2017
A case of severe nephrotoxicity associated with long-term dietary supplement use
Koraishy FM, Moeckel GW, Geller DS. A case of severe nephrotoxicity associated with long-term dietary supplement use. Clinical Nephrology - Case Studies 2017, 5: 42-47. PMID: 28766491, PMCID: PMC5642467, DOI: 10.5414/cncs109180.BooksDietary supplement useDietary supplementsSupplement useNew-onset renal failureNon-steroidal anti-inflammatory drugsAcute interstitial nephritisCourse of prednisoneAcute kidney injuryAcute tubular necrosisNephrotic range proteinuriaAnti-inflammatory drugsCherry extractKidney injuryRenal failureSerum creatinineTubular necrosisInterstitial nephritisRenal biopsyKidney diseaseSevere nephrotoxicityCyclooxygenase inhibitorSide effectsProteinuriaDaily intakeHealth benefitsHistones 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
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 mechanismsRenalase 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
2010
Identification and Regulation of Reticulon 4B (Nogo-B) in Renal Tubular Epithelial Cells
Marin EP, Moeckel G, Al-Lamki R, Bradley J, Yan Q, Wang T, Wright PL, Yu J, Sessa WC. Identification and Regulation of Reticulon 4B (Nogo-B) in Renal Tubular Epithelial Cells. American Journal Of Pathology 2010, 177: 2765-2773. PMID: 20971739, PMCID: PMC2993268, DOI: 10.2353/ajpath.2010.100199.Peer-Reviewed Original ResearchConceptsUnilateral ureteral obstructionAcute tubular necrosisEpithelial cellsRenal tubular epithelial cellsMurine kidneyIschemia/reperfusionMeasurement of fibrosisDistal nephron segmentsRecruitment of macrophagesWild-type miceInflammatory gene expressionTubular epithelial cellsDe novo expressionHuman biopsy specimensRenal injuryTubular necrosisUreteral obstructionWT miceVascular injuryHistological damageBiopsy specimensCortical tubulesDeficient miceMacrophage recruitmentTissue injury
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-1Injury
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