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
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 processes
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