2019
Hypergranulotic dyscornification: 30 cases of a striking epithelial reaction pattern
Roy SF, Ko CJ, Moeckel GW, Mcniff JM. Hypergranulotic dyscornification: 30 cases of a striking epithelial reaction pattern. Journal Of Cutaneous Pathology 2019, 46: 742-747. PMID: 31157457, DOI: 10.1111/cup.13522.Peer-Reviewed Original ResearchConceptsBenign keratosesDistinctive histopathologic findingsHistological reaction patternEpidermolytic hyperkeratosisReaction patternsBowen's diseaseRetrospective reviewMean ageProminent granular layerHistopathologic findingsEpidermoid cystKeratin immunohistochemistryClinical impressionSeborrheic keratosisPositive stainingNeck areaAbnormal keratinizationKeratohyaline granulesUnique reaction patternReproducible findingsKeratosesCytoplasmic areaGranular layerHyperkeratosisPrevious reportsDevelopment of a 2-dimensional atlas of the human kidney with imaging mass cytometry
Singh N, Avigan ZM, Kliegel JA, Shuch BM, Montgomery RR, Moeckel GW, Cantley LG. Development of a 2-dimensional atlas of the human kidney with imaging mass cytometry. JCI Insight 2019, 4: e129477. PMID: 31217358, PMCID: PMC6629112, DOI: 10.1172/jci.insight.129477.Peer-Reviewed Original ResearchConceptsCell typesIndividual cell typesCritical baseline dataRenal cell typesMass cytometryQuantitative atlasNormal human samplesHuman kidneyRelative abundanceDevelopment of therapiesHuman kidney diseaseKidney diseaseMetal-conjugated antibodiesQuantitative interrogationScarce samplesMachine-learning pipelineDiscovery purposesFuture quantitative analysisNovel abnormalityNormal human kidneySingle tissue sectionHuman samplesRenal biopsyImmune cellsCellsUrine TNF-α and IL-9 for clinical diagnosis of acute interstitial nephritis
Moledina DG, Wilson FP, Pober JS, Perazella MA, Singh N, Luciano RL, Obeid W, Lin H, Kuperman M, Moeckel GW, Kashgarian M, Cantley LG, Parikh CR. Urine TNF-α and IL-9 for clinical diagnosis of acute interstitial nephritis. JCI Insight 2019, 4: e127456. PMID: 31092735, PMCID: PMC6542610, DOI: 10.1172/jci.insight.127456.Peer-Reviewed Original ResearchConceptsAcute interstitial nephritisAcute kidney diseasePrebiopsy diagnosisKidney biopsyKidney diseaseIL-9AIN diagnosisUrine TNFInterstitial nephritisSpecific T cell subsetsAcute tubular injuryDiabetic kidney diseaseIL-9 levelsTNF-α levelsT cell subsetsAddition of biomarkersPlasma cytokinesCytokine levelsTubular injuryHighest quartileMultivariable analysisCell subsetsUrinary TNFBlood eosinophilsGlomerular diseaseUpdate on the Native Kidney Biopsy: Core Curriculum 2019
Luciano RL, Moeckel GW. Update on the Native Kidney Biopsy: Core Curriculum 2019. American Journal Of Kidney Diseases 2019, 73: 404-415. PMID: 30661724, DOI: 10.1053/j.ajkd.2018.10.011.BooksConceptsKidney biopsyKidney diseaseCore Curriculum 2019Arteriovenous fistula formationNative kidney biopsiesPercutaneous kidney biopsyKidney biopsy procedureReal-time ultrasoundGross hematuriaPerinephric hematomaFistula formationPotential complicationsLower riskBiopsyBiopsy procedureGenetic testingSpecific procedural aspectsGold standardDiseaseComplicationsSimple light microscopyPreferred methodLight microscopyTomographic imagingHematuria
2018
Reliability of deceased‐donor procurement kidney biopsy images uploaded in United Network for Organ Sharing
