2019
Regulated 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 administration
2015
Comparison of amyloid deposition in human kidney biopsies as predictor of poor patient outcome
Castano E, Palmer MB, Vigneault C, Luciano R, Wong S, Moeckel G. Comparison of amyloid deposition in human kidney biopsies as predictor of poor patient outcome. BMC Nephrology 2015, 16: 64. PMID: 25924613, PMCID: PMC4424547, DOI: 10.1186/s12882-015-0046-0.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseAmyloid depositionPatient outcomesAmyloid depositsBiopsy-proven renal amyloidosisHistological localizationHigher serum creatinineInterstitial inflammatory infiltrateStage renal diseaseUrine protein levelsGlomerular amyloid depositionGlomerular amyloid depositsPoor patient outcomesGlomerular capillary loopsHuman kidney biopsiesDifferent study groupsStudent's t-testGlomerular amyloidosisOverall survivalSerum creatinineVascular amyloidosisKidney biopsyRenal diseaseInflammatory infiltrateClinical parameters
2013
NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy
Knauf F, Asplin JR, Granja I, Schmidt IM, Moeckel GW, David RJ, Flavell RA, Aronson PS. NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy. Kidney International 2013, 84: 895-901. PMID: 23739234, PMCID: PMC3772982, DOI: 10.1038/ki.2013.207.Peer-Reviewed Original ResearchConceptsProgressive renal failureRenal failureCalcium oxalate crystal depositionCrystal-associated diseasesOverproduction of oxalateWild-type miceHigh-oxalate dietNephropathy resultsOxalate nephropathyRenal histologyKidney diseaseOxalate dietInflammatory responseNALP3 expressionDietary oxalateIntestinal oxalateOxalate homeostasisSoluble oxalateNephropathyCrystal depositionMiceMultiple disordersNALP3DietInflammation
2012
Intrarenal Dopamine Inhibits Progression of Diabetic Nephropathy
Zhang MZ, Yao B, Yang S, Yang H, Wang S, Fan X, Yin H, Fogo AB, Moeckel GW, Harris RC. Intrarenal Dopamine Inhibits Progression of Diabetic Nephropathy. Diabetes 2012, 61: 2575-2584. PMID: 22688335, PMCID: PMC3447896, DOI: 10.2337/db12-0046.Peer-Reviewed Original ResearchConceptsIntrarenal dopaminergic systemRenal dopamine productionDopaminergic systemDopamine productionDiabetic nephropathyDiabetic miceWild-type diabetic miceOxidative stressDiabetic kidney injuryIntrarenal dopamine productionRenin-angiotensin systemMarkers of inflammationType 1 diabetesAromatic amino acid decarboxylaseCyclooxygenase-2 expressionKidney injuryRenal hemodynamicsRenal transplantationUnderlying pathogenesisDopamine metabolismInhibition of expressionInhibits progressionAmino acid decarboxylaseFluid reabsorptionKidney structure
2008
Fibrocystin/Polyductin Modulates Renal Tubular Formation by Regulating Polycystin-2 Expression and Function
Kim I, Fu Y, Hui K, Moeckel G, Mai W, Li C, Liang D, Zhao P, Ma J, Chen XZ, George AL, Coffey RJ, Feng ZP, Wu G. Fibrocystin/Polyductin Modulates Renal Tubular Formation by Regulating Polycystin-2 Expression and Function. Journal Of The American Society Of Nephrology 2008, 19: 455-468. PMID: 18235088, PMCID: PMC2391052, DOI: 10.1681/asn.2007070770.Peer-Reviewed Original ResearchConceptsFibrocystin/polyductinPC2 channel activityRenal cystic phenotypeGene-targeted mutationPolycystic kidney diseaseCultured renal epithelial cellsAutosomal recessive polycystic kidney diseaseHuman autosomal recessive polycystic kidney diseaseCommon molecular pathwaysEpithelial cellsRecessive polycystic kidney diseaseRenal epithelial cellsAberrant ciliogenesisKidney diseasePolycystin-2Polycystin-2 expressionPrimary ciliaCystic phenotypeSingle mutationMolecular pathwaysGenetic modifiersPhenotypic characteristicsMutationsMolecular interactionsAutosomal dominant polycystic kidney disease