Peter S. Aronson, MD
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C. N. H. Long Professor of Medicine (Nephrology) and Professor of Cellular And Molecular Physiology
Biography
Dr. Aronson received his undergraduate education at the University of Rochester and his medical education at New York University. He was an internal medicine resident at the University of North Carolina and a research fellow at the National Institutes of Health before coming to Yale as a nephrology fellow in 1974. He joined the Yale faculty in 1977, and was Chief of the Section of Nephrology from 1987-2002. Dr. Aronson has published articles and book chapters on the mechanisms regulating sodium, chloride, acid-base, and oxalate excretion by the kidney. He has received several awards and honors for his research work, including the Young Investigator Award of the American Society of Nephrology (ASN) and American Heart Association in 1985, the Homer W. Smith Award of the ASN in 1994, Fellow of the American Association for the Advancement of Science in 1996, Fellow of the American Academy of Arts and Sciences in 2009, the Robert W. Berliner Award of the American Physiological Society (APS) in 2016, and the Walter B. Cannon Award of the APS in 2019. He served as President of the American Society of Nephrology in 2008. Dr. Aronson actively participates in the teaching of undergraduate, graduate and medical students. He was a co-recipient of the Charles W. Bohmfalk Teaching Prize in the Basic Sciences in 2005, and received the Fund for Physician-Scientist Mentorship Award in 2023. Dr. Aronson is an Associate Director of the Yale M.D.-Ph.D. Program.
Appointments
Nephrology
ProfessorPrimaryCellular & Molecular Physiology
ProfessorSecondary
Other Departments & Organizations
Education & Training
- Postdoctoral Fellow in Nephrology
- Yale School of Medicine (1977)
- Clinical Associate (Research Fellow)
- Gerontology Research Center, NIH (1974)
- Resident
- University of North Carolina School of Medicine (1972)
- MD
- New York University (1970)
- AB
- University of Rochester, General Science (1967)
Board Certifications
Nephrology
- Certification Organization
- AB of Internal Medicine
- Original Certification Date
- 1976
Internal Medicine
- Certification Organization
- AB of Internal Medicine
- Original Certification Date
- 1973
Research
Overview
Our general goal is to characterize the mechanisms regulating sodium, acid-base, and anion excretion by the kidney. Our work is primarily focused on membrane transport proteins mediating ion exchange, namely NHE isoforms mediating Na+-H+ exchange, and SLC26 isoforms mediating anion exchange. One approach involves the generation of isoform- and phospho-specific polyclonal and monoclonal antibodies to identify the cellular and subcellular sites of expression of ion exchangers in the kidney and other tissues, and to study their regulation. A complementary approach uses mice with targeted gene disruption to elucidate the physiological roles of ion exchangers and associated proteins under in vivo conditions. For example, work with mice lacking anion exchanger Slc26a6, which can function as an oxalate transporter, revealed a phenotype of calcium oxalate kidney stones. This finding in turn has motivated studies on the mechanisms and regulation of oxalate transporters and their roles in oxalate homeostasis, urolithiasis, and crystal-induced inflammation in the kidney and other tissues.
Medical Subject Headings (MeSH)
ORCID
0000-0002-1860-2419
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Felix Knauf, MD
Robert Thomson, PhD
Tong Wang, MD
Ali Abu-Alfa, MD, FASN, FAHA
Thecla Abbiati
Theresa Ermer, MD
Cell Membrane Permeability
Hyperoxaluria
Nephrolithiasis
Publications
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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIL-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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSulfate 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 StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsKidney 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 LettersAltmetricDominant 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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsRare 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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSudden 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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsKsp-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 mice
Academic Achievements and Community Involvement
honor Fellow
National AwardAmerican Academy of Arts and SciencesDetails01/01/2009United States
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The Anlyan Center
300 Cedar Street, Ste Room S255C
New Haven, CT 06519
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