Mansour SG, Hall IE, Reese PP, Jia Y, Thiessen‐Philbrook H, Moeckel G, Weng FL, Revelo MP, Khalighi MA, Trivedi A, Doshi MD, Schröppel B, Parikh CR. Reliability of deceased‐donor procurement kidney biopsy images uploaded in United Network for Organ Sharing. Clinical Transplantation 2018, 32: e13441. PMID: 30387908, PMCID: PMC6317379, DOI: 10.1111/ctr.13441.Peer-Reviewed Original ResearchSemaphorin 7A in circulating regulatory T cells is increased in autosomal-dominant polycystic kidney disease and decreases with tolvaptan treatment
Lee Y, Blount KL, Dai F, Thompson S, Scher JK, Bitterman S, Droher M, Herzog EL, Moeckel G, Karihaloo A, Dahl NK. Semaphorin 7A in circulating regulatory T cells is increased in autosomal-dominant polycystic kidney disease and decreases with tolvaptan treatment. Clinical And Experimental Nephrology 2018, 22: 906-916. PMID: 29453607, DOI: 10.1007/s10157-018-1542-x.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsAutosomal dominant polycystic kidney diseaseEnd-stage renal diseaseRenal fibrosisSEMA7A expressionADPKD patientsTolvaptan treatmentPolycystic kidney diseaseKidney diseaseNumber of PBMCsExpression of SEMA7ASubsequent renal fibrosisMarkers of inflammationRegulatory T cellsADPKD kidneysBlood mononuclear cellsImmunomodulating proteinsRenal diseaseMononuclear cellsSmall kidneysKidney fibrosisLiver fibrosisRenal cystsSemaphorin 7AT cells
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 animalsMIF-2/D-DT enhances proximal tubular cell regeneration through SLPI- and ATF4-dependent mechanisms
Ochi A, Chen D, Schulte W, Leng L, Moeckel N, Piecychna M, Averdunk L, Stoppe C, Bucala R, Moeckel G. MIF-2/D-DT enhances proximal tubular cell regeneration through SLPI- and ATF4-dependent mechanisms. American Journal Of Physiology. Renal Physiology 2017, 313: f767-f780. PMID: 28539339, PMCID: PMC6148305, DOI: 10.1152/ajprenal.00683.2016.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 4Acute Kidney InjuryAnimalsAntigens, Differentiation, B-LymphocyteApoptosisAutophagyCell HypoxiaCell LineCell ProliferationCyclin D1Disease Models, AnimalEukaryotic Initiation Factor-2FemaleGenetic Predisposition to DiseaseHistocompatibility Antigens Class IIIntramolecular OxidoreductasesKidney Tubules, ProximalMacrophage Migration-Inhibitory FactorsMaleMice, Inbred C57BLMice, KnockoutPhenotypeRegenerationReperfusion InjurySecretory Leukocyte Peptidase InhibitorSignal TransductionTime FactorsTransfectionConceptsMacrophage migration inhibitory factorSecretory leukocyte proteinase inhibitorTubular cell regenerationProximal tubular cellsD-DTCell regenerationTubular cellsIschemic acute kidney injuryIschemia-reperfusion injury modelWild-type control miceMouse proximal tubular cellsAcute kidney injuryIschemia-reperfusion injuryRenal proximal tubular cellsMigration inhibitory factorIntegrated stress responseATF4-dependent mechanismCyclin D1 expressionEukaryotic initiation factorKidney injuryTubular injuryControl miceChemokine receptorsInjury modelInflammatory contextRapamycin treatment dose‐dependently improves the cystic kidney in a new ADPKD mouse model via the mTORC1 and cell‐cycle‐associated CDK1/cyclin axis
