Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents-Pathophysiology and Biomarkers-A Review

Nadezda Petejova, Arnost Martinek, Josef Zadrazil, Marcela Kanova, Viktor Klementa, Radka Sigutova, Ivana Kacirova, Vladimir Hrabovsky, Zdenek Svagera, David Stejskal, Nadezda Petejova, Arnost Martinek, Josef Zadrazil, Marcela Kanova, Viktor Klementa, Radka Sigutova, Ivana Kacirova, Vladimir Hrabovsky, Zdenek Svagera, David Stejskal

Abstract

Acute kidney injury is a common complication in critically ill patients with sepsis and/or septic shock. Further, some essential antimicrobial treatment drugs are themselves nephrotoxic. For this reason, timely diagnosis and adequate therapeutic management are paramount. Of potential acute kidney injury (AKI) biomarkers, non-protein-coding RNAs are a subject of ongoing research. This review covers the pathophysiology of vancomycin and gentamicin nephrotoxicity in particular, septic AKI and the microRNAs involved in the pathophysiology of both syndromes. PubMED, UptoDate, MEDLINE and Cochrane databases were searched, using the terms: biomarkers, acute kidney injury, antibiotic nephrotoxicity, sepsis, miRNA and nephrotoxicity. A comprehensive review describing pathophysiology and potential biomarkers of septic and toxic acute kidney injury in septic patients was conducted. In addition, five miRNAs: miR-15a-5p, miR-192-5p, miR-155-5p, miR-486-5p and miR-423-5p specific to septic and toxic acute kidney injury in septic patients, treated by nephrotoxic antibiotic agents (vancomycin and gentamicin) were identified. However, while these are at the stage of clinical testing, preclinical and clinical trials are needed before they can be considered useful biomarkers or therapeutic targets of AKI in the context of antibiotic nephrotoxicity or septic injury.

Keywords: acute kidney injury; gentamicin; miRNA; nephrotoxicity; sepsis; vancomycin.

Conflict of interest statement

The authors declare no conflict of interest related to this manuscript or project.

Figures

Figure 1
Figure 1
Simplified pathophysiology of acute kidney injury development in sepsis and selected antibiotic treatment [6,10,42,47,48,51,55,56]. DNA—deoxyribonucleic acid, ICAM-1—intercellular adhesion molecule-1, IKK—I-kinase, IL-6—interleukin 6, IL-8—interleukin 8, MBD2—Methyl-CpG Binding Domain Protein 2, MCP-1—monocyte chemoattractant protein 1, NF-κB—nuclear factor—kappa B, PTC—proximal tubular cells, ROS—reactive oxygen species, TLR4—Toll-like receptor 4, TNFα—tumor necrosis factor alpha
Figure 2
Figure 2
Schematic pathophysiology of acute kidney injury in a critically ill patient with sepsis and nephrotoxic antibiotic treatment with selected miRNAs. AKI—acute kidney injury, GSTM1—glutathione-S-transferase Mu 1 gene, IL-6—interleukin 6, IL-1ß—interleukin 1ß, NF-κB—nuclear factor—kappa B, TNFα—tumor necrosis factor alpha, TNIP2—tumor necrosis factor alpha induced protein 3-interacting protein 2, TLR4—Toll-like receptor 4.

