2023
APOBEC-1 deletion enhances cisplatin-induced acute kidney injury
Guo X, Blanc V, Davidson N, Velazquez H, Chen T, Moledina D, Moeckel G, Safirstein R, Desir G. APOBEC-1 deletion enhances cisplatin-induced acute kidney injury. Scientific Reports 2023, 13: 22255. PMID: 38097707, PMCID: PMC10721635, DOI: 10.1038/s41598-023-49575-3.Peer-Reviewed Original Research
2020
Polycystin 2 is increased in disease to protect against stress-induced cell death
Brill AL, Fischer TT, Walters JM, Marlier A, Sewanan LR, Wilson PC, Johnson EK, Moeckel G, Cantley LG, Campbell SG, Nerbonne JM, Chung HJ, Robert ME, Ehrlich BE. Polycystin 2 is increased in disease to protect against stress-induced cell death. Scientific Reports 2020, 10: 386. PMID: 31941974, PMCID: PMC6962458, DOI: 10.1038/s41598-019-57286-x.Peer-Reviewed Original ResearchConceptsPolycystin-2General cellular homeostasisCell deathStress-induced cell deathPathological cell deathAutosomal dominant polycystic kidney diseaseEndoplasmic reticulum membraneCellular homeostasisCellular stressPrimary ciliaUbiquitous expressionExpression changesCell stressReticulum membraneTransient receptor potential cation channelHuman diseasesMultiple tissuesEndogenous roleDominant polycystic kidney diseaseTissue typesCation channelsPolycystic kidney diseaseDifferent pathological statesMultiple diseasesKidney disease
2019
Urine 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 diseaseRegulated necrosis and failed repair in cisplatin-induced chronic kidney disease
Landau SI, Guo X, Velazquez H, Torres R, Olson E, Garcia-Milian R, Moeckel GW, Desir GV, Safirstein R. Regulated necrosis and failed repair in cisplatin-induced chronic kidney disease. Kidney International 2019, 95: 797-814. PMID: 30904067, PMCID: PMC6543531, DOI: 10.1016/j.kint.2018.11.042.Peer-Reviewed Original ResearchConceptsChronic kidney diseaseKidney diseaseKidney injuryCisplatin-induced chronic kidney diseaseCisplatin-induced acute kidney injuryToll-like receptor 2Regulated necrosis pathwaysReversible kidney injuryAcute kidney injuryChronic kidney injuryProximal tubular damageKidney injury markersDoses of cisplatinEvidence of fibrosisMechanisms of progressionEffective chemotherapeutic agentWestern blot analysisFirst doseInjury markersIntraperitoneal cisplatinSignificant nephrotoxicityTubular damageKidney functionSecond doseCisplatin administrationTelavancin-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 bacteriaNephritis
2018
The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery
Stoppe C, Averdunk L, Goetzenich A, Soppert J, Marlier A, Kraemer S, Vieten J, Coburn M, Kowark A, Kim BS, Marx G, Rex S, Ochi A, Leng L, Moeckel G, Linkermann A, El Bounkari O, Zarbock A, Bernhagen J, Djudjaj S, Bucala R, Boor P. The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery. Science Translational Medicine 2018, 10 PMID: 29769287, DOI: 10.1126/scitranslmed.aan4886.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnimalsAntigens, Differentiation, B-LymphocyteAntioxidantsCardiac Surgical ProceduresCell DeathHistocompatibility Antigens Class IIHumansIncidenceInflammationKidneyLipid PeroxidationLipocalin-2Macrophage Migration-Inhibitory FactorsMice, Inbred C57BLOxidative StressProtective AgentsProtein DomainsRecombinant ProteinsReperfusion InjuryRhabdomyolysisConceptsMacrophage migration inhibitory factorAcute kidney injuryRecombinant macrophage migration inhibitory factorIschemia-reperfusion injuryCardiac surgeryMigration inhibitory factorTubular epithelial cellsKidney injuryHigher macrophage migration inhibitory factorIncidence of AKIPathogenesis of AKIUrinary Macrophage Migration Inhibitory FactorExperimental acute kidney injuryExperimental ischemia-reperfusion injuryInhibitory factorMyocardial ischemia-reperfusion injuryOxidative stressMIF serum concentrationsCardiac surgery patientsRenal tubular epithelial cellsConventional cardiac surgeryEpithelial cellsHours of reperfusionSetting of hypoxiaTubular cell injuryGranulomatosis With Polyangiitis in a Young Adult With Down Syndrome
Mensah KA, Pascha V, Moeckel G, Danve A. Granulomatosis With Polyangiitis in a Young Adult With Down Syndrome. JCR Journal Of Clinical Rheumatology 2018, 24: 153-156. PMID: 29200025, DOI: 10.1097/rhu.0000000000000633.Peer-Reviewed Original ResearchAcute Kidney InjuryAdultAntibodies, Antineutrophil CytoplasmicBiopsyBlood TransfusionDiagnosis, DifferentialDown SyndromeGlucocorticoidsGranulomatosis with PolyangiitisHemoptysisHumansImmunoglobulins, IntravenousImmunologic FactorsKidneyMalePatient Care ManagementPatient SelectionRespiration, ArtificialRespiratory InsufficiencyRituximabTomography, X-Ray ComputedTreatment OutcomePathologic Perspectives on Acute Tubular Injury Assessment in the Kidney Biopsy
