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 benefits
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
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