Research Progress in Mechanisms of Drug-induced Kidney Injury

doi:10.19803/j.1672-8629.2019.11.10

Abstract

Abstract: Objective To help gain keen insights into drug-induced kidney injury and prevent such injury by analyzing the mechanism of this disease Methods By searching PubMed, ScienceDirect and other authoritative databases, the latest literature was summarized on the pathogenesis, mechanism, typical diseases and drug safety evaluation Methods of drug-induced kidney injury. Results The clinical phenotypes of drug-induced kidney injury could be divided into four categories: acute renal injury, glomerular injury, renal tubule injury and renal calculus. The mechanisms of drug-induced kidney injury could be divided into six categories: direct action, oxidative stress, immune inflammation, acid-base balance disorder, drug effect on transporters. Typical drug-induced kidney injury included thrombotic microangiopathy, aristolochic acid nephropathy and Fanconi syndrome. More sensitive Methods for safety evaluation of drug-induced kidney injury were needed. Conclusion We should improve our understanding of the clinical phenotypes, pathogenesis and typical diseases of drug-induced kidney injury and try to establish comprehensive and reliable drug safety evaluation Methods so as to update our knowledge of drug-induced kidney injury while enhancing prevention and control of this disease.

Key words: drug-induced kidney injury, mechanism, clinical phenotype, typical disease, research progress

CLC Number:

R994.11

QIU Caixia, YANG Cuiping, JIN Hongtao. Research Progress in Mechanisms of Drug-induced Kidney Injury[J]. Chinese Journal of Pharmacovigilance, 2019, 16(11): 688-694.

