2023
HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy
Chen M, Menon M, Wang W, Fu J, Yi Z, Sun Z, Liu J, Li Z, Mou L, Banu K, Lee S, Dai Y, Anandakrishnan N, Azeloglu E, Lee K, Zhang W, Das B, He J, Wei C. HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy. Nature Communications 2023, 14: 4297. PMID: 37463911, PMCID: PMC10354075, DOI: 10.1038/s41467-023-40086-3.Peer-Reviewed Original ResearchConceptsChronic kidney diseasePro-inflammatory polarizationBone marrow-derived macrophagesRenal inflammationKidney fibrosisMacrophage activationHematopoietic cell kinaseMacrophage pro-inflammatory activityProgressive chronic kidney diseaseIschemia-reperfusion injury modelUnilateral ureteral obstruction kidneysChronic allograft injuryReperfusion injury modelPro-inflammatory activityPro-inflammatory macrophagesHck inhibitorsMarrow-derived macrophagesSuppression of autophagyAllograft injuryUUO miceRenal fibrosisKidney diseaseDiseased kidneysMacrophage numbersInjury model
2022
Infliximab Induction Lacks Efficacy and Increases BK Virus Infection in Deceased Donor Kidney Transplant Recipients: Results of the CTOT-19 Trial
Hricik D, Armstrong B, Alhamad T, Brennan D, Bromberg J, Bunnapradist S, Chandran S, Fairchild R, Foley D, Formica R, Gibson I, Kesler K, Kim SJ, Mannon R, Menon M, Newell K, Nickerson P, Odim J, Poggio E, Sung R, Shapiro R, Tinckam K, Vincenti F, Heeger P. Infliximab Induction Lacks Efficacy and Increases BK Virus Infection in Deceased Donor Kidney Transplant Recipients: Results of the CTOT-19 Trial. Journal Of The American Society Of Nephrology 2022, 34: 145-159. PMID: 36195441, PMCID: PMC10101585, DOI: 10.1681/asn.2022040454.Peer-Reviewed Original ResearchMeSH KeywordsBK VirusGraft RejectionHumansImmunosuppressive AgentsInflammationInfliximabKidney TransplantationVirus DiseasesConceptsBiopsy-proven acute rejectionBK virus infectionIntravenous infliximabPrimary end pointTransplant recipientsKidney transplantVirus infectionDe novo donor-specific antibodiesDeceased donor kidney transplant recipientsRabbit anti-thymocyte globulin (rATG) inductionAnti-thymocyte globulin inductionCLINICAL TRIAL REGISTRY NAMEDonor kidney transplant recipientsNovo donor-specific antibodiesEnd pointPhase 2 clinical trialIFX induction therapyTRIAL REGISTRY NAMEDelayed graft functionDonor-specific antibodiesKidney transplant recipientsDeceased donor kidneysTNF-α productionPrimary transplant recipientsAcute rejection
2019
A Peripheral Blood Gene Expression Signature to Diagnose Subclinical Acute Rejection
Zhang W, Yi Z, Keung KL, Shang H, Wei C, Cravedi P, Sun Z, Xi C, Woytovich C, Farouk S, Huang W, Banu K, Gallon L, Magee CN, Najafian N, Samaniego M, Djamali A, Alexander SI, Rosales IA, Smith RN, Xiang J, Lerut E, Kuypers D, Naesens M, O'Connell PJ, Colvin R, Menon MC, Murphy B. A Peripheral Blood Gene Expression Signature to Diagnose Subclinical Acute Rejection. Journal Of The American Society Of Nephrology 2019, 30: 1481-1494. PMID: 31278196, PMCID: PMC6683710, DOI: 10.1681/asn.2018111098.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiomarkersBiopsyFemaleGene Expression ProfilingGenomicsGraft RejectionGraft SurvivalHumansImmunosuppressive AgentsInflammationKaplan-Meier EstimateKidney Failure, ChronicKidney TransplantationMaleMiddle AgedOligonucleotide Array Sequence AnalysisProspective StudiesRisk FactorsSequence Analysis, RNAConceptsSubclinical acute rejectionKidney transplant recipientsAcute cellular rejectionAcute rejectionTransplant recipientsSurveillance biopsiesACR 3Graft functionHigh riskIndependent cohortPeripheral blood gene expression signaturesClinical acute rejectionFuture graft lossOngoing acute rejectionStable graft functionBlood gene expression signaturesCellular rejectionGraft lossGraft outcomeGraft survivalBorderline changesGene expression signaturesCox analysisHistologic featuresPeripheral blood