2020
Kidney tissue hypoxia dictates T cell–mediated injury in murine lupus nephritis
Chen PM, Wilson PC, Shyer JA, Veselits M, Steach HR, Cui C, Moeckel G, Clark MR, Craft J. Kidney tissue hypoxia dictates T cell–mediated injury in murine lupus nephritis. Science Translational Medicine 2020, 12 PMID: 32269165, PMCID: PMC8055156, DOI: 10.1126/scitranslmed.aay1620.Peer-Reviewed Original ResearchConceptsHypoxia-inducible factor-1Lupus nephritisT cellsTissue hypoxiaT-cell-mediated injuryCell-mediated injuryHIF-1 blockadeKidney tissue hypoxiaSystemic lupus erythematosusHuman lupus nephritisMurine lupus nephritisRenal injuryAutoimmune injuryLupus erythematosusAutoimmune diseasesImmune cellsRenal tissueMurine modelTissue damageMore hypoxicNephritisInjuryLow oxygen tensionOxygen tensionFactor 1
2019
Telavancin-associated acute kidney injury.
Cavanaugh C, Moeckel GW, Perazella MA. Telavancin-associated acute kidney injury. Clinical Nephrology 2019, 91: 187-191. PMID: 30614441, DOI: 10.5414/cn109651.Peer-Reviewed Original ResearchConceptsAcute kidney injuryKidney injuryTubular injuryCases of AKIAcute interstitial nephritisProximal tubular injuryAcute tubular injuryHuman clinical trialsSelect infectionsInterstitial nephritisIntravenous therapyKidney biopsyKidney histopathologyHistologic changesClinical trialsHistopathologic descriptionAnimal modelsLysosomal proliferationTelavancinInjurySemi-synthetic derivativesNumerous phagolysosomesStaphylococciGram-positive bacteriaNephritisChapter 83 Adaptive Immunity and Critical Illness
Schulte W, Maerz L, Moeckel G, Bucala R. Chapter 83 Adaptive Immunity and Critical Illness. 2019, 483-487. DOI: 10.1016/b978-0-323-44942-7.00083-2.Peer-Reviewed Original ResearchAcute kidney injuryCritical illnessEnd-stage renal diseaseChronic kidney diseaseChallenging clinical conditionIschemia-reperfusion injuryComplex disease processAdaptive immune systemAKI pathophysiologyKidney injuryHospitalized patientsRenal diseaseKidney diseaseInflammatory processCommon causeClinical conditionsAdaptive immunityLong-term consequencesDisease processImmune systemSubsequent treatmentInjuryIllnessDiseaseCurrent knowledge
2015
Essential Role of X-Box Binding Protein-1 during Endoplasmic Reticulum Stress in Podocytes
Hassan H, Tian X, Inoue K, Chai N, Liu C, Soda K, Moeckel G, Tufro A, Lee AH, Somlo S, Fedeles S, Ishibe S. Essential Role of X-Box Binding Protein-1 during Endoplasmic Reticulum Stress in Podocytes. Journal Of The American Society Of Nephrology 2015, 27: 1055-1065. PMID: 26303067, PMCID: PMC4814187, DOI: 10.1681/asn.2015020191.Peer-Reviewed Original ResearchConceptsX-box binding protein 1Endoplasmic reticulum stress responseEndoplasmic reticulum stressGlomerular filtration barrierPodocyte injuryReticulum stress responseBinding protein 1Reticulum stressProtein 1Filtration barrierFoot process effacementProgressive albuminuriaMouse modelProcess effacementUnfolded protein response pathwayEpithelial cellsNormal glomerular filtration barrierProtein response pathwayEndoplasmic reticulumPodocytesGenetic inactivationXBP1 pathwayInjuryJNK pathwayStress response
2014
Eculizumab Therapy for Chronic Antibody-Mediated Injury in Kidney Transplantation: An Interim Assessment.
