2024
Interleukin-16 is increased in dialysis patients but is not a cardiovascular risk factor
Brösecke F, Pfau A, Ermer T, Dein Terra Mota Ribeiro A, Rubenbauer L, Rao V, Burlein S, Genser B, Reichel M, Aronson P, Coca S, Knauf F. Interleukin-16 is increased in dialysis patients but is not a cardiovascular risk factor. Scientific Reports 2024, 14: 11323. PMID: 38760468, PMCID: PMC11101424, DOI: 10.1038/s41598-024-61808-7.Peer-Reviewed Original ResearchConceptsIL-16 levelsIL-16Dialysis patientsCardiovascular eventsConcentrations of IL-16Kidney failureUremic toxinsCardiovascular diseaseCompared to healthy individualsPlasma oxalate concentrationActivated immune cellsAssociated with cardiovascular diseaseIL-16 concentrationCytokine IL-16Cardiovascular risk factorsNo significant associationPlasma oxalateInflammatory markersImmune cellsCytokine concentrationsInterleukin-16US patientsCohort 1Cardiovascular outcomesHealthy individuals
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 strategyExcretionDominant negative mutation in oxalate transporter SLC26A6 associated with enteric hyperoxaluria and nephrolithiasis
Cornière N, Thomson RB, Thauvin S, Villoutreix BO, Karp S, Dynia DW, Burlein S, Brinkmann L, Badreddine A, Dechaume A, Derhourhi M, Durand E, Vaillant E, Froguel P, Chambrey R, Aronson PS, Bonnefond A, Eladari D. Dominant negative mutation in oxalate transporter SLC26A6 associated with enteric hyperoxaluria and nephrolithiasis. Journal Of Medical Genetics 2022, 59: 1035-1043. PMID: 35115415, PMCID: PMC9346097, DOI: 10.1136/jmedgenet-2021-108256.Peer-Reviewed Original ResearchConceptsRare heterozygous missense mutationsWild-type proteinStrong dominant-negative effectDominant negative effectDominant negative mutationMembrane surface expressionOxalate transporter SLC26A6Calcium oxalate nephrolithiasisCotransfection studiesOxalate transporterSilico analysisNegative mutationTransport activityMissense mutationsHeterozygous missense mutationEnteric hyperoxaluriaComplex multifactorial diseaseMutationsOxalate nephrolithiasisHuman populationSurface expressionCell culturesUrinary oxalate excretionMajor risk factorGenetic factors
2021
High Oxalate Concentrations Correlate with Increased Risk for Sudden Cardiac Death in Dialysis Patients
Pfau A, Ermer T, Coca S, Tio MC, Genser B, Reichel M, Finkelstein FO, März W, Wanner C, Waikar SS, Eckardt KU, Aronson P, Drechsler C, Knauf F. High Oxalate Concentrations Correlate with Increased Risk for Sudden Cardiac Death in Dialysis Patients. Journal Of The American Society Of Nephrology 2021, 32: 2375-2385. PMID: 34281958, PMCID: PMC8729829, DOI: 10.1681/asn.2020121793.Peer-Reviewed Original ResearchConceptsSudden cardiac deathCardiac deathCardiovascular eventsKidney failurePrimary composite cardiovascular end pointComposite cardiovascular end pointGerman Diabetes Dialysis StudyCox proportional hazards modelCardiovascular end pointsCohort of patientsNovel risk factorsProportional hazards modelCubic spline modelingCause mortalityChronic dialysisCardiovascular mortalityDialysis patientsStudy cohortUS patientsRisk regressionRisk factorsEuropean patientsSerum oxalate concentrationClinical significanceSeparate cohort
2020
Enteric 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
N-glycosylation critically regulates function of oxalate transporter SLC26A6
Thomson RB, Thomson CL, Aronson PS. N-glycosylation critically regulates function of oxalate transporter SLC26A6. American Journal Of Physiology - Cell Physiology 2016, 311: c866-c873. PMID: 27681177, PMCID: PMC5206297, DOI: 10.1152/ajpcell.00171.2016.Peer-Reviewed Original ResearchConceptsPlasma membraneIntegral membrane proteinsCell surface deliverySLC26A6 functionTissue-specific differencesGlycosylation mutantsMembrane proteinsN-glycosylationSurface deliveryBiotinylation studiesOxalate transporterOxalate homeostasisSecond extracellular loopExtracellular loopIntact cellsEnzymatic deglycosylation studiesTransport activityEnzymatic deglycosylationFunctional studiesDeglycosylation studiesGlycosylationPutative second extracellular loopTransport functionFunctional significanceEssential roleOxalate, 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 domain
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