Add to citation manager EndNote|Ris|BibTeX

URL: https://zgywjj.magtechjournal.com/EN/10.19803/j.1672-8629.2019.11.10

https://zgywjj.magtechjournal.com/EN/Y2019/V16/I11/688

References

[1] 郝静,袁伟杰.药物性肾损伤的诊治进展[J].实用医院临床杂志, 2012, 9(2):11-14.
[2] Ravindra L, Metha, Linda Awdishu, et al. Phenotypestandardization for drug-induced kidney disease[J]. KidneyInternational, 2015, 88(2): 226-234.
[3] Humphreys W G, Will Y, Guengerich F P. Toxicology Strategiesfor Drug Discovery-Present and Future: Introduction[J].Chem Res Toxicol, 2016, 29(4): 437.
[4] Onakpoya I J, Heneghan C J, Aronson J K. Worldwide withdrawalof medicinal products because of adverse drug reactions:a systematic review and analysis[J]. Critical Reviews inToxicology, 2016, 46(6): 477-489.
[5] Vanherweghem J L, Depierreux M, Tielemans C, et al. Rapidlyprogressive interstitial renal fibrosis in young women: associationwith slimming regimen including Chinese herbs[J]. Lancet,1993, 341(8842): 387.
[6] 邱婷婷, 张弨, 陈丁丁.6例药源性肾损伤案例报告及临床分析[J].临床药物治疗杂志, 2017, 15(6): 63-68.[7] 赵靓,郭代红,朱曼,等. 501例药源性肾损伤分析[J].中国药物警戒, 2015, 12(10):627-631.
[8] 朱曼,蔡乐,郭代红,等. 209例抗感染药物药源性肾损伤不良反应/事件报告分析[J].药物流行病学杂志, 2015(9):537-540.
[9] 周立国.药物毒理学[M]. 北京:中国医药科技出版社,2009:47-48.
[10] 曾诚.药源性肾损害[J].中国医院药学杂志,2013,33(4):319-321.
[11] Yokoyama H, Narita I, Sugiyama H, et al. Drug-inducedkidney disease: a study of the Japan Renal Biopsy Registryfrom 2007 to 2015[J]. Clinical and Experimental Nephrology,2016, 20(5): 720-730.
[12] Amy E, Blatt, Scott E, Liebman. Drug Induced Acute KidneyInjury[M]. Hosp Med Clin ，2013：525-541.
[13] Decloedt E, Maartens G. Drug-induced renal injury: Thekidney plays an important role in the elimination of many drugsand their metabolites[J]. Continuing Medical Education，2011, 29(6): 252-255.
[14] Mehta R L, Awdishu L, Davenport A, et al. PhenotypeStandardization for Drug Inducdee Kidney Disease[J].Kidneyinternational, 2015，88(2): 226-234.
[15] Perazella M A. Diagnosing drug-induced AIN in the hospitalizedpatient: a challenge for the clinician.[J]. Clinical Nephrology,2014, 81(6):0-381.
[16] Raghavan R, Shawar S. Mechanisms of Drug-Induced InterstitialNephritis[J]. Advances in Chronic Kidney Disease, 2017,24(2): 64-71.
[17] Radhakrishnan J, Perazella M A. Drug-induced glomerulardisease: attention required![J]. Clinical Journal of the AmericanSociety of Nephrology Cjasn,2015, 10(7): 1287-1290.
[18] 葛可佑, 程义勇,郭俊生,等.中国营养师培训教材[M].人民卫生出版社, 2005：569-570.
[19] 那彦群, 郭震华.实用泌尿外科学[M]. 人民卫生出版社,2009：169-170.
[20] Perazella M A. Crystal-induced acute renal failure.[J].American Journal of Medicine, 1999, 106(4): 0-459.
[21]于敏, 张双庆, 李佐刚.药物源性肾损伤发生机制的研究进展[J].中国药事, 2012, 26(12):1388-1392.
[22] Briguori C, Airoldi F, D’Andrea D, et al. Renal InsufficiencyFollowing Contrast Media Administration Trial: a randomizedcomparison of 3 preventive strategies[J]. Circulation, 2007,46(6): 1307-1308.
[23] Yarlagadda S G, Perazella M A. Drug-induced crystal nephropathy:an update.[J]. Expert Opinion on Drug Safety, 2008, 7(2):147-158.
[24] Fogazzi G B. Crystalluria: a nelgected aspect of urinarysediment analysis[J]. Nephrol Dial Transpant, 1996, 11(2):379-387.
[25] Ohsaki Y, O’Connor P, Mori T, et al. Increase of sodiumdelivery stimulates the mitochondrial respirator chain H2O2production in rat renal medullary thick ascending limb[J].Am J Physiol Renal Physiol, 2012, 302(1): F95-F102.
[26] Brian B, Ratliff, Wasan Abdlumahdi, et al. Oxidant mechanismsin renal injury and diease[J]. Antioxidants & Redox Signaling,2016, 25(3): 119-146.
