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中华肾病研究电子杂志 ›› 2024, Vol. 13 ›› Issue (02) : 106 -112. doi: 10.3877/cma.j.issn.2095-3216.2024.02.009

综述

急性肾损伤向慢性肾脏病转变研究进展
张轶男1, 朱国贞2,()   
  1. 1. 030001 太原,山西医科大学
    2. 030001 太原,山西医科大学第二医院肾内科
  • 收稿日期:2023-08-24 出版日期:2024-04-28
  • 通信作者: 朱国贞
  • 基金资助:
    山西省自然科学研究面上项目(202103021224420)

Research progress on the transition from acute kidney injury to chronic kidney disease

Yinan Zhang1, Guozhen Zhu2,()   

  1. 1. Shanxi Medical University
    2. Department of Nephrology, Second Hospital of Shanxi Medical University; Taiyuan 030001, Shanxi Province, China
  • Received:2023-08-24 Published:2024-04-28
  • Corresponding author: Guozhen Zhu
引用本文:

张轶男, 朱国贞. 急性肾损伤向慢性肾脏病转变研究进展[J]. 中华肾病研究电子杂志, 2024, 13(02): 106-112.

Yinan Zhang, Guozhen Zhu. Research progress on the transition from acute kidney injury to chronic kidney disease[J]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2024, 13(02): 106-112.

虽然一些急性肾损伤(AKI)患者获得了临床痊愈,却仍然会由于肾脏结构的改变以及适应不良性修复而发生肾组织纤维化,从而转变进展至慢性肾脏病(CKD)甚至是终末期肾脏病(ESRD)。因此,早期识别和干预AKI向CKD转变是至关重要的。本文就AKI向CKD转变的危险因素、转变机制、生物标志物和干预措施的研究进展作一综述。

Although some patients with acute kidney injury (AKI) got clinical recovery, they still experienced renal tissue fibrosis due to changes in renal structure and maladaptive repair, leading to progression to chronic kidney disease (CKD) and even end-stage renal disease (ESRD). Therefore, early identification and intervention of the AKI-to-CKD transition is crucial. This article reviewed the research progress on the risk factors, transition mechanisms, biomarkers, and intervention measures of the AKI-to-CKD transition.