Urinary Metabolic Phenotyping the slc26a6 (Chloride–Oxalate Exchanger) Null Mouse Model
Garcia-Perez I, Villaseñor A, Wijeyesekera A, Posma JM, Jiang Z, Stamler J, Aronson P, Unwin R, Barbas C, Elliott P, Nicholson J, Holmes E. Urinary Metabolic Phenotyping the slc26a6 (Chloride–Oxalate Exchanger) Null Mouse Model. Journal Of Proteome Research 2012, 11: 4425-4435. PMID: 22594923, PMCID: PMC4028149, DOI: 10.1021/pr2012544.Peer-Reviewed Original ResearchConceptsRenal stone diseaseStone diseaseNull miceUrinary metabolic signaturesBlood pressure controlWild-type miceNull mouse modelRenal stone formationRenal proximal tubulesUrinary metabolicUrinary metabolomeClear metabolic differentiationSodium homeostasisRenal stonesType miceMouse modelUrinary metabolitesOxalate balanceUrinary profilesProximal tubulesPressure controlStone formationExchanger SLC26A6Metabolic signaturesPathological processesSat1 is dispensable for active oxalate secretion in mouse duodenum
Ko N, Knauf F, Jiang Z, Markovich D, Aronson PS. Sat1 is dispensable for active oxalate secretion in mouse duodenum. American Journal Of Physiology - Cell Physiology 2012, 303: c52-c57. PMID: 22517357, PMCID: PMC3404526, DOI: 10.1152/ajpcell.00385.2011.Peer-Reviewed Original ResearchConceptsCalcium oxalate stonesMouse duodenumOxalate secretionOxalate stonesIntestinal oxalate secretionIntestinal oxalate transportSecretory fluxSAT1 expressionDisulfonic stilbene DIDSDuodenumTransporter 1SecretionMiceHyperoxalemiaBasolateral solutionHyperoxaluriaBasolateral transportersBicarbonate productionOxalate transportBasolateral membraneSAT1Apical membraneComplete removalMedium concentration
2011
Net Intestinal Transport of Oxalate Reflects Passive Absorption and SLC26A6-mediated Secretion
Knauf F, Ko N, Jiang Z, Robertson WG, Van Itallie CM, Anderson JM, Aronson PS. Net Intestinal Transport of Oxalate Reflects Passive Absorption and SLC26A6-mediated Secretion. Journal Of The American Society Of Nephrology 2011, 22: 2247-2255. PMID: 22021714, PMCID: PMC3250206, DOI: 10.1681/asn.2011040433.Peer-Reviewed Original Research
2010
Role of SLC26A6-mediated Cl⁻-oxalate exchange in renal physiology and pathophysiology.
Aronson PS. Role of SLC26A6-mediated Cl⁻-oxalate exchange in renal physiology and pathophysiology. Journal Of Nephrology 2010, 23 Suppl 16: s158-64. PMID: 21170874.Commentaries, Editorials and LettersConceptsNull miceCalcium oxalate urolithiasisProximal tubule cellsStone riskAnimal modelsOxalate urolithiasisProximal tubulesOxalate homeostasisTubule cellsApical membrane ClHyperoxaluriaRenal physiologyOxalate exchangeMiceExchange activitySubsequent studiesAnion transportersPossible mechanismHyperoxalemiaPatientsPathophysiologyUrolithiasisStriking phenotypeReabsorption
2009
Prestin's Anion Transport and Voltage-Sensing Capabilities Are Independent
Bai JP, Surguchev A, Montoya S, Aronson PS, Santos-Sacchi J, Navaratnam D. Prestin's Anion Transport and Voltage-Sensing Capabilities Are Independent. Biophysical Journal 2009, 96: 3179-3186. PMID: 19383462, PMCID: PMC2718310, DOI: 10.1016/j.bpj.2008.12.3948.Peer-Reviewed Original ResearchMeSH Keywords4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAnalysis of VarianceAnimalsAnion Transport ProteinsAntiportersCarbon RadioisotopesChloridesCHO CellsCricetinaeCricetulusElectric CapacitanceFormatesGerbillinaeIon TransportMiceMutation, MissenseOxalatesPatch-Clamp TechniquesSalicylatesSulfate TransportersConceptsClosest phylogenetic relativesTransmembrane regionSLC26 anion transporter familyMammalian outer hair cellsMembrane protein prestinPrestin's motor functionAnion transportPhylogenetic relativesAnion transporter familyTransporter familyProtein prestinChloride-binding siteGating charge movementPrestinCharge movementHair cellsOuter hair cellsResiduesMechanistic conceptsVoltage sensingTransport capabilityCellsVoltage sensorPrevious observationsUptake studies
2006
Regulation of anion exchanger Slc26a6 by protein kinase C
