开放期刊系统

高血压眼肾微血管病变的研究进展

子平 张(承德医学院附属医院,中国)
微莉 董(承德医学院附属医院,中国)

摘要

高血压肾病和高血压视网膜病变是高血压常见的两种微血管并发症。两者拥有相似的发病机制,高血压影响RAAS系统、氧化应激和代谢因素等,导致肾脏和视网膜微血管的损伤。肾脏也有着区别于视网膜的发病机制,如铁死亡。临床中,眼部微血管变化可间接反应肾脏微血管的改变,肾小球滤过率和尿微量白蛋白同样影响视网膜和脉络膜的改变。本文从发病机制、病理特点、协同与交互作用等方面总结高血压眼肾微血管病变的研究进展。

关键词

高血压;高血压肾病;高血压视网膜病变

全文:

PDF

参考

Saran R, Robinson B, Abbott K C, et al. US renal data system 2019 annual data report: epidemiology of kidney disease in the United States[J]. American journal of kidney diseases: the official journal of the National Kidney Foundation, 2020, 75(1 Suppl 1): A6-A7.

边波,万征,李永乐,等.高血压患者视网膜病变调查及其临床价值评价[J].中国慢性病预防与控制,2011,19(2):170-171.

Wong C W, Wong T Y, Cheng C Y, et al. Kidney and eye diseases: common risk factors, etiological mechanisms, and pathways[J]. Kidney international, 2014, 85(6): 1290-1302.

Mennuni S, Rubattu S, Pierelli G, et al. Hypertension and kidneys: unraveling complex molecular mechanisms underlying hypertensive renal damage[J]. Journal of human hypertension, 2014, 28(2): 74-79.

Wolf G, Butzmann U, Wenzel U O. The renin-angiotensin system and progression of renal disease: from hemodynamics to cell biology[J]. Nephron physiology, 2003, 93(1): p3-p13.

Thomas W G, Thekkumkara T J, Baker K M. Proceedings of the Symposium ‘Angiotensin AT1 Receptors: From Molecular Physiology to Therapeutics’: MOLECULAR MECHANISMS OF ANGIOTENSIN II (AT1a) RECEPTOR ENDOCYTOSIS[J]. Clinical and Experimental Pharmacology and Physiology, 1996, 23(S3): 74-80.

Queisser N, Oteiza P I, Stopper H, et al. Aldosterone induces oxidative stress, oxidative DNA damage and NF-κB-activation in kidney tubule cells[J]. Molecular carcinogenesis, 2011, 50(2): 123-135.

Wagner J, Danser A H J, Derkx F H, et al. Demonstration of renin mRNA, angiotensinogen mRNA, and angiotensin converting enzyme mRNA expression in the human eye: evidence for an intraocular renin-angiotensin system[J]. British Journal of Ophthalmology, 1996, 80(2): 159-163.

Benigni A, Cassis P, Remuzzi G. Angiotensin II revisited: new roles in inflammation, immunology and aging[J]. EMBO molecular medicine, 2010, 2(7): 247-257.

Cuadrado A, Manda G, Hassan A, et al. Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach[J]. Pharmacological reviews, 2018, 70(2): 348-383.

Touyz R M, Rios F J, Alves-Lopes R, et al. Oxidative stress: a unifying paradigm in hypertension[J]. Canadian journal of cardiology, 2020, 36(5): 659-670.

Lee M Y, Griendling K K. Redox signaling, vascular function, and hypertension[J]. Antioxidants & redox signaling, 2008, 10(6): 1045-1059.

Santana-Garrido Á, Reyes-Goya C, Fernández-Bobadilla C, et al. NADPH oxidase–induced oxidative stress in the eyes of hypertensive rats[J]. Molecular Vision, 2021, 27: 161.

Dong Z, Dai H, Feng Z, et al. Mechanism of herbal medicine on hypertensive nephropathy[J]. Molecular Medicine Reports, 2021, 23(4): 1.

