Progress in Pathogenesis and Treatment of Enteric Hyperoxaluria
-
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。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.
-
[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.
点击查看大图
计量
- 文章访问数: 3588
- HTML全文浏览量: 902
- PDF下载量: 168
- 被引次数: 0