Li A, Fan S, Xu Y, Meng J, Shen X, Mao J, Zhang L, Zhang X, Moeckel G, Wu D, Wu G, Liang C. Rapamycin treatment dose‐dependently improves the cystic kidney in a new ADPKD mouse model via the mTORC1 and cell‐cycle‐associated CDK1/cyclin axis. Journal Of Cellular And Molecular Medicine 2017, 21: 1619-1635. PMID: 28244683, PMCID: PMC5543471, DOI: 10.1111/jcmm.13091.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibiotics, AntineoplasticCDC2 Protein KinaseCell CycleCyclinsDose-Response Relationship, DrugFemaleFounder EffectGene Expression RegulationHumansIntegrasesKidneyMaleMiceMice, TransgenicMicrofilament ProteinsPolycystic Kidney, Autosomal DominantPromoter Regions, GeneticSignal TransductionSirolimusTOR Serine-Threonine KinasesTRPP Cation ChannelsConceptsAutosomal dominant polycystic kidney diseaseEnd-stage renal diseaseMouse modelCyclin-dependent kinase 1Kidney/body weight ratioPreclinical trialsVivo preclinical resultsBody weight ratioCre transgenic miceHigh-dose rapamycinStandardized animal modelHuman autosomal dominant polycystic kidney diseaseRapamycin (mTOR) inhibitor rapamycinDominant polycystic kidney diseaseMonths of ageOrthologous mouse modelConditional knockout miceDose-dependent mannerPolycystic kidney diseaseAberrant epithelial cell proliferationEpithelial cell proliferationNew molecular targetsADPKD therapyRenal functionADPKD mouse model
2016
Eculizumab Therapy for Chronic Antibody‐Mediated Injury in Kidney Transplant Recipients: A Pilot Randomized Controlled Trial
Kulkarni S, Kirkiles‐Smith N, Deng YH, Formica RN, Moeckel G, Broecker V, Bow L, Tomlin R, Pober JS. Eculizumab Therapy for Chronic Antibody‐Mediated Injury in Kidney Transplant Recipients: A Pilot Randomized Controlled Trial. American Journal Of Transplantation 2016, 17: 682-691. PMID: 27501352, DOI: 10.1111/ajt.14001.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAntibodies, Monoclonal, HumanizedChronic DiseaseComplement C5Complement Inactivating AgentsEarly Intervention, EducationalFemaleFollow-Up StudiesGlomerular Filtration RateGraft RejectionGraft SurvivalHumansIsoantibodiesKidney Failure, ChronicKidney Function TestsKidney TransplantationLiving DonorsMaleMiddle AgedPilot ProjectsPrognosisRisk FactorsTissue DonorsTransplant RecipientsYoung AdultConceptsDe novo donor-specific antibodiesComplement inhibitionTreatment groupsNovo donor-specific antibodiesAntibody-Mediated InjuryC1q-positive patientsDonor-specific antibodiesKidney transplant recipientsPrimary end pointEndothelial cell injuryMo of observationEculizumab therapyEculizumab treatmentHumoral injuryTransplant recipientsKidney transplantRenal functionKidney functionChronic settingEGFR trajectoriesTreatment periodCell injuryPatientsEnd pointPercentage change
2015
Comparison of amyloid deposition in human kidney biopsies as predictor of poor patient outcome
Castano E, Palmer MB, Vigneault C, Luciano R, Wong S, Moeckel G. Comparison of amyloid deposition in human kidney biopsies as predictor of poor patient outcome. BMC Nephrology 2015, 16: 64. PMID: 25924613, PMCID: PMC4424547, DOI: 10.1186/s12882-015-0046-0.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseAmyloid depositionPatient outcomesAmyloid depositsBiopsy-proven renal amyloidosisHistological localizationHigher serum creatinineInterstitial inflammatory infiltrateStage renal diseaseUrine protein levelsGlomerular amyloid depositionGlomerular amyloid depositsPoor patient outcomesGlomerular capillary loopsHuman kidney biopsiesDifferent study groupsStudent's t-testGlomerular amyloidosisOverall survivalSerum creatinineVascular amyloidosisKidney biopsyRenal diseaseInflammatory infiltrateClinical parameters
2013
Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells
