2022
Blood Transcriptomes of SARS-CoV-2–Infected Kidney Transplant Recipients Associated with Immune Insufficiency Proportionate to Severity
Sun Z, Zhang Z, Banu K, Al Azzi Y, Reghuvaran A, Fredericks S, Planoutene M, Hartzell S, Kim Y, Pell J, Tietjen G, Asch W, Kulkarni S, Formica R, Rana M, Maltzman JS, Zhang W, Akalin E, Heeger PS, Cravedi P, Menon MC. Blood Transcriptomes of SARS-CoV-2–Infected Kidney Transplant Recipients Associated with Immune Insufficiency Proportionate to Severity. Journal Of The American Society Of Nephrology 2022, 33: 2108-2122. PMID: 36041788, PMCID: PMC9678030, DOI: 10.1681/asn.2022010125.Peer-Reviewed Original ResearchConceptsKidney transplant recipientsImmune activation pathwaysImmunosuppressant useKTR cohortAcute illnessBlood transcriptomeAcute casesT cellsCOVID-19Most kidney transplant recipientsPost-acute COVID-19Adaptive immune system activationManagement of immunosuppressionReinstitution of immunosuppressionAcute COVID-19Serum inflammatory cytokinesCOVID-19 severity scoreCOVID-19 infectionImmune system activationUpregulation of neutrophilActivation pathwayTransplant recipientsChart reviewImmune signaturesLymphocyte countInfliximab 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 ResearchConceptsBiopsy-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
2017
Analysis of OPTN/UNOS registry suggests the number of HLA matches and not mismatches is a stronger independent predictor of kidney transplant survival
Yacoub R, Nadkarni GN, Cravedi P, He JC, Delaney VB, Kent R, Chauhan KN, Coca SG, Florman SS, Heeger PS, Murphy B, Menon MC. Analysis of OPTN/UNOS registry suggests the number of HLA matches and not mismatches is a stronger independent predictor of kidney transplant survival. Kidney International 2017, 93: 482-490. PMID: 28965746, DOI: 10.1016/j.kint.2017.07.016.Peer-Reviewed Original ResearchMeSH KeywordsDelayed Graft FunctionGraft RejectionGraft SurvivalHistocompatibilityHistocompatibility TestingHLA AntigensHumansKidney TransplantationPredictive Value of TestsProtective FactorsRegistriesRetrospective StudiesRisk FactorsTime FactorsTissue and Organ ProcurementTreatment OutcomeUnited StatesConceptsDelayed graft functionGraft survivalHLA matchingGraft functionDeceased donor kidney transplant patientsDeceased donor kidney transplant recipientsOne-year acute rejection ratesDeath-censored graft survivalOne-year acute rejectionOPTN/UNOS registryDonor kidney transplant recipientsAcute rejection ratesKidney transplant patientsKidney transplant recipientsOrgan Sharing databaseKidney transplant survivalDegree of HLAStrong independent predictorUNOS registryAcute rejectionGraft outcomeTransplant recipientsTransplant patientsHLA matchIndependent predictors
2016
Biopsy transcriptome expression profiling to identify kidney transplants at risk of chronic injury: a multicentre, prospective study
O'Connell PJ, Zhang W, Menon MC, Yi Z, Schröppel B, Gallon L, Luan Y, Rosales IA, Ge Y, Losic B, Xi C, Woytovich C, Keung KL, Wei C, Greene I, Overbey J, Bagiella E, Najafian N, Samaniego M, Djamali A, Alexander SI, Nankivell BJ, Chapman JR, Smith RN, Colvin R, Murphy B. Biopsy transcriptome expression profiling to identify kidney transplants at risk of chronic injury: a multicentre, prospective study. The Lancet 2016, 388: 983-993. PMID: 27452608, PMCID: PMC5014570, DOI: 10.1016/s0140-6736(16)30826-1.Peer-Reviewed Original ResearchConceptsChronic allograft damage indexAllograft lossKidney transplantPathological variablesChronic injuryEarly allograft lossKidney transplant recipientsRenal allograft recipientsFunction 3 monthsBaseline clinical variablesDevelopment of fibrosisAllograft recipientsNormal allograftsRenal allograftsTransplant recipientsAllograft fibrosisMulticentre studyProgressive injuryProspective studyClinical variablesIndependent cohortLower riskFibrosisPredictive valueTransplant
2014
Intronic locus determines SHROOM3 expression and potentiates renal allograft fibrosis
Menon MC, Chuang PY, Li Z, Wei C, Zhang W, Luan Y, Yi Z, Xiong H, Woytovich C, Greene I, Overbey J, Rosales I, Bagiella E, Chen R, Ma M, Li L, Ding W, Djamali A, Saminego M, O’Connell P, Gallon L, Colvin R, Schroppel B, He JC, Murphy B. Intronic locus determines SHROOM3 expression and potentiates renal allograft fibrosis. Journal Of Clinical Investigation 2014, 125: 208-221. PMID: 25437874, PMCID: PMC4382250, DOI: 10.1172/jci76902.Peer-Reviewed Original ResearchMeSH KeywordsAllograftsAnimalsBeta CateninDisease SusceptibilityEnhancer Elements, GeneticFibrosisGene ExpressionGenetic Association StudiesGenetic LociHEK293 CellsHumansIntronsKidneyKidney DiseasesKidney TransplantationMaleMiceMicrofilament ProteinsPolymorphism, Single NucleotideQuantitative Trait LociRiskSmad3 ProteinTranscription Factor 7-Like 2 ProteinTranscriptional ActivationTransforming Growth Factor beta1ConceptsChronic allograft nephropathyChronic kidney diseaseAllograft fibrosisTGF-β1Development of CANRisk allelesKidney transplant recipientsRenal allograft recipientsGlomerular filtration rateRenal allograft fibrosisTGF-β1 administrationUnilateral ureteric obstructionRenal tubular cellsTranscription factor 7Canonical TGF-β1Cell-specific knockdownAllograft injuryAllograft nephropathyAllograft recipientsTransplant recipientsProspective cohortRenal functionInterstitial fibrosisUreteric obstructionKidney disease