster model of hyperoxaluria[J]. Medical Science Monitor,2019,25:3662-3667. doi: 10.12659/MSM.913637
[27]	Asplin J R. The management of patients with enteric hyperoxaluria[J]. Urolithiasis,2016,44(1):33-43. doi: 10.1007/s00240-015-0846-5
[28]	Joshi S,Khan S R. Opportunities for future therapeutic interventions for hyperoxaluria:targeting oxidative stress[J]. Expert Opinion on Therapeutic Targets,2019,23(5):379-391. doi: 10.1080/14728222.2019.1599359
[29]	Knauf F,Asplin J R,Granja I,et al. NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy[J]. Kidney Int,2013,84(5):895-901. doi: 10.1038/ki.2013.207
[30]	Anders H, Suarez-Alvarez B, Grigorescu M, et al. The macrophage phenotype and inflammasome component NLRP3 contributes to nephrocalcinosis-related chronic kidney disease independent from IL-1–mediated tissue injury[J]. Kidney International, 2018, 93（3）: 656-669.

相关文章(20)

[1]	彭达, 张爱军. 正常高值血压者尿NGAL与血流介导的血管舒张功能的相关性, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20240121
[2]	李波, 孙杨, 缪应雷. 炎症性肠病的肠道微生态变化及对策, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20240401
[3]	牛俊杰, 姬文娟, 于拽拽. 肠道菌群、血清ET、PCT水平与脓毒症病情程度、预后的相关性, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20240420
[4]	李媛媛, 宋亚贤, 徐玉善, 曾晓甫, 袁惠, 徐兆, 江艳. 肠道菌群代谢物TMAO与非酒精性脂肪性肝病的关系, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20240210
[5]	陀晓宇, 李超, 郭丽萍, 赵华君. 尿AD7c-NTP与P300检查在AD源性MCI诊断的价值, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20230407
[6]	李吉, 柯坤彬, 张白羽, 刘裔道, 白晶, 董滔, 王振丞, 秦德强, 王梦悦, 李颢. 云南德宏州傣族人群CaSR基因SNP与含钙肾结石和高钙尿的关联性, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20230520
[7]	徐琳, 高开成, 贾杰, 李煜阳, 王华伟, 况轶群, 赵昱. 参苓白术散对甲基苯丙胺诱导小鼠肠道菌群改变的作用机制研究, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20230829
[8]	邓绍友, 赵玉兰, 王佩锦, 李蓉, 李进涛, 郑红. 恒古骨伤愈合剂联合广谱抗生素改善db/db小鼠胰岛素抵抗和肠道菌群, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20230530
[9]	梁彩红, 孟明耀, 李欣欣, 熊晶晶, 李檬, 刘梅, 侯宗柳, 黄永坤. 肠道菌群代谢物脱氧胆酸对人脐带间充质干细胞hUC-MSCs增殖及细胞周期的影响, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20230402
[10]	李丹, 万绪莲, 李律宇, 云宇, 罗光云, 刘韦兵, 林公府, 李宁, 黎勇坤, 段为钢. 尿酸酶缺失大鼠肠道菌群的变化, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20230205
[11]	李露, 田云粉. 肠道菌群与儿童非酒精性脂肪性肝病的研究进展, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20230708
[12]	刘四香, 黄永坤, 王明英, 胡红卫, 马敏, 凌昱. 功能性便秘患儿的肠道菌群分析及治疗干预, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20220309
[13]	唐娟, 念馨. 肠道微生态与肥胖相关性研究进展, 昆明医科大学学报.
[14]	梁睿, 淳于纬训, 沈焘, 孙乐, 李云峰. 肠道菌群和免疫在结直肠肿瘤中作用研究进展, 昆明医科大学学报.
[15]	薛平燕, 江艳, 徐玉善, 袁惠, 李璇, 宋亚贤, 刘华. 肠道菌群结构在非酒精性脂肪性肝病患者中的改变, 昆明医科大学学报. doi: 10.12259/j.issn.2095-610X.S20201120
[16]	张锦山, 沈绍聪, 李律, 王奇, 尤庶敏, 张才军. 不同葡萄糖浓度对大鼠草酸钙结石模型的影响, 昆明医科大学学报.
[17]	王瑞涛, 贾庆安, 牟怡平, 耿智敏, 刘昌. 胆宁片调节肠道菌群移位消除胆道炎症及预防胆石形成的临床评价, 昆明医科大学学报.
[18]	魏静. 迷迭香叶中鼠尾草酸的提取工艺研究, 昆明医科大学学报.
[19]	张建华. 上尿路腔内碎石术后并发尿源性脓毒症休克的处理和预防, 昆明医科大学学报.
[20]	宋华. 还原型谷胱甘肽联合甘草酸二铵治疗肝硬化的临床疗效观察, 昆明医科大学学报.