Featured Publications
Podocyte histone deacetylase activity regulates murine and human glomerular diseases
Inoue K, Gan G, Ciarleglio M, Zhang Y, Tian X, Pedigo CE, Cavanaugh C, Tate J, Wang Y, Cross E, Groener M, Chai N, Wang Z, Justice A, Zhang Z, Parikh CR, Wilson FP, Ishibe S. Podocyte histone deacetylase activity regulates murine and human glomerular diseases. Journal Of Clinical Investigation 2019, 129: 1295-1313. PMID: 30776024, PMCID: PMC6391095, DOI: 10.1172/jci124030.Peer-Reviewed Original ResearchConceptsEarly growth response 1Histone deacetylase 1Proteinuric patientsKidney diseaseHDAC2 activityValproic acidVeterans Aging Cohort StudyEnd-stage kidney diseaseDegree of proteinuriaGlomerular filtration rateAging Cohort StudyInhibition of HDAC1Proteinuric kidney diseaseHuman glomerular diseasesGlomerular disease modelsConnectivity Map databaseCohort studyFiltration rateGlomerular diseaseHistone deacetylase activityProteinuric kidneysHDAC inhibitorsProteinuriaMRNA expressionGenetic ablation
2023
Comparative evaluation of glomerular morphometric techniques reveals differential technical artifacts between focal segmental glomerulosclerosis and normal glomeruli
Reghuvaran A, Lin Q, Basgen J, Banu K, Shi H, Vashist A, Pell J, Perinchery S, He J, Moledina D, Wilson F, Menon M. Comparative evaluation of glomerular morphometric techniques reveals differential technical artifacts between focal segmental glomerulosclerosis and normal glomeruli. Physiological Reports 2023, 11: e15688. PMID: 37423891, PMCID: PMC10329935, DOI: 10.14814/phy2.15688.Peer-Reviewed Original Research
2022
Urine Uromodulin as a Biomarker of Kidney Tubulointerstitial Fibrosis
Melchinger H, Calderon-Gutierrez F, Obeid W, Xu L, Shaw MM, Luciano RL, Kuperman M, Moeckel GW, Kashgarian M, Wilson FP, Parikh CR, Moledina DG. Urine Uromodulin as a Biomarker of Kidney Tubulointerstitial Fibrosis. Clinical Journal Of The American Society Of Nephrology 2022, 17: 1284-1292. PMID: 35948365, PMCID: PMC9625093, DOI: 10.2215/cjn.04360422.Peer-Reviewed Original ResearchConceptsInterstitial fibrosis/tubular atrophyUrine uromodulinTubular atrophyThick ascending limbUrine albuminSerum creatinineKidney biopsyTubulointerstitial fibrosisMultivariable linear regression modelsTime of biopsyKidney's thick ascending limbAcademic medical centerHuman kidney biopsiesKidney tubulointerstitial fibrosisTubular healthMultivariable analysisHistologic featuresHistologic findingsHistologic changesKidney fibrosisIndependent associationFibrotic modelMultivariable modelMedical CenterMurine model
2021
Renal negative pressure treatment as a novel therapy for heart failure-induced renal dysfunction
Rao VS, Maulion C, Asher JL, Ivey-Miranda J, Cox ZL, Moreno-Villagomez J, Mahoney D, Turner JM, Wilson FP, Wilcox CS, Testani J. Renal negative pressure treatment as a novel therapy for heart failure-induced renal dysfunction. AJP Regulatory Integrative And Comparative Physiology 2021, 321: r588-r594. PMID: 34405731, DOI: 10.1152/ajpregu.00115.2021.Peer-Reviewed Original ResearchConceptsRenal plasma flowGlomerular filtration rateCongestive HFTubular pressureHeart failure hospitalizationPara-aminohippurate clearanceCentral venous pressureHigh fractional excretionNegative pressure therapyUrinary collecting systemNegative pressure treatmentSimilar diuresisFailure hospitalizationRenal dysfunctionCardiac tamponadeIothalamate clearanceFractional excretionRenal parametersKidney functionRenal congestionRenal responseRight kidneyVenous pressurePressure therapyControl kidneys
2020
First-in-Human Experience With Peritoneal Direct Sodium Removal Using a Zero-Sodium Solution
Rao VS, Turner JM, Griffin M, Mahoney D, Asher J, Jeon S, Yoo PS, Boutagy N, Feher A, Sinusas A, Wilson FP, Finkelstein F, Testani JM. First-in-Human Experience With Peritoneal Direct Sodium Removal Using a Zero-Sodium Solution. Circulation 2020, 141: 1043-1053. PMID: 31910658, PMCID: PMC7331276, DOI: 10.1161/circulationaha.119.043062.Peer-Reviewed Original ResearchConceptsStandard PD solutionExperimental heart failureHeart failurePD solutionsAdverse eventsPeritoneal dialysisSignificant discomfortSodium removalEnd-stage renal diseaseEnd pointElevated right atrial pressureMaintenance of euvolemiaPrimary end pointSecondary end pointsRight atrial pressureHuman proofLoss of responseSolute removalPorcine experimentsAtrial pressureRenal diseaseLoop diureticsSerum electrolytesHuman studiesPeritoneal membrane
2013
Cdc42 Deficiency Causes Ciliary Abnormalities and Cystic Kidneys
Choi SY, Chacon-Heszele MF, Huang L, McKenna S, Wilson FP, Zuo X, Lipschutz JH. Cdc42 Deficiency Causes Ciliary Abnormalities and Cystic Kidneys. Journal Of The American Society Of Nephrology 2013, 24: 1435-1450. PMID: 23766535, PMCID: PMC3752951, DOI: 10.1681/asn.2012121236.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCdc42 GTP-Binding ProteinCell ProliferationCiliaDisease Models, AnimalFibrosisIn Vitro TechniquesKidney Diseases, CysticKidney Tubules, CollectingKidney Tubules, DistalMiceMice, KnockoutMice, TransgenicMitogen-Activated Protein Kinase KinasesPhenotypeSignal TransductionVesicular Transport ProteinsZebrafishZebrafish ProteinsConceptsCiliary proteinsSynergistic genetic interactionMitogen-activated protein kinase activationSmall GTPase Cdc42Role of Cdc42Protein kinase activationKnockdown of Cdc42Trafficking complexGTPase Cdc42Genetic interactionsSec10 knockdownPolycystic kidney diseaseCyst cellsCdc42 knockdownPrimary ciliaPhotoreceptor ciliaCdc42Kinase activationExocystMAPK activationCiliogenesisSec10Same pathwayPathways resultsCdc42 deficiency