Hassan HA, Mentone S, Karniski LP, Rajendran VM, Aronson PS. Regulation of anion exchanger Slc26a6 by protein kinase C. American Journal Of Physiology - Cell Physiology 2006, 292: c1485-c1492. PMID: 17151144, DOI: 10.1152/ajpcell.00447.2006.Peer-Reviewed Original ResearchMeSH KeywordsAcetophenonesAnimalsAnion Transport ProteinsAntiportersBenzopyransBiological Transport, ActiveCarbazolesCell MembraneChloridesCytoplasmEnzyme ActivationFemaleFormatesIn Vitro TechniquesIndolesMaleimidesMiceOocytesOxalatesProtein Kinase C-deltaProtein TransportSulfate TransportersTetradecanoylphorbol AcetateXenopusConceptsPKC activationOxalate secretionIntestinal oxalate secretionFormate exchangeRenal proximal tubulesAnion exchanger pendrinPancreatic ductExchanger pendrinProximal tubulesSmall intestineSLC26A6 expressionNaCl reabsorptionCalcium independentSimilar extentPotential rolePKC-delta activationProtein kinase CActivationSecretionSlc26a6Immunofluorescence microscopyXenopus oocytesPMAPhysiological significanceOocyte plasma membraneEssential roles of CFEX-mediated Cl−–oxalate exchange in proximal tubule NaCl transport and prevention of urolithiasis
Aronson PS. Essential roles of CFEX-mediated Cl−–oxalate exchange in proximal tubule NaCl transport and prevention of urolithiasis. Kidney International 2006, 70: 1207-1213. PMID: 16883319, DOI: 10.1038/sj.ki.5001741.Commentaries, Editorials and LettersAnimalsAntiportersCalcium OxalateChloride-Bicarbonate AntiportersChloridesDisease Models, AnimalFormatesHomeostasisHumansHyperoxaluriaImmunohistochemistryIntestinal AbsorptionIon ExchangeKidney Tubules, ProximalMiceMice, KnockoutModels, BiologicalNephrolithiasisOocytesOxalatesSodium ChlorideSulfate TransportersXenopusRole of SLC26‐Mediated Cl−/Base Exchange in Proximal Tubule NaCl Transport
Aronson PS. Role of SLC26‐Mediated Cl−/Base Exchange in Proximal Tubule NaCl Transport. Novartis Foundation Symposia 2006, 273: 148-163. PMID: 17120766, DOI: 10.1002/0470029579.ch10.Commentaries, Editorials and Letters
2002
Specificity of Anion Exchange Mediated by Mouse Slc26a6*
Jiang Z, Grichtchenko II, Boron WF, Aronson PS. Specificity of Anion Exchange Mediated by Mouse Slc26a6*. Journal Of Biological Chemistry 2002, 277: 33963-33967. PMID: 12119287, DOI: 10.1074/jbc.m202660200.Peer-Reviewed Original ResearchConceptsProximal tubule cellsP-aminohippurateTubule cellsOxalate-sulfate exchangeTransport of oxalatePH recordingRenal tubular fluidTubular fluidVoltage-clamp measurementsBrush border membraneFormate exchangeOxalate exchangeMeasurement of uptakeClamp measurementsBorder membraneSlc26a6Two-electrode voltage clamp measurementsXenopus oocytesPresent studyHigh oxalate concentrationsApical membraneOocytesMouse orthologueCellsCFEXIon exchangers mediating NaCl transport in the renal proximal tubule
Aronson PS. Ion exchangers mediating NaCl transport in the renal proximal tubule. Cell Biochemistry And Biophysics 2002, 36: 147-153. PMID: 12139400, DOI: 10.1385/cbb:36:2-3:147.Commentaries, Editorials and LettersConceptsProximal tubulesNaCl absorptionOxalate-sulfate exchangeLoop of HenleProximal tubule cellsNaCl transportRenal proximal tubulesRecycling of formateRole of NHE3NHE3 null miceTubule cellsNull micePerfusion solutionNephron segmentsIsoform-specific antibodiesApical membraneRenal brush border vesiclesMammalian proximal tubuleBrush border vesiclesSulfate cotransportBrush border membrane vesiclesTubulesFormate exchangeNHE3Stimulation
1997
Ion exchangers mediating NaCl transport in the proximal tubule.
Aronson PS. Ion exchangers mediating NaCl transport in the proximal tubule. Wiener Klinische Wochenschrift 1997, 109: 435-40. PMID: 9261983.Commentaries, Editorials and LettersConceptsApical membraneBasolateral membraneBrush border membraneMembrane traffickingNHE3 protein expressionMembrane ion exchangerIntracellular vesiclesMammalian proximal tubuleBorder membraneDifferential regulationProximal tubule cellsInhibitor sensitivityPossible regulationFormate transportExchange activityProtein expressionCl- channelsTubule cellsMembranePolyclonal antibodiesVesiclesCellsNHE3Oxalate-sulfate exchangeRegulation
1996
Mechanisms of stimulation of proximal tubule chloride transport by formate and oxalate
Wang T, Egbert AL, Abbiati T, Aronson PS, Giebisch G. Mechanisms of stimulation of proximal tubule chloride transport by formate and oxalate. American Journal Of Physiology 1996, 271: f446-f450. PMID: 8770178, DOI: 10.1152/ajprenal.1996.271.2.f446.Peer-Reviewed Original Research