Moeckel GW. Pathologic Perspectives on Acute Tubular Injury Assessment in the Kidney Biopsy. Seminars In Nephrology 2018, 38: 21-30. PMID: 29291758, DOI: 10.1016/j.semnephrol.2017.09.003.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryApoptosisBiopsyEndoplasmic Reticulum StressHumansKidneyKidney TubulesOrganellesConceptsAcute tubular injuryKidney biopsy analysisRenal pathology laboratoryTissue injury markersClinical time courseCell injury pathwaysTime courseNephrologists' managementInjury markersTubular injuryTubular lesionsKidney biopsyPathophysiological mechanismsTreatment modalitiesPatient managementDrug choiceEtiologic mechanismsInjury pathwaysToxic injuryPathologic perspectiveToxic etiologyBiopsy samplesClinical practiceBiopsy analysisPathology practice
2017
MIF-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 contextHistones and Neutrophil Extracellular Traps Enhance Tubular Necrosis and Remote Organ Injury in Ischemic AKI
Nakazawa D, Kumar SV, Marschner J, Desai J, Holderied A, Rath L, Kraft F, Lei Y, Fukasawa Y, Moeckel GW, Angelotti ML, Liapis H, Anders HJ. Histones and Neutrophil Extracellular Traps Enhance Tubular Necrosis and Remote Organ Injury in Ischemic AKI. Journal Of The American Society Of Nephrology 2017, 28: 1753-1768. PMID: 28073931, PMCID: PMC5461800, DOI: 10.1681/asn.2016080925.Peer-Reviewed Original ResearchConceptsNeutrophil extracellular trap formationExtracellular trap formationNeutrophil extracellular trapsTubular necrosisExtracellular trapsCell necrosisTubular epithelial cell deathTubular epithelial cell necrosisRemote organ dysfunctionRemote organ injuryRemote organ damageRenal ischemic injuryTubular cell necrosisIschemia-reperfusion injuryRemote tissue injuryAdditive protective effectEpithelial cell necrosisTUNEL-positive cellsEpithelial cell deathNovel molecular targetsTrap formationIschemic AKISevere AKIKidney injuryMultiorgan dysfunction
2014
GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury
Huen SC, Huynh L, Marlier A, Lee Y, Moeckel GW, Cantley LG. GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2014, 26: 1334-1345. PMID: 25388222, PMCID: PMC4446881, DOI: 10.1681/asn.2014060612.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnalysis of VarianceAnimalsBlotting, WesternCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorImmunohistochemistryKidney Tubules, ProximalMacrophage ActivationMaleMiceMice, Inbred C57BLMultivariate AnalysisPhenotypeRandom AllocationReal-Time Polymerase Chain ReactionReperfusion InjurySignal TransductionUp-RegulationConceptsIschemia/reperfusion injuryMacrophage alternative activationBone marrow-derived macrophagesAlternative activationMarrow-derived macrophagesTubular cellsGM-CSFReperfusion injuryReparative phenotypeTubular proliferationKidney ischemia/reperfusion injuryRenal ischemia/reperfusion injuryMouse proximal tubule cellsInitial kidney damageRepair phaseProximal tubule cellsTubular factorsIschemic injuryKidney damageProinflammatory macrophagesRenal repairMacrophage activationTubule cellsPharmacologic inhibitionMacrophagesBile Acid Nephropathy in a Bodybuilder Abusing an Anabolic Androgenic Steroid
Luciano RL, Castano E, Moeckel G, Perazella MA. Bile Acid Nephropathy in a Bodybuilder Abusing an Anabolic Androgenic Steroid. American Journal Of Kidney Diseases 2014, 64: 473-476. PMID: 24953892, DOI: 10.1053/j.ajkd.2014.05.010.Peer-Reviewed Case Reports and Technical NotesConceptsAcute kidney injurySevere cholestatic liver diseaseCholestatic liver diseaseLiver diseaseAcute tubular injury/necrosisCases of AKIEnd-stage liver diseaseBile acid injurySevere obstructive jaundiceAcute tubular injuryAnabolic androgenic steroidsAnabolic-androgenic steroid useCholemic nephrosisHepatorenal syndromeKidney injuryTubular injuryObstructive jaundiceHemodynamic changesTubular toxicitySteroid useAcid injuryHepatic diseaseTubular cellsHeterogeneous lesionsNephropathyRenalase 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 activationAcute 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 ResearchMeSH KeywordsAcute Kidney InjuryAdultCalcium PhosphatesHumansHypercalcemiaHypercalciuriaMaleSarcoidosisConceptsAcute 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 findingRecessive 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
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 casesProteinuriaMedicationsComplicationsDysfunction
2008
Apoptosis 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
A woman with chronic hepatitis C infection and nephrotic syndrome who developed multiple renal lesions after interferon alfa therapy
Fisher ME, Rossini M, Simmons E, Harris RC, Moeckel G, Zent R. A woman with chronic hepatitis C infection and nephrotic syndrome who developed multiple renal lesions after interferon alfa therapy. American Journal Of Kidney Diseases 2004, 44: 567-573. PMID: 15332232, DOI: 10.1053/j.ajkd.2004.04.051.Peer-Reviewed Original Research