References

    1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int. Suppl. 2012;2:1–138.
    1. Chawla L.S., Bellomo R., Bihorac A., Goldstein S.L., Siew E.D., Bagshaw S.M., Bittleman D., Cruz D., Endre Z., Fitzgerald R.L., et al. Acute kidney disease and renal recovery: Consensus report of the Acute Disease Quality Initiative (ADQI) 16 Workgroup. Nat. Rev. Nephrol. 2017;13:241–257. doi: 10.1038/nrneph.2017.2.
    1. Uchino S., Kellum J.A., Bellomo R., Doig G.S., Morimatsu H., Morgera S., Schetz M., Tan I., Bouman C., Macedo E., et al. Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Acute renal failure in critically ill patients: A multinational, multicenter study. JAMA. 2005;294:813–818.
    1. Jiang L., Zhu Y., Luo X., Wen Y., Du B., Wang M., Zhao Z., Yin Y., Zhu B., Xi X. Epidemiology of acute kidney injury in intensive care units in Beijing: The multi-center BAKIT study. BMC Nephrol. 2019;20:468. doi: 10.1186/s12882-019-1660-z.
    1. Singer M., Deutschman C.S., Seymour C.W., Shankar-Hari M., Annane D., Bauer M., Bellomo R., Bernard G.R., Chiche J.D., Coopersmith C.M., et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA. 2016;315:801–810. doi: 10.1001/jama.2016.0287.
    1. Poston J.T., Koyner J.L. Sepsis associated acute kidney injury. BMJ. 2019;364:k4891. doi: 10.1136/bmj.k4891.
    1. Gómez H., Kellum J.A. Sepsis-induced acute kidney injury. Curr. Opin. Crit. Care. 2016;22:546–553. doi: 10.1097/MCC.0000000000000356.
    1. Ronco C., Bellomo R., Kellum J.A. Acute kidney injury. Lancet. 2019;394:1949–1964.
    1. Anders H.J., Banas B., Schlöndorff D. Signaling danger: Toll-like receptors and their potential roles in kidney disease. J. Am. Soc. Nephrol. 2004;15:854–867. doi: 10.1097/01.ASN.0000121781.89599.16.
    1. Kawai T., Akira S. Signaling to NF-kappaB by Toll-like receptors. Trends Mol. Med. 2007;13:460–469.
    1. Morrell E.D., Kellum J.A., Pastor-Soler N.M., Hallows K.R. Septic acute kidney injury: Molecular mechanisms and the importance of stratification and targeting therapy. Crit. Care. 2014;18:501. doi: 10.1186/s13054-014-0501-5.
    1. Wei Q. Novel strategy for septic acute kidney injury rescue: Maintenance of the tubular integrity. Kidney Int. 2020;97:847–849.
    1. Nakano D., Kitada K., Wan N., Zhang Y., Wiig H., Wararat K., Yanagita M., Lee S., Jia L., Titze J.M., et al. Lipopolysaccharide induces filtrate leakage from renal tubular lumina into the interstitial space via a proximal tubular Toll-like receptor 4-dependent pathway and limits sensitivity to fluid therapy in mice. Kidney Int. 2020;97:904–912. doi: 10.1016/j.kint.2019.11.024.
    1. Kashani K., Cheungpasitporn W., Ronco C. Biomarkers of acute kidney injury: The pathway from discovery to clinical adoption. Clin. Chem. Lab. Med. 2017;55:1074–1089. doi: 10.1515/cclm-2016-0973.
    1. Klein S.J., Brandtner A.K., Lehner G.F., Ulmer H., Bagshaw S.M., Wiedermann C.J., Joannidis M. Biomarkers for prediction of renal replacement therapy in acute kidney injury: A systematic review and meta-analysis. Intensive Care Med. 2018;44:323–336. doi: 10.1007/s00134-018-5126-8.
    1. Schrezenmeier E.V., Barasch J., Budde K., Westhoff T., Schmidt-Ott K.M. Biomarkers in acute kidney injury-pathophysiological basis and clinical performance. Acta Physiol. 2017;219:554–572. doi: 10.1111/apha.12764.
    1. Teo S.H., Endre Z.H. Biomarkers in acute kidney injury (AKI) Best Pract. Res. Clin. Anaesthesiol. 2017;31:331–344. doi: 10.1016/j.bpa.2017.10.003.
