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
2023
SLC26A1 is a major determinant of sulfate homeostasis in humans
Pfau A, López-Cayuqueo K, Scherer N, Wuttke M, Wernstedt A, Fassrainer D, Smith D, van de Kamp J, Ziegeler K, Eckardt K, Luft F, Aronson P, Köttgen A, Jentsch T, Knauf F. SLC26A1 is a major determinant of sulfate homeostasis in humans. Journal Of Clinical Investigation 2023, 133: e161849. PMID: 36719378, PMCID: PMC9888379, DOI: 10.1172/jci161849.Peer-Reviewed Original ResearchConceptsSulfate homeostasisIntervertebral disc disordersWhole-exome sequencingMajor determinantBack painPatient presentingMusculoskeletal healthDisc disordersPlasma sulfateSulfate reabsorptionFunctional expression assaysCartilage healthHomozygous mutationPotential targetPopulation studiesNumerous physiological processesRecent evidenceExome analysisHomeostasisHyposulfatemiaExpression assaysPivotal roleClinical geneticsAdditional variantsHumans
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
Gerhard Giebisch and the Gift of Mentorship.
Aronson PS. Gerhard Giebisch and the Gift of Mentorship. Kidney360 2020, 1: 977-981. PMID: 35369559, PMCID: PMC8815600, DOI: 10.34067/kid.0004402020.Commentaries, Editorials and LettersHumansMentors
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
2014
Cyclic GMP Kinase II (cGKII) Inhibits NHE3 by Altering Its Trafficking and Phosphorylating NHE3 at Three Required Sites IDENTIFICATION OF A MULTIFUNCTIONAL PHOSPHORYLATION SITE*
Chen T, Kocinsky HS, Cha B, Murtazina R, Yang J, Tse CM, Singh V, Cole R, Aronson PS, de Jonge H, Sarker R, Donowitz M. Cyclic GMP Kinase II (cGKII) Inhibits NHE3 by Altering Its Trafficking and Phosphorylating NHE3 at Three Required Sites IDENTIFICATION OF A MULTIFUNCTIONAL PHOSPHORYLATION SITE*. Journal Of Biological Chemistry 2014, 290: 1952-1965. PMID: 25480791, PMCID: PMC4303652, DOI: 10.1074/jbc.m114.590174.Peer-Reviewed Original ResearchAnimalsBinding SitesCaco-2 CellsCell MembraneCyclic GMP-Dependent Protein Kinase Type IIDexamethasoneHumansIntestinal MucosaMass SpectrometryMiceMicrovilliMutagenesisPhosphorylationProtein Structure, TertiaryProtein TransportSerineSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSurface PropertiesTransfection
2013
Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension
Jacques T, Picard N, Miller RL, Riemondy KA, Houillier P, Sohet F, Ramakrishnan SK, Büsst CJ, Jayat M, Cornière N, Hassan H, Aronson PS, Hennings JC, Hübner CA, Nelson RD, Chambrey R, Eladari D. Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension. Journal Of The American Society Of Nephrology 2013, 24: 1104-1113. PMID: 23766534, PMCID: PMC3699825, DOI: 10.1681/asn.2012080787.Peer-Reviewed Original ResearchConceptsDistal nephronTransgenic miceSame sodium intakeHigh salt intakeCause of hypertensionHigh-salt dietSodium-driven chloride/bicarbonate exchangerNet NaCl absorptionArterial hypertensionSalt intakeSodium intakeEpithelial sodium channel ENaCPathogenic roleNormal miceHypertensionRenal absorptionExchanger pendrinPrimary abnormalityVascular volumeAppropriate downregulationIntercalated cellsChloride absorptionSodium channel ENaCActivity of transportersPrimary activationEzrin Is Required for the Functional Regulation of the Epithelial Sodium Proton Exchanger, NHE3
Hayashi H, Tamura A, Krishnan D, Tsukita S, Suzuki Y, Kocinsky HS, Aronson PS, Orlowski J, Grinstein S, Alexander RT. Ezrin Is Required for the Functional Regulation of the Epithelial Sodium Proton Exchanger, NHE3. PLOS ONE 2013, 8: e55623. PMID: 23405179, PMCID: PMC3566197, DOI: 10.1371/journal.pone.0055623.Peer-Reviewed Original ResearchMeSH KeywordsActin CytoskeletonAnimalsColonCyclic AMPCytoskeletal ProteinsDogsEpithelial CellsFluorescence Recovery After PhotobleachingHumansMadin Darby Canine Kidney CellsMaleMembrane ProteinsMiceMice, KnockoutMicrofilament ProteinsMicrovilliOctoxynolPhosphorylationProtein TransportRNA, Small InterferingSodiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersConceptsApical actin cytoskeletonNHE3 activitySodium hydrogen exchanger isoform 3CAMP-dependent inhibitionEzrin knockdown miceERM proteinsActin cytoskeletonSodium-proton exchangerApical cytoskeletonApical localizationFunctional regulationWild-type animalsEpithelial cell culture modelEzrinProton exchangersFluorescent recoveryEpithelial phenotypeCytoskeletonMolecular determinantsCell culture modelExchanger isoform 3Functional studiesNon-targeting siRNAApical membraneIsoform 3
2011
Effects of pH on Potassium: New Explanations for Old Observations