Kulkarni S, Nancy K, Formica R, Moeckel G, Pober J. Eculizumab Therapy for Chronic Antibody-Mediated Injury in Kidney Transplantation: An Interim Assessment. Transplantation 2014, 98: 79. DOI: 10.1097/00007890-201407151-00247.Peer-Reviewed Original ResearchPodocyte-associated talin1 is critical for glomerular filtration barrier maintenance
Tian X, Kim JJ, Monkley SM, Gotoh N, Nandez R, Soda K, Inoue K, Balkin DM, Hassan H, Son SH, Lee Y, Moeckel G, Calderwood DA, Holzman LB, Critchley DR, Zent R, Reiser J, Ishibe S. Podocyte-associated talin1 is critical for glomerular filtration barrier maintenance. Journal Of Clinical Investigation 2014, 124: 1098-1113. PMID: 24531545, PMCID: PMC3934159, DOI: 10.1172/jci69778.Peer-Reviewed Original ResearchConceptsNephrotic syndromeFoot process effacementLoss of talin1Glomerular filtration barrierGlomerular injuryMurine modelProcess effacementKidney's glomerular filtration barrierFiltration barrierGlomerular basement membraneSevere proteinuriaKidney failurePharmacologic inhibitionSyndromeBarrier maintenanceCalpain activityIntegrin activationEpithelial cellsPodocytesModest reductionΒ1 integrin activationBasement membranePathogenesisInjuryCytoskeletal protein talin1Renalase Prevents AKI Independent of Amine Oxidase Activity
Wang L, Velazquez H, Moeckel G, Chang J, Ham A, Lee HT, Safirstein R, Desir GV. Renalase Prevents AKI Independent of Amine Oxidase Activity. Journal Of The American Society Of Nephrology 2014, 25: 1226-1235. PMID: 24511138, PMCID: PMC4033373, DOI: 10.1681/asn.2013060665.Peer-Reviewed Original ResearchConceptsIschemic injuryCatecholamine levelsRecombinant renalaseAmine oxidase activityHuman proximal tubular cellsCisplatin-induced AKITreatment of AKIWild-type miceHK-2 cellsProximal tubular cellsOxidase activityKidney injuryRenal injuryC-Jun N-terminal kinaseExtracellular signal-regulated kinaseP38 mitogen-activated protein kinaseToxic injuryRenalase proteinTubular cellsSignal-regulated kinaseIntracellular signaling cascadesRenalaseInjuryMitogen-activated protein kinaseN-terminal kinase
2013
Met Activation Is Required for Early Cytoprotection after Ischemic Kidney Injury
Mason S, Hader C, Marlier A, Moeckel G, Cantley LG. Met Activation Is Required for Early Cytoprotection after Ischemic Kidney Injury. Journal Of The American Society Of Nephrology 2013, 25: 329-337. PMID: 24136921, PMCID: PMC3904569, DOI: 10.1681/asn.2013050473.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnimalsApoptosisBcl-Associated Death ProteinGene Knockdown TechniquesKidneyKidney Tubules, ProximalMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutOrgan SpecificityPhosphatidylinositol 3-KinasesPhosphorylationProtein Processing, Post-TranslationalProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine KinasesReperfusion InjuryRibosomal Protein S6 Kinases, 70-kDaSignal TransductionConceptsIschemia/reperfusionKidney injuryIschemic injuryProximal tubulesInitial tubular injuryMET receptor expressionProximal tubule responseTubular cell survivalIschemic kidney injuryProximal tubule epithelial cellsRenal proximal tubule epithelial cellsTubular cell proliferationTubular cell apoptosisPI3K/Akt activationProapoptotic factor BadTubule epithelial cellsCell survivalTubule responseSerum creatinineTubular injuryKidney repairLiver abnormalitiesReceptor expressionInjuryMET activationWarfarin-related nephropathy in a patient with mild IgA nephropathy on dabigatran and aspirin
Moeckel GW, Luciano RL, Brewster UC. Warfarin-related nephropathy in a patient with mild IgA nephropathy on dabigatran and aspirin. Clinical Kidney Journal 2013, 6: 507-509. PMID: 26120444, PMCID: PMC4438392, DOI: 10.1093/ckj/sft076.Peer-Reviewed Case Reports and Technical NotesAcute kidney injuryTubular injuryIgA nephropathyMild IgA nephropathyAcute tubular injuryLong-term anticoagulationDirect thrombin inhibitorKidney injurySevere hematuriaRenal biopsyGlomerular pathologyDabigatranPatientsThrombin inhibitorsNephropathyInjuryWarfarinAnticoagulationHematuriaAspirinBiopsyPathologyAcute kidney injury in a patient with sarcoidosis: hypercalciuria and hypercalcemia leading to calcium phosphate deposition.