[27] Geiszt M, Kopp J B, Varnai P, et al. Identification of renox,an NADPH oxidase in kidney[J]. Proc Natl Acad Sci USA,2000, 97(14): 8010-8014.
[28] Newburger P E, Ezekowitz R A, Whitney C, et al. Inductionof phagocyte cytochrome b heavy chain gene expression byinterferon gamma[J]. Proc Natl Acad Sci USA, 1988, 85(14):5215-5219.
[29] Holterman C E, Thibodeau J F, Kennedy C R J. NADPHoxidase 5 and renal disease[J]. Current Opinion in Nephrologyand Hypertension, 2014, 24(1): 81-87.
[30] Zou A P, Li N, Cowley A W. Production and Actions of Superoxidein the Renal Medulla[J]. Hypertension, 2001, 37(2): 547-553.
[31] Brodsky S V, Gao S, Li H, et al. Hyperglycemic switch frommitochondrial nitric oxide to superoxide production in endothelialcells[J]. AJP Heart and Circulatory Physiology, 2002, 283(5): H2130-H2139.
[32] Li J M, Shah A M. Endothelial call superoxide generation:regulation and relevance for cardiovascular pathophysiology[J].Am J Physiol Regul Intergr Comp Physiol, 2004, 287(5):R1014-R1030.
[33] Lodha S, Dani D, Mehta R, et al. Angiotensin II-InducedMesangial Cell Apoptosis: Role of Oxidative Stress[J]. MolecularMedicine, 2003, 8(12): 830-840.
[34] Sverrisson K, Axelsson J, Rippe A, et al. Acute reactiveoxygen species (ROS)-dependent effects of IL-1β, TNF-α,and IL-6 on the glomerular filtration barrier (GFB) in vivo[J].American Journal of Physiology - Renal Physiology, 2015,309(9): F800-F806.
[35] Brian B, Ratliff, Wasan Abdlumahdi, et al. Oxidant mechanismsin renal injury and diease[J]. Antioxidants & Redox Signaling,2016, 25(3): 119-146.
[36] Kurts C, Panzer U, Anders H J, et al. The immune system andkidney disease basic concepts and clinical implications[J].Nat Rev Immunol, 2013, 13(10): 738-753.
[37] Ludwig-Portugall I, Bartok E, Dhana E, et al. An NLRP3-specific inflammasome inhibitor attenuates crystal-inducedkidney fibrosis in mice[J]. Kidney International, 2016, 90(3):525-539.
[38] Dhana E, Ludwig-Portugall I, Kurts C . Role of immune cellsin crystal-induced kidney fibrosis[J]. Matrix Biology, 2018(68):280-292.
[39] Sinico R A, Mezzina N, Trezzi B, et al. Immunology of membranousnephropathy: from animal models to humans[J]. Clinical &Experimental Immunology, 2016, 183(2): 157-165.
[40] Lionaki S, Gakiopoulou H, Boletis J N. Understanding thecomlement-mediated glomerular diseases: focus on membran-oprolifeatvie and C3 glomerulopathies[J]. APMIS, 2016(124): 725-735.
[41] Al-Hussain T, Hussein M H, Mana H A, et al. Renal Involvementin Monoclonal Gammopathy[J]. Advances in Anatomic Pathology,2015, 22(2): 121-134.
[42] Bridoux F, Leung N, Hutchison C A, et al. Diagnosis ofmonoclonal gammopathy of renal significance.[J]. KidneyInternational, 2015, 87(4): 698-711.
[43] Tecklenborg J, Clayton D, Siebert S, et al. The role of theimmune system in kidney disease[J]. Clinical & ExperimentalImmunology, 2018, 192(2): 142-150.
[44] Brain R Matlaga, Ojas D Shah, Dean G Assimos. Drug-Induced Urinary Calculi[J]. Rev Urol, 2003, 5(4): 227-231.
[45] DuBose T D. Molecular and pathophysiologic mechanisms ofhyperkalemic metabolic acidosis[J]. Trans Am Clin ClimatolAssoc, 2000, （111）: 122-134.
[46] Yin J , Wang J. Renal drug transporters and their significancein drug–drug interactions[J]. Acta Pharmaceutica SinicaB, 2016, 6(5): 363-373.
[47] Burckhardt G, Wolff N A. Structure of renal organic anionand cation transporters.[J]. Am J Physiol Renal Physiol,2000, 278(6): F853-F866.