    1. Izquierdo-Garcia J.L., Nin N., Cardinal-Fernandez P., Rojas Y., de Paula M., Granados R., Martínez-Caro L., Ruíz-Cabello J., Lorente J.A. Identification of novel metabolomic biomarkers in an experimental model of septic acute kidney injury. Am. J. Physiol. Renal Physiol. 2019;316:F54–F62. doi: 10.1152/ajprenal.00315.2018.
    1. Chebotareva N., Bobkova I., Shilov E. Heat shock proteins and kidney disease: Perspectives of HSP therapy. Cell Stress Chaperones. 2017;22:319–343. doi: 10.1007/s12192-017-0790-0.
    1. Morales-Buenrostro L.E., Salas-Nolasco O.I., Barrera-Chimal J., Casas-Aparicio G., Irizar-Santana S., Pérez-Villalva R., Bobadilla N.A. Hsp72 is a novel biomarker to predict acute kidney injury in critically ill patients. PLoS ONE. 2014;9:e109407. doi: 10.1371/journal.pone.0109407.
    1. Dozmorov M.G., Giles C.B., Koelsch K.A., Wren J.D. Systematic classification of non-coding RNAs by epigenomic similarity. BMC Bioinform. 2013;14:S2. doi: 10.1186/1471-2105-14-S14-S2.
    1. Fan P.C., Chen C.C., Chen Y.C., Chang Y.S., Chu P.H. MicroRNAs in acute kidney injury. Hum. Genom. 2016;10:29. doi: 10.1186/s40246-016-0085-z.
    1. Giza D.E., Fuentes-Mattei E., Bullock M.D., Tudor S., Goblirsch M.J., Fabbri M., Lupu F., Yeung S.J., Vasilescu C., Calin G.A. Cellular and viral microRNAs in sepsis: Mechanisms of action and clinical applications. Cell Death Differ. 2016;23:1906–1918. doi: 10.1038/cdd.2016.94.
    1. Benz F., Roy S., Trautwein C., Roderburg C., Luedde T. Circulating MicroRNAs as Biomarkers for Sepsis. Int. J. Mol. Sci. 2016;17:78. doi: 10.3390/ijms17010078.
    1. Lin Z., Liu Z., Wang X., Qiu C., Zheng S. MiR-21-3p Plays a Crucial Role in Metabolism Alteration of Renal Tubular Epithelial Cells during Sepsis Associated Acute Kidney Injury via AKT/CDK2-FOXO1 Pathway. Biomed. Res. Int. 2019;2019:2821731. doi: 10.1155/2019/2821731.
    1. Ge Q.M., Huang C.M., Zhu X.Y., Bian F., Pan S.M. Differentially expressed miRNAs in sepsis-induced acute kidney injury target oxidative stress and mitochondrial dysfunction pathways. PLoS ONE. 2017;12:e0173292. doi: 10.1371/journal.pone.0173292.
    1. Ishimoto Y., Inagi R. Mitochondria: A therapeutic target in acute kidney injury. Nephrol. Dial. Transplant. 2016;31:1062–1069. doi: 10.1093/ndt/gfv317.
    1. Shen Y., Yu J., Jing Y., Zhang J. MiR-106a aggravates sepsis-induced acute kidney injury by targeting THBS2 in mice model. Acta Cir. Bras. 2019;34:e201900602. doi: 10.1590/s0102-865020190060000002.
    1. Taber S.S., Pasko D.A. The epidemiology of drug-induced disorders: The kidney. Expert Opin. Drug Saf. 2008;7:679–690. doi: 10.1517/14740330802410462.
    1. Rhodes A., Evans L.E., Alhazzani W., Levy M.M., Antonelli M., Ferrer R., Kumar A., Sevransky J.E., Sprung C.L., Nunnally M.E., et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43:304–377. doi: 10.1007/s00134-017-4683-6.
    1. Wilhelm-Leen E., Montez-Rath M.E., Chertow G. Estimating the Risk of Radiocontrast-Associated Nephropathy. J. Am. Soc. Nephrol. 2017;28:653–659. doi: 10.1681/ASN.2016010021.
    1. Perazella M.A., Markowitz G.S. Drug-induced acute interstitial nephritis. Nat. Rev. Nephrol. 2010;6:461–470. doi: 10.1038/nrneph.2010.71.
    1. Petejova N., Martinek A., Zadrazil J., Teplan V. Acute toxic kidney injury. Ren. Fail. 2019;41:576–594. doi: 10.1080/0886022X.2019.1628780.
    1. Arimura Y., Yano T., Hirano M., Sakamoto Y., Egashira N., Oishi R. Mitochondrial superoxide production contributes to vancomycin-induced renal tubular cell apoptosis. Free Radic. Biol. Med. 2012;52:1865–1873. doi: 10.1016/j.freeradbiomed.2012.02.038.