Aronson PS, Giebisch G. Effects of pH on Potassium: New Explanations for Old Observations. Journal Of The American Society Of Nephrology 2011, 22: 1981-1989. PMID: 21980112, PMCID: PMC3231780, DOI: 10.1681/asn.2011040414.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCholinergic signaling inhibits oxalate transport by human intestinal T84 cells
Hassan HA, Cheng M, Aronson PS. Cholinergic signaling inhibits oxalate transport by human intestinal T84 cells. American Journal Of Physiology - Cell Physiology 2011, 302: c46-c58. PMID: 21956166, PMCID: PMC3328906, DOI: 10.1152/ajpcell.00075.2011.Peer-Reviewed Original ResearchConceptsC-SrcT84 cellsHuman intestinal cell line T84PKC-δ inhibitor rottlerinSrc inhibitor PP2Intestinal cell line T84Human intestinal T84 cellsSurface expressionMuscarinic receptorsRegulation downstreamInhibitor PP2Phosphorylation studiesBiotinylation studiesInhibitor rottlerinKnockdown studiesPharmacological inhibitorsIntestinal T84 cellsIntestinal oxalate secretionPhospholipase CIntestinal ion transportPKC activationSignificant translocationCalcium oxalate urolithiasisPKCAnion exchanger SLC26A6
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
ESRD as a Window into America's Cost Crisis in Health Care
Knauf F, Aronson PS. ESRD as a Window into America's Cost Crisis in Health Care. Journal Of The American Society Of Nephrology 2009, 20: 2093-2097. PMID: 19729435, DOI: 10.1681/asn.2009070715.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2008
Phenotypic and Functional Analysis of Human SLC26A6 Variants in Patients With Familial Hyperoxaluria and Calcium Oxalate Nephrolithiasis
Monico CG, Weinstein A, Jiang Z, Rohlinger AL, Cogal AG, Bjornson BB, Olson JB, Bergstralh EJ, Milliner DS, Aronson PS. Phenotypic and Functional Analysis of Human SLC26A6 Variants in Patients With Familial Hyperoxaluria and Calcium Oxalate Nephrolithiasis. American Journal Of Kidney Diseases 2008, 52: 1096-1103. PMID: 18951670, PMCID: PMC2710965, DOI: 10.1053/j.ajkd.2008.07.041.Peer-Reviewed Original ResearchConceptsPrimary hyperoxaluria type 1Oxalate transportMajor risk factorCalcium oxalate nephrolithiasisUrine oxalate levelsCalcium oxalate urolithiasisRare variantsHyperoxaluria type 1Calcium oxalate stonesAdditional missense variantsUrine oxalateOxalate excretionRisk factorsOxalate nephrolithiasisOxalate urolithiasisHyperoxaluriaAbstractTextAdult subjectsType 1Oxalate stonesPotential modifiersStudy designOxalate levelsGood healthMissense variants
2007
Specificity and Regulation of Renal Sulfate Transporters
Markovich D, Aronson PS. Specificity and Regulation of Renal Sulfate Transporters. Annual Review Of Physiology 2007, 69: 361-375. PMID: 17002596, DOI: 10.1146/annurev.physiol.69.040705.141319.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsProximal tubulesSulfate reabsorptionProximal tubular cellsRenal expressionApical membraneKnockout mouse studiesTubular cellsNet reabsorptionNaCl reabsorptionMouse studiesMajor roleReabsorptionSulfate homeostasisCFEXKidneyFamily membersPhysiological roleCurrent dataNormal cellular functionBasolateral membraneTubulesSLC26 family members
2006
Essential 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 TransportersXenopusIon exchangers mediating Na+, HCO3 - and Cl- transport in the renal proximal tubule.
Aronson PS. Ion exchangers mediating Na+, HCO3 - and Cl- transport in the renal proximal tubule. Journal Of Nephrology 2006, 19 Suppl 9: s3-s10. PMID: 16736438.Commentaries, Editorials and LettersConceptsProximal tubulesNaCl absorptionApical membrane ClNull miceOxalate-sulfate exchangePendrin-null miceProximal tubule cellsBrush borderFormate exchangeRenal proximal tubulesSlc26a6-null miceAcid secretionPendrin expressionFunctional expression studiesTubule cellsNaCl reabsorptionCl absorptionBrush border membraneSulfate cotransportLines of evidenceExchanger isoformsTubulesMiceFamily membersBorder membrane
2005
Expression of kidney-specific cadherin distinguishes chromophobe renal cell carcinoma from renal oncocytoma
Mazal PR, Exner M, Haitel A, Krieger S, Thomson RB, Aronson PS, Susani M. Expression of kidney-specific cadherin distinguishes chromophobe renal cell carcinoma from renal oncocytoma. Human Pathology 2005, 36: 22-28. PMID: 15712178, DOI: 10.1016/j.humpath.2004.09.011.Peer-Reviewed Original ResearchConceptsChromophobe renal cell carcinomaRenal cell carcinomaPapillary renal cell carcinomaCell carcinomaRenal oncocytomaKidney-specific cadherinColloidal iron stainingDuct carcinomaRenal carcinomaClear cell renal cell carcinomaHale's colloidal iron stainingCell renal cell carcinomaClear cell renal carcinomaEpithelial membrane antigenMalignant biological behaviorCell renal carcinoma