[48] Atsushi Yonezawa, Ken-ichi Inui. Organic cation transporterOCT/SLC22A and H+/organic cation antiporter MATE/SLC47A are key molecules for nephrotoxicity of platinumagents[J]. Biochemical Pharmacology, 2011, 81(5): 563-568.
[49] Ciarimboli G, Deuster D, Knief A, et al. Organic CationTransporter 2 Mediates Cisplatin-Induced Oto and Nephrotoxicityand Is a Target for Protective Interventions[J]. The AmericanJournal of Pathology, 2010, 176(3): 1169-1180.
[50] Filipski K K, Mathijssen R H, Mikkelsen T S, et al. Contributionof Organic Cation Transporter 2 (OCT2) to Cisplatin-InducedNephrotoxicity[J]. Clinical Pharmacology & Therapeutics,2009, 86(4): 396-402.
[51] Shatzel J J, Taylor J A . Syndromes of Thrombotic Microangiopathy[J]. Medical Clinics of North America, 2017, 101(2): 395-415.
[52] Izzedine H, Perazella M A. Anticancer Drug-Induced AcuteKidney Injury.[J]. Kidney International Reports, 2017, 2(4):504.
[53] 陈文, 李安, 程虹,等.马兜铃酸肾病的临床与病理表现[J]. 中华医学杂志, 2001, 81(18):1101-1105.
[54] 谌贻璞. 马兜铃酸肾病的研究进展[C]. 2005珠海国际肾脏病学术周论文集.2005:1-3.
[55] Wen Y J, Qu L, Li X M. Ischemic injury underlies the pathogenesisof aristolochic acid-induced acute kidney injury[J]. TranslationalResearch the Journal of Laboratory & Clinical Medicine,2008, 152(1): 38-46.
[56] Zhenzhou Jiang, Qingli Bao, Lixin Sun, et al. Possible role ofmtDNA depletion and respiratory chain defects in aristolochicacid I-induced acute nephrotoxicity[J]. Toxicology and AppliedPharmacology, 2013, 266(2): 198-203.
[57] Verhelst D, Monge M, Meynard J L, et al. Fanconi syndrome andrenal failure induced by tenofovir: A first case report[J]. AmericanJournal of Kidney Diseases, 2002, 40(6): 1331-1333.
[58] 邱宣,周晓冰,李波.体外模型在药源性肾毒性评价中的研究进展[J].中国新药杂志, 2017,(15): 1792-1796.
[59] Mossoba M E, Flynn T J, Vohra S, et al. Evaluation of “DreamHerb,” Calea zacatechichi, for Nephrotoxicity Using HumanKidney Proximal Tubule Cells[J]. Journal of Toxicology,2016, 2016(1): 1-7.
[60] Hynes J, Nadanaciva S, Swiss R, et al. A high-throughputdual parameter assay for assessing drug-induced mitochondrialdysfunction provides additional predictivity over two establishedmitochondrial toxicity assays[J]. Toxicology in Vitro, 2013,
27(2): 560-569.[61] Zhe M, Xuexiao C, Xiao G, et al. Establishment and Validationof an In Vitro Screening Method for Traditional Chinese Medicine-Induced Nephrotoxicity[J]. Evidence-Based Complementaryand Alternative Medicine, 2018:1-15.
[62] Weber E J, Himmelfarb J, Kelly E J. Concise Review: Currentand Emerging Biomarkers of Nephrotoxicity.[J]. Curr OpinToxicol, 2017, （4）: 16-21.
[63] D?津克, 李尧. 预测肾近曲小管细胞毒性的体外试验:CN 104641237 A[P]. 2015.
[64] Pavkovic M, Vaidya V S. MicroRNAs and Drug-inducedKidney Injury[J]. Pharmacol Ther, 2016，（163）:48-57.
[65] 周晓冰.大鼠与Beagle犬肾毒性生物标志物及肠道病毒71型灭活疫苗临床前安全性的研究[D]. 北京协和医学院, 2014.
[66] 劳乔聪, 俞航萍, 汤保华,等. 斑马鱼模型在药物肾毒性评价中的应用[C].中国毒理学会湖北科技论坛, 2015.
[67] Gautier J C, Zhou X, Yang Y, et al. Evaluation of novelbiomarkers of nephrotoxicity in Cynomolgus monkeys treatedwith gentamicin[J]. Toxicology & Applied Pharmacology,2016, （303）: 1-10.
[68] Qu Y, An F, Luo Y, et al. A nephron model for study of drug-induced acute kidney injury and assessment of drug-inducednephrotoxicity.[J]. Biomaterials, 2017,（155）:41-53.
[69] Li Z, Jiang L, Zhu Y, et al. Assessment of hepatic metabolism-dependent nephrotoxicity on an organs-on-a-chip microdevice[J]. Toxicology in Vitro, 2018,（ 46）: 1-8.