    1. Moledina D.G., Perazella M.A. PPIs and kidney disease: From AIN to CKD. J. Nephrol. 2016;29:611–616. doi: 10.1007/s40620-016-0309-2.
    1. Ong L.Z., Tambyah P.A., Lum L.H., Low Z.J., Cheng I., Murali T.M., Wan M.Q., Chua H.R. Aminoglycoside-associated acute kidney injury in elderly patients with and without shock. J. Antimicrob. Chemother. 2016;71:3250–3257. doi: 10.1093/jac/dkw296.
    1. Rybak M.J., Lomaestro B.M., Rotschafer J.C., Moellering R.C., Jr., Craig W.A., Billeter M., Dalovisio J.R., Levine D.P. Therapeutic monitoring of vancomycin in adults summary of consensus recommendations from the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the Society of Infectious Diseases Pharmacists. Pharmacotherapy. 2009;29:1275–1279. doi: 10.1592/phco.29.11.1275.
    1. Zamoner W., Prado I.R.S., Balbi A.L., Ponce D. Vancomycin dosing, monitoring and toxicity: Critical review of the clinical practice. Clin. Exp. Pharmacol. Physiol. 2019 doi: 10.1111/1440-1681.13066.
    1. Rybak M.J., Le J., Lodise T.P., Levine D.P., Bradley J.S., Liu C., Mueller B.A., Pai M.P., Wong-Beringer A., Rotschafer J.C., et al. Executive Summary: Therapeutic Monitoring of Vancomycin for Serious Methicillin-Resistant Staphylococcus aureus Infections: A Revised Consensus Guideline and Review of the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, the Pediatric Infectious Diseases Society, and the Society of Infectious Diseases Pharmacists. Pharmacotherapy. 2020;40:363–367.
    1. Chavada R., Ghosh N., Sandaradura I., Maley M., Van Hal S.J. Establishment of an AUC0-24 Threshold for Nephrotoxicity Is a Step towards Individualized Vancomycin Dosing for Methicillin-Resistant Staphylococcus aureus Bacteremia. Antimicrob. Agents Chemother. 2017;61 doi: 10.1128/AAC.02535-16.
    1. Hanrahan T.P., Kotapati C., Roberts M.J., Rowland J., Lipman J., Roberts J.A., Udy A. Factors associated with vancomycin nephrotoxicity in the critically ill. Anaesth. Intensive Care. 2015;43:594–599. doi: 10.1177/0310057X1504300507.
    1. Sakamoto Y., Yano T., Hanada Y., Takeshita A., Inagaki F., Masuda S., Matsunaga N., Koyanagi S., Ohdo S. Vancomycin induces reactive oxygen species-dependent apoptosis via mitochondrial cardiolipin peroxidation in renal tubular epithelial cells. Eur. J. Pharmacol. 2017;800:48–56. doi: 10.1016/j.ejphar.2017.02.025.
    1. Kane-Gill S.L., Ostermann M., Shi J., Joyce E.L., Kellum J.A. Evaluating Renal Stress Using Pharmacokinetic Urinary Biomarker Data in Critically Ill Patients Receiving Vancomycin and/or Piperacillin-Tazobactam: A Secondary Analysis of the Multicenter Sapphire Study. Drug Saf. 2019;42:1149–1155. doi: 10.1007/s40264-019-00846-x.
    1. Rhodes N.J., Prozialeck W.C., Lodise T.P., Venkatesan N., O’Donnell J.N., Pais G., Cluff C., Lamar P.C., Neely M.N., Gulati A., et al. Evaluation of Vancomycin Exposures Associated with Elevations in Novel Urinary Biomarkers of Acute Kidney Injury in Vancomycin-Treated Rats. Antimicrob. Agents Chemother. 2016;60:5742–5751. doi: 10.1128/AAC.00591-16.
    1. Pang H.M., Qin X.L., Liu T.T., Wei W.X., Cheng D.H., Lu H., Guo Q., Jing L. Urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin as early biomarkers for predicting vancomycin-associated acute kidney injury: A prospective study. Eur. Rev. Med. Pharmacol. Sci. 2017;21:4203–4213.