Manjunath V, Moeckel G, Dahl NK. Acute kidney injury in a patient with sarcoidosis: hypercalciuria and hypercalcemia leading to calcium phosphate deposition. Clinical Nephrology 2013, 80: 151-5. PMID: 23845267, DOI: 10.5414/cn107258.Peer-Reviewed Original ResearchConceptsAcute kidney injuryAcute tubular necrosisKidney injuryOH vitamin D levelsVitamin D levelsCalcium oxalate nephrolithiasisRenal functionTubular necrosisKidney biopsyKidney functionCalcium phosphate depositionD levelsGiant cell formationOxalate nephrolithiasisSarcoidosisRandall's plaqueHypercalcemiaHypercalciuriaPatientsInjuryPhosphate depositionPlaquesCell formationCalcium phosphate crystalsDifferent mechanismsBabesiosis-Induced Acute Kidney Injury With Prominent Urinary Macrophages
Luciano RL, Moeckel G, Palmer M, Perazella MA. Babesiosis-Induced Acute Kidney Injury With Prominent Urinary Macrophages. American Journal Of Kidney Diseases 2013, 62: 801-805. PMID: 23643302, DOI: 10.1053/j.ajkd.2013.02.376.Peer-Reviewed Case Reports and Technical NotesConceptsAcute kidney injuryAcute tubular injuryKidney injuryTubular injuryDialysis-requiring acute kidney injuryAcute interstitial nephritisMultiorgan system failureSubsequent kidney biopsySevere symptomatic diseaseUrinary macrophagesUrinary findingsInterstitial nephritisKidney biopsySymptomatic diseaseMassive hemolysisSevere babesiosisVolume depletionCommon causeProfound hemolysisErythrocyte fragmentsUrine sedimentInjuryLarge macrophagesPigment toxicityUnique findingRenalase protects against cisplatin acute kidney injury in mice
Desir G, Wang L, Velazquez H, Moeckel G, Safirstein R. Renalase protects against cisplatin acute kidney injury in mice. The FASEB Journal 2013, 27: 910.7-910.7. DOI: 10.1096/fasebj.27.1_supplement.910.7.Peer-Reviewed Original ResearchCisplatin acute kidney injuryAcute kidney injuryRenalase expressionKidney injuryCisplatin-induced acute kidney injuryIschemic acute kidney injuryRenal injury scoreUseful therapeutic optionHK-2 cellsImportant clinical syndromeRenalase deficiencyTubular necrosisPro-survival signalsTherapeutic optionsClinical syndromeInjury scorePlasma creatinineKO miceEffective therapyRenalaseBCL2 expressionMarked reductionProtective actionCaspase-3Injury
2011
Podocyte COX-2 Exacerbates Diabetic Nephropathy by Increasing Podocyte (Pro)renin Receptor Expression
Cheng H, Fan X, Moeckel GW, Harris RC. Podocyte COX-2 Exacerbates Diabetic Nephropathy by Increasing Podocyte (Pro)renin Receptor Expression. Journal Of The American Society Of Nephrology 2011, 22: 1240-1251. PMID: 21737546, PMCID: PMC3137572, DOI: 10.1681/asn.2010111149.Peer-Reviewed Original ResearchConceptsCOX-2 transgenic miceDiabetic nephropathyFoot process effacementCOX-2Transgenic miceGlomerular injuryReceptor expressionHigh glucoseRenin-angiotensin systemMesangial matrix expansionCOX-2 inhibitionWild-type miceCOX-2 inhibitorsCyclooxygenase-2 expressionGlomerular basement membraneStreptozotocin modelProgressive albuminuriaSegmental thickeningMesangial expansionDiabetic mellitusCell injuryAnimal modelsInjuryIncreased expressionNephropathy
2010
Nephrotoxicity From Chemotherapeutic Agents: Clinical Manifestations, Pathobiology, and Prevention/Therapy
Perazella MA, Moeckel GW. Nephrotoxicity From Chemotherapeutic Agents: Clinical Manifestations, Pathobiology, and Prevention/Therapy. Seminars In Nephrology 2010, 30: 570-581. PMID: 21146122, DOI: 10.1016/j.semnephrol.2010.09.005.Peer-Reviewed Original ResearchConceptsKidney lesionsChemotherapeutic agentsKidney injuryNephrotoxic chemotherapeutic agentsAcute kidney injuryChronic kidney injuryHost risk factorsDrug-induced nephrotoxicityPrevention/therapyGlomerular injuryClinical manifestationsRisk factorsRenal handlingNephrotoxicityVexing complicationInjuryLesionsDrugsInnate toxicityAgentsMost casesProteinuriaMedicationsComplicationsDysfunctionTGF-β Receptor Deletion in the Renal Collecting System Exacerbates Fibrosis