图1 急性肾损伤-慢性肾脏病转变机制注:RAAS:肾素-血管紧张素-醛固酮系统
图2 生物标志物注:KIM-1:肾损伤分子-1;NGAL:中性粒细胞明胶酶相关脂质运载蛋白;L-FABP:肝型脂肪酸结合蛋白;TIMP-2:金属蛋白酶组织抑制剂-2;IGFBP7:胰岛素样生长因子结合蛋白7;NLRP3:核苷酸结合的低聚结构域样受体蛋白3;bFGF:碱性成纤维细胞生长因子;NT-proBNP:N-末端B型利钠肽原;MMP-7:基质金属蛋白酶-7
[1]
Kung CW, Chou YH. Acute kidney disease: an overview of the epidemiology, pathophysiology, and management [J]. Kidney Res Clin Pract, 2023, Epub ahead of print.
[2]
Guzzi F, Cirillo L, Roperto RM, et al. Molecular mechanisms of the acute kidney injury to chronic kidney disease transition: an updated view [J]. Int J Mol Sci, 2019, 20(19): 4941.
[3]
Thakar CV, Christianson A, Himmelfarb J, et al. Acute kidney injury episodes and chronic kidney disease risk in diabetes mellitus [J]. Clin J Am Soc Nephrol, 2011, 6(11): 2567-2572.
[4]
Kurzhagen JT, Dellepiane S, Cantaluppi V, et al. AKI: an increasingly recognized risk factor for CKD development and progression [J]. J Nephrol, 2020, 33(6): 1171-1187.
[5]
Saranya GR, Viswanathan P. Gut microbiota dysbiosis in AKI to CKD transition [J]. Biomed Pharmacother, 2023, 161: 114447.
[6]
Chen JY, Tsai I, Pan HC, et al. The impact of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers on clinical outcomes of acute kidney disease patients: a systematic review and meta-analysis [J]. Front Pharmacol, 2021, 12: 665250.
[7]
Ciarambino T, Crispino P, Giordano M. Gender and renal insufficiency: opportunities for their therapeutic management? [J]. Cells, 2022, 11(23): 3820.
[8]
Wang Z, Zhang C. From AKI to CKD: maladaptive repair and the underlying mechanisms [J]. Int J Mol Sci, 2022, 23(18): 10880.
[9]
McWilliam SJ, Wright RD, Welsh GI, et al. The complex interplay between kidney injury and inflammation [J]. Clin Kidney J, 2021, 14(3): 780-788.
[10]
Tinti F, Lai S, Noce A, et al. Chronic kidney disease as a systemic inflammatory syndrome: update on mechanisms involved and potential treatment [J]. Life (Basel), 2021, 11(5): 419.
[11]
Wu YS, Liang S, Li DY, et al. Cell cycle dysregulation and renal fibrosis [J]. Front Cell Dev Biol, 2021, 9: 714320.
[12]
Yang L, Besschetnova TY, Brooks CR, et al. Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury [J]. Nat Med, 2010, 16(5): 535-543.
[13]
Zhang X, Agborbesong E, Li X. The role of mitochondria in acute kidney injury and chronic kidney disease and its therapeutic potential [J]. Int J Mol Sci, 2021, 22(20): 11253.
[14]
Bartoszewska S, Collawn JF. Unfolded protein response (UPR) integrated signaling networks determine cell fate during hypoxia [J]. Cell Mol Biol Lett, 2020, 25: 18.
[15]
Chen F, Gao Q, Wei A, et al. Histone deacetylase 3 aberration inhibits Klotho transcription and promotes renal fibrosis [J]. Cell Death Differ, 2021, 28(3): 1001-1012.
[16]
Fontecha-Barriuso M, Martin-Sanchez D, Ruiz-Andres O, et al. Targeting epigenetic DNA and histone modifications to treat kidney disease [J]. Nephrol Dial Transplant, 2018, 33(11): 1875-1886.
[17]
Zhou Q, Chen W, Yu XQ. Long non-coding RNAs as novel diagnostic and therapeutic targets in kidney disease [J]. Chronic Dis Transl Med, 2020, 5(4): 252-257.
[18]
Venkatachalam MA, Weinberg JM, Kriz W, et al. Failed tubule recovery, AKI-CKD transition, and kidney disease progression [J]. J Am Soc Nephrol, 2015, 26(8): 1765-1776.
[19]
Zhu Z, Hu J, Chen Z, et al. Transition of acute kidney injury to chronic kidney disease: role of metabolic reprogramming [J]. Metabolism, 2022, 131: 155194.
[20]
Baudoux T, Jadot I, Declèves AE, et al. Experimental aristolochic acid nephropathy: a relevant model to study AKI-to-CKD transition [J]. Front Med (Lausanne), 2022, 9: 822870.
[21]
Aggarwal D, Singh G. Effects of single and dual RAAS blockade therapy on progressive kidney disease transition to CKD in rats [J]. Naunyn Schmiedebergs Arch Pharmacol, 2020, 393(4): 615-627.
[22]
Ciarambino T, Crispino P, Giordano M. Gender and renal insufficiency: opportunities for their therapeutic management? [J]. Cells, 2022, 11(23): 3820.
[23]
McCoy IE, Hsu JY, Bonventre JV, et al. Acute kidney injury associates with long-term increases in plasma TNFR1, TNFR2, and KIM-1: findings from the CRIC study [J]. J Am Soc Nephrol, 2022, 33(6): 1173-1181.
[24]
Tuan PNH, Quyen DBQ, Van Khoa H, et al. Serum and urine neutrophil gelatinase-associated lipocalin levels measured at admission predict progression to chronic kidney disease in sepsis-associated acute kidney injury patients [J]. Dis Markers, 2020, 2020: 8883404.