    1. Pais G.M., Avedissian S.N., O′Donnell J.N., Rhodes N.J., Lodise T.P., Prozialeck W.C., Lamar P.C., Cluff C., Gulati A., Fitzgerald J.C., et al. Comparative Performance of Urinary Biomarkers for Vancomycin-Induced Kidney Injury According to Timeline of Injury. Antimicrob. Agents Chemother. 2019;63 doi: 10.1128/AAC.00079-19.
    1. Wang J., Li H., Qiu S., Dong Z., Xiang X., Zhang D. MBD2 upregulates miR-301a-5p to induce kidney cell apoptosis during vancomycin-induced AKI. Cell Death Dis. 2017;8:e3120. doi: 10.1038/cddis.2017.509.
    1. Olbricht C.J., Fink M., Gutjahr E. Alterations in lysosomal enzymes of the proximal tubule in gentamicin nephrotoxicity. Kidney Int. 1991;39:639–646. doi: 10.1038/ki.1991.76.
    1. Gentamicin 40 mg/mL Injection. [(accessed on 7 July 2020)]; Available online: .
    1. Romero F., Pérez M., Chávez M., Parra G., Durante P. Effect of uric acid on gentamicin-induced nephrotoxicity in rats-role of matrix metalloproteinases 2 and 9. Basic Clin. Pharmacol. Toxicol. 2009;105:416–424. doi: 10.1111/j.1742-7843.2009.00466.x.
    1. Martínez-Salgado C., López-Hernández F.J., López-Novoa J.M. Glomerular nephrotoxicity of aminoglycosides. Toxicol. Appl. Pharmacol. 2007;223:86–98. doi: 10.1016/j.taap.2007.05.004.
    1. Udupa V., Prakash V. Gentamicin induced acute renal damage and its evaluation using urinary biomarkers in rats. Toxicol. Rep. 2018;6:91–99. doi: 10.1016/j.toxrep.2018.11.015.
    1. Campos M.A.A., de Almeida L.A., Grossi M.F., Tagliati C.A. In vitro evaluation of biomarkers of nephrotoxicity through gene expression using gentamicin. J. Biochem. Mol. Toxicol. 2018;32:e22189. doi: 10.1002/jbt.22189.
    1. Kagawa T., Zarybnicky T., Omi T., Shirai Y., Toyokuni S., Oda S., Yokoi T. A scrutiny of circulating microRNA biomarkers for drug-induced tubular and glomerular injury in rats. Toxicology. 2019;415:26–36. doi: 10.1016/j.tox.2019.01.011.
    1. Hori Y., Aoki N., Kuwahara S., Hosojima M., Kaseda R., Goto S., Iida T., De S., Kabasawa H., Kaneko R., et al. Megalin Blockade with Cilastatin Suppresses Drug-Induced Nephrotoxicity. J. Am. Soc. Nephrol. 2017;28:1783–1791. doi: 10.1681/ASN.2016060606.
    1. Balakumar P., Rohilla A., Thangathirupathi A. Gentamicin-induced nephrotoxicity: Do we have a promising therapeutic approach to blunt it? Pharmacol. Res. 2010;62:179–186. doi: 10.1016/j.phrs.2010.04.004.
    1. Xu G., Mo L., Wu C., Shen X., Dong H., Yu L., Pan P., Pan K. The miR-15a-5p-XIST-CUL3 regulatory axis is important for sepsis-induced acute kidney injury. Ren. Fail. 2019;41:955–966. doi: 10.1080/0886022X.2019.1669460.
    1. Lou Y., Huang Z. microRNA-15a-5p participates in sepsis by regulating the inflammatory response of macrophages and targeting TNIP2. Exp. Ther. Med. 2020;19:3060–3068. doi: 10.3892/etm.2020.8547.
    1. Wang Z.M., Wan X.H., Sang G.Y., Zhao J.D., Zhu Q.Y., Wang D.M. miR-15a-5p suppresses endometrial cancer cell growth via Wnt/β-catenin signaling pathway by inhibiting WNT3A. Eur. Rev. Med. Pharmacol. Sci. 2017;21:4810–4818.
    1. Chen D., Wu D., Shao K., Ye B., Huang J., Gao Y. MiR-15a-5p negatively regulates cell survival and metastasis by targeting CXCL10 in chronic myeloid leukemia. Am. J. Transl. Res. 2017;9:4308–4316.
    1. Shang J., He Q., Chen Y., Yu D., Sun L., Cheng G., Liu D., Xiao J., Zhao Z. miR-15a-5p suppresses inflammation and fibrosis of peritoneal mesothelial cells induced by peritoneal dialysis via targeting VEGFA. J. Cell. Physiol. 2019;234:9746–9755. doi: 10.1002/jcp.27660.
    1. Caserta S., Kern F., Cohen J., Drage S., Newbury S.F., Llewelyn M.J. Circulating Plasma microRNAs can differentiate Human Sepsis and Systemic Inflammatory Response Syndrome (SIRS) Sci. Rep. 2016;6:28006. doi: 10.1038/srep28006.
