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 animalsRapamycin 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
2013
Acute 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 mechanisms
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