[25]
Cooper DS, Claes D, Goldstein SL, et al. Follow-up renal assessment of injury long-term after acute kidney injury (FRAIL-AKI) [J]. Clin J Am Soc Nephrol, 2016, 11(1): 21-29.
[26]
Ichikawa D, Kamijo-Ikemori A, Sugaya T, et al. Utility of urinary tubular markers for monitoring chronic tubulointerstitial injury after ischemia-reperfusion [J]. Nephrology (Carlton), 2018, 23(4): 308-316.
[27]
Cho WY, Lim SY, Yang JH, et al. Urinary tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-binding protein 7 as biomarkers of patients with established acute kidney injury [J]. Korean J Intern Med, 2020, 35(3): 662-671.
[28]
Zheng Z, Xu K, Li C, et al. NLRP3 associated with chronic kidney disease progression after ischemia/reperfusion-induced acute kidney injury [J]. Cell Death Discov, 2021, 7(1): 324.
[29]
Xing Z, Gong K, Hu N, et al. The reduction of uromodulin, complement factor H, and their interaction is associated with acute kidney injury to chronic kidney disease transition in a four-time cisplatin-injected rat model [J]. Int J Mol Sci, 2023, 24(7): 6636.
[30]
Menez S, Moledina DG, Garg AX, et al. Results from the TRIBE-AKI study found associations between post-operative blood biomarkers and risk of chronic kidney disease after cardiac surgery [J]. Kidney Int, 2021, 99(3): 716-724.
[31]
Liu Z, Tan RJ, Liu Y. The many faces of matrix metalloproteinase-7 in kidney diseases [J]. Biomolecules, 2020, 10(6): 960.
[32]
Yin J, Wang F, Kong Y, et al. Antithrombin III prevents progression of chronic kidney disease following experimental ischaemic-reperfusion injury [J]. J Cell Mol Med, 2017, 21(12): 3506-3514.
[33]
Zhao JY, Wu YB. Huaier extract attenuates acute kidney injury to chronic kidney disease transition by inhibiting endoplasmic reticulum stress and apoptosis via miR-1271 upregulation [J]. Biomed Res Int, 2020, 2020: 9029868.
[34]
Wu M, Chen W, Miao M, et al. Anti-anemia drug FG4592 retards the AKI-to-CKD transition by improving vascular regeneration and antioxidative capability [J]. Clin Sci (Lond), 2021, 135(14): 1707-1726.
[35]
Nishida K, Watanabe H, Murata R, et al. Recombinant long-acting thioredoxin ameliorates AKI to CKD transition via modulating renal oxidative stress and inflammation [J]. Int J Mol Sci, 2021, 22(11): 5600.
[36]
Chen DQ, Cao G, Zhao H, et al. Combined melatonin and poricoic acid A inhibits renal fibrosis through modulating the interaction of Smad3 and β-catenin pathway in AKI-to-CKD continuum [J]. Ther Adv Chronic Dis, 2019, 10: 2040622319869116.
[37]
Abdelmageed MM, Kefaloyianni E, Arthanarisami A, et al. TNF or EGFR inhibition equally block AKI-to-CKD transition: opportunities for etanercept treatment [J]. Nephrol Dial Transplant, 2023, 38(5): 1139-1150.
[38]
Zahan MS, Ahmed KA, Moni A, et al. Kidney protective potential of lactoferrin: pharmacological insights and therapeutic advances [J]. Korean J Physiol Pharmacol, 2022, 26(1): 1-13.
[39]
Jia Y, Kang X, Tan L, et al. Nicotinamide mononucleotide attenuates renal interstitial fibrosis after AKI by suppressing tubular DNA damage and senescence [J]. Front Physiol, 2021, 12: 649547.
[40]
Lok SWY, Yiu WH, Li H, et al. The PAR-1 antagonist vorapaxar ameliorates kidney injury and tubulointerstitial fibrosis [J]. Clin Sci (Lond), 2020, 134(21): 2873-2891.
[41]
Yu Y, Chen M, Guo Q, et al. Human umbilical cord mesenchymal stem cell exosome-derived miR-874-3p targeting RIPK1/PGAM5 attenuates kidney tubular epithelial cell damage [J]. Cell Mol Biol Lett, 2023, 28(1): 12.
[42]
Mapuskar KA, Vasquez-Martinez G, Mayoral-Andrade G, et al. Mitochondrial oxidative metabolism: an emerging therapeutic target to improve CKD outcomes [J]. Biomedicines, 2023, 11(6): 1573.
[43]
Li C, Shen Y, Huang L, et al. Senolytic therapy ameliorates renal fibrosis postacute kidney injury by alleviating renal senescence [J]. FASEB J, 2021, 35(1): e21229.
[44]
Li J, Gong X. Tetramethylpyrazine: an active ingredient of Chinese herbal medicine with therapeutic potential in acute kidney injury and renal fibrosis [J]. Front Pharmacol, 2022, 13: 820071.
[45]
Kurata Y, Nangaku M. Use of antibiotics as a therapeutic approach to prevent AKI-to-CKD progression [J]. Kidney Int, 2023, 104(3): 418-420.
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