    1. Caserta S., Mengozzi M., Kern F., Newbury S.F., Ghezzi P., Llewelyn M.J. Severity of Systemic Inflammatory Response Syndrome Affects the Blood Levels of Circulating Inflammatory-Relevant MicroRNAs. Front. Immunol. 2018;8:1977. doi: 10.3389/fimmu.2017.01977.
    1. Zou Y.F., Wen D., Zhao Q., Shen P.Y., Shi H., Zhao Q., Chen Y.X., Zhang W. Urinary MicroRNA-30c-5p and MicroRNA-192-5p as potential biomarkers of ischemia-reperfusion-induced kidney injury. Exp. Biol. Med. 2017;242:657–667. doi: 10.1177/1535370216685005.
    1. Cai H., Jiang Z., Yang X., Lin J., Cai Q., Li X. Circular RNA HIPK3 contributes to hyperglycemia and insulin homeostasis by sponging miR-192-5p and upregulating transcription factor forkhead box O1. Endocr. J. 2020;67:397–408. doi: 10.1507/endocrj.EJ19-0271.
    1. Baker M.A., Wang F., Liu Y., Kriegel A.J., Geurts A.M., Usa K., Xue H., Wang D., Kong Y., Liang M. MiR-192-5p in the Kidney Protects Against the Development of Hypertension. Hypertension. 2019;73:399–406. doi: 10.1161/HYPERTENSIONAHA.118.11875.
    1. Chen J., Wang J., Li H., Wang S., Xiang X., Zhang D. p53 activates miR-192-5p to mediate vancomycin induced AKI. Sci. Rep. 2016;6:38868. doi: 10.1038/srep38868.
    1. Elton T.S., Selemon H., Elton S.M., Parinandi N.L. Regulation of the MIR155 host gene in physiological and pathological processes. Gene. 2013;532:1–12. doi: 10.1016/j.gene.2012.12.009.
    1. Pfeiffer D., Roßmanith E., Lang I., Falkenhagen D. miR-146a, miR-146b, and miR-155 increase expression of IL-6 and IL-8 and support HSP10 in an In vitro sepsis model. PLoS ONE. 2017;12:e0179850. doi: 10.1371/journal.pone.0179850.
    1. Alexander M., Hu R., Runtsch M.C., Kagele D.A., Mosbruger T.L., Tolmachova T., Seabra M.C., Round J.L., Ward D.M., O’Connell R.M. Exosome-delivered microRNAs modulate the inflammatory response to endotoxin. Nat. Commun. 2015;6:7321. doi: 10.1038/ncomms8321.
    1. Johnson B.J., Le T.T., Dobbin C.A., Banovic T., Howard C.B., Flores F.D.M.L., Vanags D., Naylor D.J., Hill G.R., Suhrbier A. Heat shock protein 10 inhibits lipopolysaccharide-induced inflammatory mediator production. J. Biol. Chem. 2005;280:4037–4047. doi: 10.1074/jbc.M411569200.
    1. Saikumar J., Hoffmann D., Kim T.M., Gonzalez V.R., Zhang Q., Goering P.L., Brown R.P., Bijol V., Park P.J., Waikar S.S., et al. Expression, circulation, and excretion profile of microRNA-21, -155, and -18a following acute kidney injury. Toxicol. Sci. 2012;129:256–267. doi: 10.1093/toxsci/kfs210.
    1. Lu C., Chen B., Chen C., Li H., Wang D., Tan Y., Weng H. CircNr1h4 regulates the pathological process of renal injury in salt-sensitive hypertensive mice by targeting miR-155-5p. J. Cell. Mol. Med. 2020;24:1700–1712. doi: 10.1111/jcmm.14863.
    1. Wang Y., Zheng Z.J., Jia Y.J., Yang Y.L., Xue Y.M. Role of p53/miR-155-5p/sirt1 loop in renal tubular injury of diabetic kidney disease. J. Transl. Med. 2018;16:146. doi: 10.1186/s12967-018-1486-7.
    1. Viñas J.L., Burger D., Zimpelmann J., Haneef R., Knoll W., Campbell P., Gutsol A., Carter A., Allan D.S., Burns K.D. Transfer of microRNA-486-5p from human endothelial colony forming cell-derived exosomes reduces ischemic kidney injury. Kidney Int. 2016;90:1238–1250. doi: 10.1016/j.kint.2016.07.015.
    1. Xu J., Li R., Workeneh B., Dong Y., Wang X., Hu Z. Transcription factor FoxO1, the dominant mediator of muscle wasting in chronic kidney disease, is inhibited by microRNA-486. Kidney Int. 2012;82:401–411. doi: 10.1038/ki.2012.84.
