2022
Effect of pulsed intravenous methylprednisolone with alternative low-dose prednisone on high-risk IgA nephropathy: a 18-month prospective clinical trial
Li Y, Fu R, Gao J, Wang L, Duan Z, Tian L, Ge H, Ma X, Zhang Y, Li K, Xu P, Tian X, Chen Z. Effect of pulsed intravenous methylprednisolone with alternative low-dose prednisone on high-risk IgA nephropathy: a 18-month prospective clinical trial. Scientific Reports 2022, 12: 255. PMID: 34996948, PMCID: PMC8742122, DOI: 10.1038/s41598-021-03691-0.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, IntravenousAdministration, OralAdultDisease ProgressionDrug TaperingDrug Therapy, CombinationFemaleGlomerulonephritis, IGAGlucocorticoidsHumansKidney Failure, ChronicMaleMethylprednisolonePrednisoneProspective StudiesProteinuriaPulse Therapy, DrugRemission InductionRisk AssessmentRisk FactorsTime FactorsTreatment OutcomeConceptsLow-dose prednisoneComplete remissionFP groupIntravenous methylprednisoloneHigh-risk IgA nephropathyOxford MEST-C scoreChinese Clinical Trial RegistryPulsed intravenous methylprednisoloneACEI/ARBClinical Trials RegistryProspective clinical trialsMEST-C scoreFavorable safety profilePercentage of CROral prednisoneTotal remissionAdult patientsNephropathy patientsPrednisone regimenCushing's syndromeMore patientsPrimary outcomeTrials RegistryClinical outcomesIgA nephropathy
2021
Distinct Roles of Type I and Type III Interferons during a Native Murine β Coronavirus Lung Infection
Sharma L, Peng X, Qing H, Hilliard BK, Kim J, Swaminathan A, Tian J, Israni-Winger K, Zhang C, Habet V, Wang L, Gupta G, Tian X, Ma Y, Shin HJ, Kim SH, Kang MJ, Ishibe S, Young LH, Kotenko S, Compton S, Wilen CB, Wang A, Dela Cruz CS. Distinct Roles of Type I and Type III Interferons during a Native Murine β Coronavirus Lung Infection. Journal Of Virology 2021, 96: e01241-21. PMID: 34705554, PMCID: PMC8791255, DOI: 10.1128/jvi.01241-21.Peer-Reviewed Original ResearchConceptsType I interferonType III interferonsI interferonIII interferonsCoronavirus infectionInterferon deficiencyViral clearanceViral loadLung infectionType IHealthy young patientsImproved host survivalHost survivalRole of interferonMurine coronavirus infectionMajor health care threatViral burdenYounger patientsEarly diseaseIntranasal routeInterferon treatmentSublethal infectionEarly treatmentLethal infectionTissue injuryAMP-Kinase mediates regulation of glomerular volume and podocyte survival
Banu K, Lin Q, Basgen JM, Planoutene M, Wei C, Reghuvaran AC, Tian X, Shi H, Garzon F, Garzia A, Chun N, Cumpelik A, Santeusanio AD, Zhang W, Das B, Salem F, LI L, Ishibe S, Cantley LG, Kaufman L, Lemley KV, Ni Z, He JC, Murphy B, Menon MC. AMP-Kinase mediates regulation of glomerular volume and podocyte survival. JCI Insight 2021, 6: e150004. PMID: 34473647, PMCID: PMC8525649, DOI: 10.1172/jci.insight.150004.Peer-Reviewed Original ResearchAdenylate KinaseAdolescentAdultAgedAlbuminuriaAnimalsCell SizeCell SurvivalChildChild, PreschoolFemaleGene Knockdown TechniquesGlomerulonephritis, MembranousGlomerulosclerosis, Focal SegmentalHumansHypertrophyInfantKidney GlomerulusMaleMiceMicrofilament ProteinsMiddle AgedNephrectomyNephrosis, LipoidNephrotic SyndromePodocytesProportional Hazards ModelsProto-Oncogene Proteins c-fynYoung Adult
2020
Inhibiting calpain 1 and 2 in cyclin G associated kinase–knockout mice mitigates podocyte injury
