2022
Oxalate homeostasis
Ermer T, Nazzal L, Tio M, Waikar S, Aronson P, Knauf F. Oxalate homeostasis. Nature Reviews Nephrology 2022, 19: 123-138. PMID: 36329260, PMCID: PMC10278040, DOI: 10.1038/s41581-022-00643-3.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsKidney diseaseOxalate homeostasisAnti-inflammatory medicationsChronic kidney diseaseKidney replacement therapySudden cardiac deathProgressive kidney diseaseOutlook of patientsOxalate nephropathyCardiovascular complicationsSystemic inflammationCardiac deathReplacement therapySecondary hyperoxaluriaKidney failureElevated plasmaConsequent impairmentNovel therapeuticsPatientsDiseaseEffective elimination strategiesEndogenous sourcesHomeostasisElimination strategyExcretion
2020
Assessment of Plasma Oxalate Concentration in Patients With CKD
Pfau A, Wytopil M, Chauhan K, Reichel M, Coca SG, Aronson PS, Eckardt KU, Knauf F. Assessment of Plasma Oxalate Concentration in Patients With CKD. Kidney International Reports 2020, 5: 2013-2020. PMID: 33163722, PMCID: PMC7609998, DOI: 10.1016/j.ekir.2020.08.029.Peer-Reviewed Original ResearchChronic kidney diseasePlasma oxalate concentrationGerman Chronic Kidney Disease (GCKD) studyChronic Kidney Disease studyObservational cohort studyGlomerular filtration rateLarge patient cohortKidney Disease studyKidney stone diseaseCKD progressionMedian eGFROngoing multicenterCohort studyKidney diseasePatient cohortPresent studyFiltration rateClinical trialsStone diseaseLarge cohortOxalate homeostasisPatientsDisease StudyPlasma samplesMaintenance of samplesEnteric Oxalate Secretion Mediated by Slc26a6 Defends against Hyperoxalemia in Murine Models of Chronic Kidney Disease
Neumeier LI, Thomson RB, Reichel M, Eckardt KU, Aronson PS, Knauf F. Enteric Oxalate Secretion Mediated by Slc26a6 Defends against Hyperoxalemia in Murine Models of Chronic Kidney Disease. Journal Of The American Society Of Nephrology 2020, 31: 1987-1995. PMID: 32660969, PMCID: PMC7461683, DOI: 10.1681/asn.2020010105.Peer-Reviewed Original ResearchConceptsEnteric oxalate secretionPlasma oxalate concentrationOxalate secretionModel of CKDChronic kidney diseaseIntestine of miceWild-type miceHealthy kidney functionOxalate clearanceWestern blot analysisKidney injuryKidney functionOxalate excretionWeekly injectionsKidney diseaseCKD modelExtrarenal clearanceOxalate transporter SLC26A6CKDMurine modelSignificant elevationOxalate homeostasisTransporter expressionMiceProtein expression
2016
Oxalate, inflammasome, and progression of kidney disease
Ermer T, Eckardt KU, Aronson PS, Knauf F. Oxalate, inflammasome, and progression of kidney disease. Current Opinion In Nephrology & Hypertension 2016, 25: 363-371. PMID: 27191349, PMCID: PMC4891250, DOI: 10.1097/mnh.0000000000000229.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsChronic kidney diseaseProgressive renal failureRenal inflammationRenal failurePlasma oxalateKidney diseaseInflammasome activationElevated plasma oxalate levelsNOD-like receptor familyProgressive renal damageGlomerular filtration rateMore rapid progressionWarrants clinical trialsPlasma oxalate levelsRenal damageEnteric hyperoxaluriaMacrophage infiltrationIL-1βFiltration rateClinical trialsRapid progressionInflammasome proteinsMice protectsUrinary oxalatePyrin domainOxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice
Mulay SR, Eberhard JN, Pfann V, Marschner JA, Darisipudi MN, Daniel C, Romoli S, Desai J, Grigorescu M, Kumar SV, Rathkolb B, Wolf E, Hrabě de Angelis M, Bäuerle T, Dietel B, Wagner CA, Amann K, Eckardt KU, Aronson PS, Anders HJ, Knauf F. Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice. American Journal Of Physiology. Renal Physiology 2016, 310: f785-f795. PMID: 26764204, PMCID: PMC5504458, DOI: 10.1152/ajprenal.00488.2015.Peer-Reviewed Original ResearchConceptsC57BL/6 miceChronic kidney disease researchOxalate-rich dietChronic kidney diseaseFemale C57BL/6 miceArterial hypertensionCardiovascular complicationsKidney disease researchAtubular glomeruliInterstitial inflammationRenal histologyTubular damageKidney diseaseCardiac fibrosisMetabolic acidosisNormochromic anemiaTissue involvementHistological changesHuman CKDCKDExperimental animalsComplicationsInducible modelControl dietFibrosis
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