    1. Regmi A., Liu G., Zhong X., Hu S., Ma R., Gou L., Zafar M.I., Chen L. Evaluation of Serum microRNAs in Patients with Diabetic Kidney Disease: A Nested Case-Controlled Study and Bioinformatics Analysis. Med. Sci. Monit. 2019;25:1699–1708. doi: 10.12659/MSM.913265.
    1. Chai X., Si H., Song J., Chong Y., Wang J., Zhao G. miR-486-5p Inhibits Inflammatory Response, Matrix Degradation and Apoptosis of Nucleus Pulposus Cells through Directly Targeting FOXO1 in Intervertebral Disc Degeneration. Cell. Physiol. Biochem. 2019;52:109–118.
    1. Yuan X.P., Liu L.S., Chen C.B., Zhou J., Zheng Y.T., Wang X.P., Han M., Wang C.X. MicroRNA-423-5p facilitates hypoxia/reoxygenation-induced apoptosis in renal proximal tubular epithelial cells by targeting GSTM1 via endoplasmic reticulum stress. Oncotarget. 2017;8:82064–82077. doi: 10.18632/oncotarget.18289.
    1. Wang W., Gao J., Wang F. MiR-663a/MiR-423-5p are involved in the pathogenesis of lupus nephritis via modulating the activation of NF-κB by targeting TNIP2. Am. J. Transl. Res. 2017;9:3796–3803.
    1. Xu Y., Zhang J., Fan L., He X. miR-423-5p suppresses high-glucose-induced podocyte injury by targeting Nox4. Biochem. Biophys. Res. Commun. 2018;505:339–345. doi: 10.1016/j.bbrc.2018.09.067.
    1. Montomoli J., Donati A., Ince C. Acute Kidney Injury and Fluid Resuscitation in Septic Patients: Are We Protecting the Kidney? Nephron. 2019;143:170–173. doi: 10.1159/000501748.
    1. O’Connor M.E., Prowle J.R. Fluid Overload. Crit. Care Clin. 2015;31:803–821. doi: 10.1016/j.ccc.2015.06.013.
    1. Bellomo R., Kellum J.A., Ronco C., Wald R., Martensson J., Maiden M., Bagshaw S.M., Glassford N.J., Lankadeva Y., Vaara S.T., et al. Acute kidney injury in sepsis. Intensive Care Med. 2017;43:816–828. doi: 10.1007/s00134-017-4755-7.
    1. Gaudry S., Hajage D., Benichou N., Chaïbi K., Barbar S., Zarbock A., Lumlertgul N., Wald R., Bagshaw S.M., Srisawat N., et al. Delayed versus early initiation of renal replacement therapy for severe acute kidney injury: A systematic review and individual patient data meta-analysis of randomised clinical trials. Lancet. 2020;395:1506–1515. doi: 10.1016/S0140-6736(20)30531-6.
    1. Gaudry S., Hajage D., Schortgen F., Martin-Lefevre L., Pons B., Boulet E., Boyer A., Chevrel G., Lerolle N., Carpentier D., et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit. N. Engl. J. Med. 2016;375:122–133. doi: 10.1056/NEJMoa1603017.
    1. Karkar A., Ronco C. Prescription of CRRT: A pathway to optimize therapy. Ann. Intensive Care. 2020;10:32. doi: 10.1186/s13613-020-0648-y.
    1. Romagnoli S., Ricci Z., Ronco C. CRRT for sepsis-induced acute kidney injury. Curr. Opin. Crit. Care. 2018;24:483–492. doi: 10.1097/MCC.0000000000000544.
    1. Petejova N., Martinek A., Zahalkova J., Duricova J., Brozmannova H., Urbanek K., Grundmann M., Plasek J., Kacirova I. Vancomycin pharmacokinetics during high-volume continuous venovenous hemofiltration in critically ill septic patients. Biomed. Pap. Med. Faculty Univ. Palacky Olomouc Czech Repub. 2014;158:65–72. doi: 10.5507/bp.2012.092.
    1. Petejova N., Zahalkova J., Duricova J., Kacirova I., Brozmanova H., Urbanek K., Grundmann M., Martinek A. Gentamicin pharmacokinetics during continuous venovenous hemofiltration in critically ill septic patients. J. Chemother. 2012;24:107–112. doi: 10.1179/1120009X12Z.0000000006.

Source: PubMed

Sponsorer och medarbetare

Medicinska tillstånd

Läkemedelsinterventioner

3
Prenumerera