Jane-wit D, Manes TD, Yi T, Qin L, Clark P, Kirkiles-Smith NC, Abrahimi P, Devalliere J, Moeckel G, Kulkarni S, Tellides G, Pober JS. Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells. Circulation 2013, 128: 2504-2516. PMID: 24045046, PMCID: PMC3885874, DOI: 10.1161/circulationaha.113.002972.Peer-Reviewed Original ResearchConceptsCardiac allograft vasculopathyPanel reactive antibodyNuclear factor-κB signalingFactor-κB signalingAllograft vasculopathyT cellsEndothelial cellsMembrane attack complexAlloreactive T cell activationChronic antibody-mediated rejectionNoncanonical nuclear factorProinflammatory gene programAntibody-mediated rejectionDonor-specific antibodiesGraft endothelial cellsLate allograft lossAlloreactive T cellsAllogeneic endothelial cellsT cell activationAttack complexHuman T cellsAllograft lossHeart transplantationTransplantation patientsLesion pathogenesisNALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy
Knauf F, Asplin JR, Granja I, Schmidt IM, Moeckel GW, David RJ, Flavell RA, Aronson PS. NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy. Kidney International 2013, 84: 895-901. PMID: 23739234, PMCID: PMC3772982, DOI: 10.1038/ki.2013.207.Peer-Reviewed Original ResearchConceptsProgressive renal failureRenal failureCalcium oxalate crystal depositionCrystal-associated diseasesOverproduction of oxalateWild-type miceHigh-oxalate dietNephropathy resultsOxalate nephropathyRenal histologyKidney diseaseOxalate dietInflammatory responseNALP3 expressionDietary oxalateIntestinal oxalateOxalate homeostasisSoluble oxalateNephropathyCrystal depositionMiceMultiple disordersNALP3DietInflammationRecessive mutations in DGKE cause atypical hemolytic-uremic syndrome
Lemaire M, Frémeaux-Bacchi V, Schaefer F, Choi M, Tang WH, Le Quintrec M, Fakhouri F, Taque S, Nobili F, Martinez F, Ji W, Overton JD, Mane SM, Nürnberg G, Altmüller J, Thiele H, Morin D, Deschenes G, Baudouin V, Llanas B, Collard L, Majid MA, Simkova E, Nürnberg P, Rioux-Leclerc N, Moeckel GW, Gubler MC, Hwa J, Loirat C, Lifton RP. Recessive mutations in DGKE cause atypical hemolytic-uremic syndrome. Nature Genetics 2013, 45: 531-536. PMID: 23542698, PMCID: PMC3719402, DOI: 10.1038/ng.2590.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAtypical Hemolytic Uremic SyndromeChildChild, PreschoolDiacylglycerol KinaseExomeFemaleGenes, RecessiveHemolytic-Uremic SyndromeHumansImmunoenzyme TechniquesInfantMaleMolecular Sequence DataMutationRenal Insufficiency, ChronicThrombocytopeniaThrombotic Microangiopathies
2010
LATE‐ONSET OMEPRAZOLE‐ASSOCIATED ACUTE INTERSTITIAL NEPHRITIS
Ni N, Moeckel GW, Kumar C. LATE‐ONSET OMEPRAZOLE‐ASSOCIATED ACUTE INTERSTITIAL NEPHRITIS. Journal Of The American Geriatrics Society 2010, 58: 2443-2444. PMID: 21143456, DOI: 10.1111/j.1532-5415.2010.03194.x.Peer-Reviewed Original ResearchSecond Prize: A Sealed Bladder Cuff Technique During Laparoscopic Nephroureterectomy Utilizing the LigaSure™ Electrosurgical Device: Laboratory and Clinical Experience
Lambert EH, Schachter LR, Altamar HO, Tikhonenkov S, Moeckel G, Miller NL, Herrell SD. Second Prize: A Sealed Bladder Cuff Technique During Laparoscopic Nephroureterectomy Utilizing the LigaSure™ Electrosurgical Device: Laboratory and Clinical Experience. Journal Of Endourology 2010, 24: 327-332. PMID: 20078234, DOI: 10.1089/end.2009.0187.Peer-Reviewed Original ResearchConceptsLaparoscopic nephroureterectomyUrothelial tumorsPorcine modelUrothelial tissuesUpper tract urothelial tumorsBladder cuff techniqueBladder cuff excisionRadical nephrectomy specimensPostoperative day 10Transitional cell tumorsMean burst pressureBladder leakageCuff resectionCuff techniqueOpen nephroureterectomyBladder cuffCuff excisionDistal ureterCautery artifactIntraoperative cystoscopyOncological principlesNephrectomy specimensCell tumorsUreteral orificeInvasive approach
