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
SLC26A6 Plays a Major Role in Release of Soluble Oxalate from Macrophages Following Internalization of Calcium Oxalate Crystals
Najenson A, Wagner T, Bachmann S, Thomson R, Knauf F, Aronson P. SLC26A6 Plays a Major Role in Release of Soluble Oxalate from Macrophages Following Internalization of Calcium Oxalate Crystals. Journal Of The American Society Of Nephrology 2023, 34: 490-490. DOI: 10.1681/asn.20233411s1490b.Peer-Reviewed Original ResearchSLC26A1 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 strategyExcretionNew Insights into the Pivotal Roles of Claudins in Proximal Tubule Electrolyte Reabsorption
Aronson PS. New Insights into the Pivotal Roles of Claudins in Proximal Tubule Electrolyte Reabsorption. Journal Of The American Society Of Nephrology 2022, 33: 659-661. PMID: 35264457, PMCID: PMC8970453, DOI: 10.1681/asn.2022020157.Commentaries, Editorials and LettersDominant 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 Increase Risk for Sudden Cardiac Death in Dialysis Patients
Pfau A, Ermer T, Coca S, Tio M, Genser B, Reichel M, Finkelstein F, März W, Wanner C, Waikar S, Eckardt K, Aronson P, Drechsler C, Knauf F. High Oxalate Concentrations Increase Risk for Sudden Cardiac Death in Dialysis Patients. Journal Of The American Society Of Nephrology 2021, 32: 226-226. DOI: 10.1681/asn.20213210s1226a.Peer-Reviewed Original ResearchA New Physiological Model to Study Regulation of SLC26A6-Mediated Oxalate Transport in Mouse and Human Intestinal Tissue
Schorr M, Holthaus D, Vallone V, Thomson R, Stachelscheid H, Aronson P, Knauf F. A New Physiological Model to Study Regulation of SLC26A6-Mediated Oxalate Transport in Mouse and Human Intestinal Tissue. Journal Of The American Society Of Nephrology 2021, 32: 202-203. DOI: 10.1681/asn.20213210s1202d.Peer-Reviewed Original ResearchHigh 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 cohortDeletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse
Thomson R, Dynia DW, Burlein S, Thomson BR, Booth C, Knauf F, Wang T, Aronson P. Deletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse. American Journal Of Physiology. Renal Physiology 2021, 320: f1106-f1122. PMID: 33938239, PMCID: PMC8285649, DOI: 10.1152/ajprenal.00556.2020.Peer-Reviewed Original ResearchConceptsKsp-cadherinCell adhesion moleculeAtypical memberKidney developmentMammalian kidneyAdult mammalian kidneyBasolateral membraneNormal kidney developmentEpithelial cellsAdhesion moleculesMutant animalsExpression analysisSpecific expressionE-cadherin expressionWestern blot analysisEpithelial phenotypePrincipal proteinE-cadherinBlot analysisMouse linesAquaporin-2CadherinCritical roleDevelopmental delayKnockout miceAuthor Reply to Comment on “Assessment of Plasma Oxalate Concentration in Patients With CKD” by Oka et al.
Pfau A, Wytopil M, Chauhan K, Reichel M, Coca S, Aronson PS, Eckardt KU, Knauf F. Author Reply to Comment on “Assessment of Plasma Oxalate Concentration in Patients With CKD” by Oka et al. Kidney International Reports 2021, 6: 1194-1195. PMID: 33912771, PMCID: PMC8071653, DOI: 10.1016/j.ekir.2021.02.027.Peer-Reviewed Original Research
2020
Assessment of Blood Oxalate Concentrations in Patients with CKD
Pfau A, Wytopil M, Chauhan K, Reichel M, Coca S, Aronson P, Eckardt K, Knauf F. Assessment of Blood Oxalate Concentrations in Patients with CKD. Journal Of The American Society Of Nephrology 2020, 31: 177-177. DOI: 10.1681/asn.20203110s1177a.Peer-Reviewed Original ResearchGerhard 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 LettersAssessment of Plasma Oxalate Concentration in Patients With CKD
Pfau A, Wytopil M, Chauhan K, Reichel M, Coca SG, Aronson PS, Eckardt KU, Knauf F. Assessment of Plasma Oxalate Concentration in Patients With CKD. Kidney International Reports 2020, 5: 2013-2020. PMID: 33163722, PMCID: PMC7609998, DOI: 10.1016/j.ekir.2020.08.029.Peer-Reviewed Original ResearchChronic kidney diseasePlasma oxalate concentrationGerman Chronic Kidney Disease (GCKD) studyChronic Kidney Disease studyObservational cohort studyGlomerular filtration rateLarge patient cohortKidney Disease studyKidney stone diseaseCKD progressionMedian eGFROngoing multicenterCohort studyKidney diseasePatient cohortPresent studyFiltration rateClinical trialsStone diseaseLarge cohortOxalate homeostasisPatientsDisease StudyPlasma samplesMaintenance of samplesEnteric 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 expressionIn memoriam: Gerhard Giebisch, MD, 1927–2020
Aronson P. In memoriam: Gerhard Giebisch, MD, 1927–2020. Kidney International 2020, 98: 2-5. DOI: 10.1016/j.kint.2020.04.023.Commentaries, Editorials and Letters
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
2017
Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease
Ermer T, Kopp C, Asplin JR, Granja I, Perazella MA, Reichel M, Nolin TD, Eckardt KU, Aronson PS, Finkelstein FO, Knauf F. Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease. Kidney International Reports 2017, 2: 1050-1058. PMID: 29270514, PMCID: PMC5733827, DOI: 10.1016/j.ekir.2017.06.002.Peer-Reviewed Original ResearchEnd-stage renal diseasePlasma oxalate concentrationRenal diseaseCalcium oxalate supersaturationPlasma of patientsTraditional therapeutic regimensExtended treatment timeTherapeutic regimensExtended hemodialysisUremic toxin removalHemodialysisTherapeutic strategiesTreatment sessionsPatientsBaseline pDialysis equipmentHemodialfiltrationWeeksTreatment timeOxalate concentrationRespective treatmentsDiseasePrevious reportsTreatment modeHours
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