Sano Y, Kanematsu E H, Yoshiura M, et al. Uric acid as biochemical marker for retinal and optic nerve damage after occlusion and reperfusion of common carotid and vertebral arteries in rat[J]. Japanese journal of ophthalmology, 1992, 36(1): 76-83.

张红艳,唐英杰,贾丽霞.高血压视网膜病变危险因素分析[J].现代中西医结合杂志,2007,16(23):3304-3305.

Ohta Y, Tsuchihashi T, Kiyohara K, et al. Increased uric acid promotes decline of the renal function in hypertensive patients: a 10-year observational study[J]. Internal Medicine, 2013, 52(13): 1467-1472.

Kang D H, Nakagawa T, Feng L, et al. A role for uric acid in the progression of renal disease[J]. Journal of the American Society of Nephrology, 2002, 13(12): 2888-2897.

黄华翠,柯晓,谢光素,等.老年高血压肾病相关危险因素分析[J].中国医药导报,2021,18(29):52-55.

Chen Y, Wang K, Yang J, et al. Mechanism of ferroptosis in hypertensive nephropathy[J]. Translational Andrology and Urology, 2022, 11(5): 617.

Du X, Ma X, Tan Y, et al. B cell-derived anti-beta 2 glycoprotein I antibody mediates hyperhomocysteinemia-aggravated hypertensive glomerular lesions by triggering ferroptosis[J]. Signal Transduction and Targeted Therapy, 2023, 8(1): 103.

Xie T, Bai Z, Chen Z, et al. Inhibition of ferroptosis ameliorates hypertensive nephropathy through p53/Nrf2/p21 pathway by Taohongsiwu decoction: based on network pharmacology and experimental validation[J]. Journal of Ethnopharmacology, 2023, 312: 116506.

Lim L S, Cheung C Y, Sabanayagam C, et al. Structural changes in the retinal microvasculature and renal function[J]. Investigative ophthalmology & visual science, 2013, 54(4): 2970-2976.

Chua J, Chin C W L, Hong J, et al. Impact of hypertension on retinal capillary microvasculature using optical coherence tomographic angiography[J]. Journal of hypertension, 2019, 37(3): 572-580.

Vadalà M, Castellucci M, Guarrasi G, et al. Retinal and choroidal vasculature changes associated with chronic kidney disease[J]. Graefe’s Archive for Clinical and Experimental Ophthalmology, 2019, 257: 1687-1698.

郭宝珠,王琳琳,潘星,等.肾病综合征患者血清同型半胱氨酸,D-二聚体和B型钠尿肽水平表达及与血栓栓塞的关系分析[J].Progress in Modern Biomedicine,2021(10).

Kuang Z, Wang Y, Feng S, et al. Association between plasma homocysteine and microalbuminuria in untreated patients with essential hypertension: a case-control study[J]. Kidney and Blood Pressure Research, 2018, 42(6): 1303-1311.

Chrysant S G, Chrysant G S. The current status of homocysteine as a risk factor for cardiovascular disease: a mini review[J]. Expert review of cardiovascular therapy, 2018, 16(8): 559-565.

Lei X, Zeng G, Zhang Y, et al. Association between homocysteine level and the risk of diabetic retinopathy: a systematic review and meta-analysis[J]. Diabetology & metabolic syndrome, 2018, 10: 1-8.

赵勋,李金萍.血清hs-CRP、Hcy水平与高血压性视网膜病变的关系研究[J].中外医学研究,2023,21(22):89-92.



DOI: http://dx.doi.org/10.12345/yzlcyxzz.v7i12.22899

Refbacks

  • 当前没有refback。
版权所有(c)2025 子平 张, 微莉 董 Creative Commons License
此作品已接受知识共享署名-非商业性使用 4.0国际许可协议的许可。
  • :+65-62233778 QQ:2249355960 :contact@s-p.sg