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
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
Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion
Knauf F, Thomson RB, Heneghan JF, Jiang Z, Adebamiro A, Thomson CL, Barone C, Asplin JR, Egan ME, Alper SL, Aronson PS. Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion. Journal Of The American Society Of Nephrology 2016, 28: 242-249. PMID: 27313231, PMCID: PMC5198290, DOI: 10.1681/asn.2016030279.Peer-Reviewed Original ResearchConceptsIntestinal oxalate secretionWild-type miceCystic fibrosisIntestinal tissueOxalate secretionIncidence of hyperoxaluriaCalcium oxalate stone formationNet intestinal absorptionOxalate stone formationCoexpression of CFTRIntestinal transport processesWestern blot analysisOxalate absorptionMouse modelIntestinal absorptionGlucose absorptionUssing chambersStone formationFibrosisMiceSecretionReduced expressionCystic fibrosis transmembrane conductance regulator (CFTR) geneHyperoxaluriaPatients
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
Sat1 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
2010
The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice
Leviel F, Hübner CA, Houillier P, Morla L, Moghrabi S, Brideau G, Hatim H, Parker MD, Kurth I, Kougioumtzes A, Sinning A, Pech V, Riemondy KA, Miller RL, Hummler E, Shull GE, Aronson PS, Doucet A, Wall SM, Chambrey R, Eladari D. The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. Journal Of Clinical Investigation 2010, 120: 1627-1635. PMID: 20389022, PMCID: PMC2860930, DOI: 10.1172/jci40145.Peer-Reviewed Original ResearchConceptsNa-Cl cotransporterSodium transportMaintenance of euvolemiaTransepithelial NaCl absorptionDucts of miceEpithelial sodium channelIntravascular volumeIndependent Cl-/HCO3Sodium balanceMouse CCDAmiloride-sensitive epithelial sodium channelSodium absorptionExcretion resultsFluid homeostasisGenetic ablationNaCl absorptionSodium channelsMiceCl-/HCO3NaCl transportSlc4a8Genetic disruptionNovel roleHydrochlorothiazideDuctRole 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
2007
Role of Anion Transporter SLC26A6 (CFEX) in Prevention of Hyperoxaluria and Urolithiasis
Aronson P. Role of Anion Transporter SLC26A6 (CFEX) in Prevention of Hyperoxaluria and Urolithiasis. AIP Conference Proceedings 2007, 900: 141-148. DOI: 10.1063/1.2723570.Commentaries, Editorials and LettersProximal tubulesNull miceOxalate secretionPlasma oxalate concentrationIntestinal oxalate secretionCalcium oxalate urolithiasisFormate exchangeOxalate exchangePrevention of hyperoxaluriaHigh incidenceOxalate urolithiasisHyperoxaluriaCFEXApical membraneRenal brush border vesiclesNet absorptionMiceBrush border vesiclesTubulesUrolithiasisSecretionXenopus oocytesAnion transportersFunctional expression
2006
Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6
Jiang Z, Asplin JR, Evan AP, Rajendran VM, Velazquez H, Nottoli TP, Binder HJ, Aronson PS. Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6. Nature Genetics 2006, 38: 474-478. PMID: 16532010, DOI: 10.1038/ng1762.Peer-Reviewed Original ResearchConceptsCalcium oxalate urolithiasisOxalate urolithiasisPlasma oxalate concentrationIntestinal oxalate secretionUrinary oxalate concentrationCommon urologic diseaseNet intestinal absorptionAnion exchanger SLC26A6Dietary oxalate restrictionSlc26a6-null miceSignificant hyperoxaluriaOxalate restrictionUrologic diseasesHigh incidenceIntestinal absorptionExchanger SLC26A6Mutant miceUrolithiasisMiceMajor constitutive roleNet absorptionOxalate secretionHyperoxaluriaOxalate concentrationEpithelial tissuesIon 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
2004
Renal and intestinal transport defects in Slc26a6-null mice
Wang Z, Wang T, Petrovic S, Tuo B, Riederer B, Barone S, Lorenz JN, Seidler U, Aronson PS, Soleimani M. Renal and intestinal transport defects in Slc26a6-null mice. American Journal Of Physiology - Cell Physiology 2004, 288: c957-c965. PMID: 15574486, DOI: 10.1152/ajpcell.00505.2004.Peer-Reviewed Original ResearchConceptsWild-type miceProximal tubulesSlc26a6-null miceHCO3- secretionKidney proximal tubulesApical membrane ClNull miceBaseline rateNormal blood pressureCl-/formate exchangeBlood pressureKidney functionElectrolyte profileMucosal tissuesIntestinal physiologyUssing chambersSmall intestineMiceFluid absorptionNaCl absorptionStatistical significanceCl-/HCO3NaCl transportDuodenumTubules
2002
Formate-stimulated NaCl absorption in the proximal tubule is independent of the pendrin protein
Karniski LP, Wang T, Everett LA, Green ED, Giebisch G, Aronson PS. Formate-stimulated NaCl absorption in the proximal tubule is independent of the pendrin protein. American Journal Of Physiology. Renal Physiology 2002, 283: f952-f956. PMID: 12372770, DOI: 10.1152/ajprenal.00182.2002.Peer-Reviewed Original ResearchConceptsProximal tubulesChloride/formate exchangeNaCl reabsorptionChloride reabsorptionElectroneutral NaCl reabsorptionNaCl absorptionRole of pendrinFormate exchangePds-knockout mouseRecycling of formatePendrin proteinReabsorptionMicePendrinBrush border membrane vesiclesTubulesPresent studyChloride transportApical membrane
1999
Mechanism of proximal tubule bicarbonate absorption in NHE3 null mice
Wang T, Yang C, Abbiati T, Schultheis P, Shull G, Giebisch G, Aronson P. Mechanism of proximal tubule bicarbonate absorption in NHE3 null mice. American Journal Of Physiology 1999, 277: f298-f302. PMID: 10444585, DOI: 10.1152/ajprenal.1999.277.2.f298.Peer-Reviewed Original Research
1998
Renal and intestinal absorptive defects in mice lacking the NHE3 Na+/H+ exchanger
Schultheis P, Clarke L, Meneton P, Miller M, Soleimani M, Gawenis L, Riddle T, Duffy J, Doetschman T, Wang T, Giebisch G, Aronson P, Lorenz J, Shull G. Renal and intestinal absorptive defects in mice lacking the NHE3 Na+/H+ exchanger. Nature Genetics 1998, 19: 282-285. PMID: 9662405, DOI: 10.1038/969.Peer-Reviewed Original ResearchConceptsAcid-base balanceAbsorptive defectsNHE3-deficient miceFluid volume homeostasisRenal proximalSlight diarrheaPlasma aldosteroneBlood pressureHomozygous mutant miceExchanger mRNANHE2 isoformsBlood analysisMutant miceCompensatory mechanismsFluid absorptionNHE3 functionVolume homeostasisMiceDistribution of NHE3Cl-/HCO3Channel activityNHE3KidneyATPase mRNAIntestine