2009
Placental Insufficiency Associated with Loss of Cited1 Causes Renal Medullary Dysplasia
Sparrow DB, Boyle SC, Sams RS, Mazuruk B, Zhang L, Moeckel GW, Dunwoodie SL, de Caestecker MP. Placental Insufficiency Associated with Loss of Cited1 Causes Renal Medullary Dysplasia. Journal Of The American Society Of Nephrology 2009, 20: 777-786. PMID: 19297558, PMCID: PMC2663829, DOI: 10.1681/asn.2008050547.Peer-Reviewed Original ResearchConceptsRenal medullary dysplasiaPlacental insufficiencyTissue oxygenationLower urinary tract obstructionUrinary tract obstructionCITED1 expressionIntrauterine growth retardationTract obstructionRenal functionMedullary growthRenal dysplasiaDysplasiaGrowth retardationRenal medullaMutant miceDecreased numberInsufficiencyEarly nephrogenesisNumber of studiesMiceGenetic lossOxygenationUreteric budCircumstantial evidenceInfants
2008
NFATc1 Identifies a Population of Proximal Tubule Cell Progenitors
Langworthy M, Zhou B, de Caestecker M, Moeckel G, Baldwin HS. NFATc1 Identifies a Population of Proximal Tubule Cell Progenitors. Journal Of The American Society Of Nephrology 2008, 20: 311-321. PMID: 19118153, PMCID: PMC2637056, DOI: 10.1681/asn.2008010094.Peer-Reviewed Original ResearchConceptsProximal tubular cell injuryBALB/c miceAcute kidney injuryTubular cell injuryWild-type miceProximal tubule segmentsKidney injurySerum creatinineCalcineurin inhibitorsC miceSustained injuryNFATc1 activityPTC proliferationCell injuryProximal tubulesNFATc1 expressionSevere injuriesTubule cellsInjuryMercuric chlorideEpithelial regenerationNephron segmentsCyclosporin AMiceTubule segmentsApoptosis of the Thick Ascending Limb Results in Acute Kidney Injury
Srichai MB, Hao C, Davis L, Golovin A, Zhao M, Moeckel G, Dunn S, Bulus N, Harris RC, Zent R, Breyer MD. Apoptosis of the Thick Ascending Limb Results in Acute Kidney Injury. Journal Of The American Society Of Nephrology 2008, 19: 1538-1546. PMID: 18495962, PMCID: PMC2488270, DOI: 10.1681/asn.2007101101.Peer-Reviewed Original ResearchConceptsAcute kidney injuryKidney injuryToxin-induced acute kidney injurySevere acute kidney injuryNovel transgenic mouse modelAdministration of gancyclovirIschemia/reperfusionBlood urea nitrogenTransgenic mouse modelToxin-induced injuryThick ascending limbHerpes simplex virus 1 thymidine kinase geneCreatinine levelsNeutrophil infiltrationAcute injuryControl miceInjury resultsMouse modelTransgenic miceUrea nitrogenProximal tubulesTAL cellsAscending limbInjuryTubular segments
2005
Role of integrin α1β1 in the regulation of renal medullary osmolyte concentration
Moeckel GW, Zhang L, Chen X, Rossini M, Zent R, Pozzi A. Role of integrin α1β1 in the regulation of renal medullary osmolyte concentration. American Journal Of Physiology. Renal Physiology 2005, 290: f223-f231. PMID: 16106035, DOI: 10.1152/ajprenal.00371.2004.Peer-Reviewed Original ResearchConceptsIntegrin alpha1-null miceOsmolyte accumulationTonicity enhancer-binding proteinExtracellular matrix receptors integrinsOrganic osmolytesProtective organic osmolytesMEK inhibitor PD 98059Inositol uptakeInhibitor PD 98059Enhancer-binding proteinRenal medullary cellsTubular necrosisGene transcriptionOsmolyte transportersReceptor integrinPD 98059Altered signalingDifferent osmotic conditionsOsmolyte concentrationMammalian kidneyCell behaviorImportant mediatorERK1/2 phosphorylationOsmotic conditionsDuct cells