Tian X, Inoue K, Zhang Y, Wang Y, Sperati CJ, Pedigo CE, Zhao T, Yan M, Groener M, Moledina DG, Ebenezer K, Li W, Zhang Z, Liebermann D, Greene L, Greer P, Parikh CR, Ishibe S. Inhibiting calpain 1 and 2 in cyclin G associated kinase–knockout mice mitigates podocyte injury. JCI Insight 2020, 5: e142740. PMID: 33208557, PMCID: PMC7710277, DOI: 10.1172/jci.insight.142740.Peer-Reviewed Original ResearchConceptsCalpain-1Chronic kidney diseaseDegree of proteinuriaCalpain inhibitor IIIGlomeruli of patientsProgressive proteinuriaCalpain protease activityGlobal glomerulosclerosisGlomerular injuryKidney functionKidney diseaseKidney failureCalcium dysregulationPodocyte injuryPodocyte-specific deletionPodocyte damageG associated kinaseProtective roleCalpain activationProteinuriaGlomerulosclerosisMiceReduced expressionStriking increaseInjuryEstablishment of a novel nomogram for the clinically diagnostic prediction of minimal change disease, −a common cause of nephrotic syndrome
Yan G, Liu G, Tian X, Tian L, Wang H, Ren P, Ma X, Fu R, Chen Z. Establishment of a novel nomogram for the clinically diagnostic prediction of minimal change disease, −a common cause of nephrotic syndrome. BMC Nephrology 2020, 21: 396. PMID: 32928127, PMCID: PMC7490860, DOI: 10.1186/s12882-020-02058-3.Peer-Reviewed Original ResearchMeSH KeywordsAdultArea Under CurveBlood PressureComplement C1qComplement C3Complement C4DiastoleFemaleGlomerular Filtration RateHemoglobinsHumansImmunoglobulin EImmunoglobulin GImmunoglobulin MMaleMiddle AgedNephrosis, LipoidNephrotic SyndromeNomogramsRegression AnalysisReproducibility of ResultsSensitivity and SpecificityYoung AdultConceptsDiastolic blood pressurePrimary glomerular diseaseNephrotic syndromeAdult patientsRenal biopsyChange diseaseGlomerular diseaseBackgroundMinimal change diseaseMinimal change diseaseLASSO regression analysisRenal biopsy procedureNon-MCD groupLogistic regression modelsDiagnostic prediction modelNovel nomogramPatient demographicsBlood pressureSerum levelsOverall incidenceClinical manifestationsMCD patientsMCD diagnosisCommon causeInvasive proceduresMethodA total
2019
Podocyte histone deacetylase activity regulates murine and human glomerular diseases
Inoue K, Gan G, Ciarleglio M, Zhang Y, Tian X, Pedigo CE, Cavanaugh C, Tate J, Wang Y, Cross E, Groener M, Chai N, Wang Z, Justice A, Zhang Z, Parikh CR, Wilson FP, Ishibe S. Podocyte histone deacetylase activity regulates murine and human glomerular diseases. Journal Of Clinical Investigation 2019, 129: 1295-1313. PMID: 30776024, PMCID: PMC6391095, DOI: 10.1172/jci124030.Peer-Reviewed Original ResearchConceptsEarly growth response 1Histone deacetylase 1Proteinuric patientsKidney diseaseHDAC2 activityValproic acidVeterans Aging Cohort StudyEnd-stage kidney diseaseDegree of proteinuriaGlomerular filtration rateAging Cohort StudyInhibition of HDAC1Proteinuric kidney diseaseHuman glomerular diseasesGlomerular disease modelsConnectivity Map databaseCohort studyFiltration rateGlomerular diseaseHistone deacetylase activityProteinuric kidneysHDAC inhibitorsProteinuriaMRNA expressionGenetic ablation
2017
Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury
Zhou H, Tian X, Tufro A, Moeckel G, Ishibe S, Goodwin J. Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury. Scientific Reports 2017, 7: 9833. PMID: 28852159, PMCID: PMC5575043, DOI: 10.1038/s41598-017-10490-z.Peer-Reviewed Original ResearchConceptsKnockout miceGlucocorticoid receptorNephrotic syndromeSimilar renal functionMainstay of therapyReceptor knockout miceTreatment of proteinuriaFoot process effacementMechanism of actionImmunomodulatory therapyRenal functionGlomerular injuryProtein excretionKO miceCommon disorderNephrotoxic serumPodocyte injuryPodocyte-specific deletionMouse modelSlit diaphragm proteinsWild-type podocytesProcess effacementProteinuriaUnstimulated conditionsKnockout animals