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 StatementsMeSH KeywordsHomeostasisHumansHyperoxaluriaKidneyOxalatesRenal DialysisRenal InsufficiencyRenal Insufficiency, ChronicConceptsKidney 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
2018
Characterization of renal NaCl and oxalate transport in Slc26a6−/− mice
Knauf F, Velazquez H, Pfann V, Jiang Z, Aronson PS. Characterization of renal NaCl and oxalate transport in Slc26a6−/− mice. American Journal Of Physiology. Renal Physiology 2018, 316: f128-f133. PMID: 30427220, PMCID: PMC6383200, DOI: 10.1152/ajprenal.00309.2018.Peer-Reviewed Original ResearchConceptsWild-type miceNaCl homeostasisBlood pressureProximal tubulesFree-flow micropuncture studiesSurface proximal tubulesLow-salt dietMean blood pressureLower blood pressureUrine flow rateLack of effectFurosemide infusionNet renal secretionSodium excretionUrine oxalateFractional excretionMicropuncture studiesNaCl deliveryRenal secretionApical membrane ClExchanger SLC26A6MiceRenal NaClNaCl transportHomeostasis
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 role
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 Statements
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
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 TransportersXenopusPendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent
Vallet M, Picard N, Loffing-Cueni D, Fysekidis M, Bloch-Faure M, Deschênes G, Breton S, Meneton P, Loffing J, Aronson PS, Chambrey R, Eladari D. Pendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent. Journal Of The American Society Of Nephrology 2006, 17: 2153-2163. PMID: 16825334, DOI: 10.1681/asn.2005101054.Peer-Reviewed Original ResearchConceptsHydrochlorothiazide administrationAldosterone secretionExtracellular fluid volume regulationElevated plasma aldosterone levelsPlasma aldosterone levelsDifferent mouse modelsFluid volume regulationPendrin protein expressionAldosterone levelsSecondary hyperaldosteronismEpithelial sodium channelChloride transportApical Cl-/HCO3Chloride reabsorptionRat modelPendrin expressionMouse modelKnockout miceSemiquantitative immunoblottingNaCl loadingGamma-ENaC subunitsBiologic effectsExperimental modelSodium channelsProtein expression
2004
The Cl−/HCO3− exchanger pendrin in the rat kidney is regulated in response to chronic alterations in chloride balance
Quentin F, Chambrey R, Trinh-Trang-Tan MM, Fysekidis M, Cambillau M, Paillard M, Aronson PS, Eladari D. The Cl−/HCO3− exchanger pendrin in the rat kidney is regulated in response to chronic alterations in chloride balance. American Journal Of Physiology. Renal Physiology 2004, 287: f1179-f1188. PMID: 15292050, DOI: 10.1152/ajprenal.00211.2004.Peer-Reviewed Original ResearchConceptsChronic furosemide administrationBlood pressure regulationDiet-induced changesAcid-base statusNaCl dietFurosemide administrationChronic alterationsControl ratsRenal membrane fractionsChloride balanceChronic changesNaCl balanceExchanger pendrinSemiquantitative immunoblottingPressure regulationRat kidneyConsistent inverse relationshipPD expressionNaCl depletionType BProtein abundanceRatsPendrinInverse relationshipExpression
1991
Na+-H+ Exchanger and Its Role in Essential Hypertension and Diabetes Mellitus
Huot S, Aronson P. Na+-H+ Exchanger and Its Role in Essential Hypertension and Diabetes Mellitus. Diabetes Care 1991, 14: 521-535. PMID: 1650693, DOI: 10.2337/diacare.14.6.521.Commentaries, Editorials and LettersConceptsDiabetes mellitusEssential hypertensionInsulin-dependent diabetes mellitusHigh blood pressureSubgroup of patientsBlood pressureHypertensionAnimal modelsPathophysiological statesTransepithelial absorptionAltered activityCellular mechanismsMellitusPatientsIntracellular pHPossible roleCell volume regulationVolume regulationCell growthRecent cDNA cloningNephropathyUbiquitous transport systems