Gewin L, Bulus N, Mernaugh G, Moeckel G, Harris RC, Moses HL, Pozzi A, Zent R. TGF-β Receptor Deletion in the Renal Collecting System Exacerbates Fibrosis. Journal Of The American Society Of Nephrology 2010, 21: 1334-1343. PMID: 20576806, PMCID: PMC2938601, DOI: 10.1681/asn.2010020147.Peer-Reviewed Original ResearchConceptsRenal collecting systemTGF-beta signalingRenal fibrosisReceptor deletionCollecting systemTGF-beta type II receptorUnilateral ureteral obstructionReceptor-mediated functionsRenal interstitial fibroblastsTGF-beta activationType II receptorParadoxic increaseUreteral obstructionII receptorsInterstitial fibroblastsInterstitial cellsFibrosisDuct cellsCollagen synthesisUreteric bud developmentInjuryMiceMatrix productionEnhanced levelsSignaling
2009
Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction
Ma H, Saenko M, Opuko A, Togawa A, Soda K, Marlier A, Moeckel GW, Cantley LG, Ishibe S. Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction. Kidney International 2009, 76: 868-876. PMID: 19675527, DOI: 10.1038/ki.2009.304.Peer-Reviewed Original ResearchConceptsUreteral obstructionFibrotic responseKnockout miceMet receptorAcute tubular necrosisPlasminogen activator inhibitor-1Unilateral ureteral obstructionTubular cell proliferationActivator inhibitor-1Conditional knockout miceHepatocyte growth factorKidney injuryRenal injuryTubular necrosisFunctional recoveryInterstitial fibrosisCre miceRenal repairNephron injuryControl littermatesObstructionGrowth factorMiceInhibitor-1InjuryDistinct Roles for Basal and Induced COX-2 in Podocyte Injury
Cheng H, Fan X, Guan Y, Moeckel GW, Zent R, Harris RC. Distinct Roles for Basal and Induced COX-2 in Podocyte Injury. Journal Of The American Society Of Nephrology 2009, 20: 1953-1962. PMID: 19643929, PMCID: PMC2736764, DOI: 10.1681/asn.2009010039.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminuriaAnimalsAntibiotics, AntineoplasticApoptosisCell AdhesionCell Line, TransformedCell SurvivalCyclooxygenase 2DinoprostoneDoxorubicinGlomerulonephritisMaleMiceMice, Inbred StrainsMice, TransgenicPodocytesPuromycinReceptors, Prostaglandin EReceptors, ThromboxaneRNA, MessengerThromboxanesConceptsCyclooxygenase-2Thromboxane receptorCOX-2 knockout miceSelective deletionCOX-2 deletionInduced COX-2Receptor subtype 4COX-2 metabolitesFoot process effacementGlomerular injuryPodocyte injuryProstanoid receptorsAttenuated albuminuriaWild-type podocytesSubtype 4Transgenic miceProcess effacementTP antagonistPodocyte survivalInjuryMore prostaglandinsGenetic deletionMicePodocytesGreater expression
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
2004
Lack of Integrin α1β1 Leads to Severe Glomerulosclerosis after Glomerular Injury
Chen X, Moeckel G, Morrow JD, Cosgrove D, Harris RC, Fogo AB, Zent R, Pozzi A. Lack of Integrin α1β1 Leads to Severe Glomerulosclerosis after Glomerular Injury. American Journal Of Pathology 2004, 165: 617-630. PMID: 15277235, PMCID: PMC1618576, DOI: 10.1016/s0002-9440(10)63326-3.Peer-Reviewed Original ResearchConceptsSevere glomerulosclerosisGlomerular injuryIntegrin alpha1-null miceSeverity of fibrosisCollagen IV accumulationWild-type miceHost genetic susceptibilityMetabolism of collagenReactive oxygen species productionFibrotic lesionsIntegrin alpha1beta1Oxygen species productionAdriamycin treatmentMesangial cellsMatrix accumulationGenetic susceptibilityInjuryGlomerulosclerosisFibrosisCell proliferationROS productionSpecies productionROS synthesisIntegrin α1β1Mice