2023
Genome-wide Association Study for AKI
Bhatraju P, Stanaway I, Palmer M, Menon R, Schaub J, Menez S, Srivastava A, Wilson F, Kiryluk K, Palevsky P, Naik A, Sakr S, Jarvik G, Parikh C, Ware L, Ikizler T, Siew E, Chinchilli V, Coca S, Garg A, Go A, Kaufman J, Kimmel P, Himmelfarb J, Wurfel M. Genome-wide Association Study for AKI. Kidney360 2023, 4: 870-880. PMID: 37273234, PMCID: PMC10371295, DOI: 10.34067/kid.0000000000000175.Peer-Reviewed Original ResearchConceptsGenome-wide association studiesGene locusAssociation studiesSingle-cell RNA sequencing dataHealthy living donorsLoop of HenleThick ascending limbWide significant associationsGenetic variantsGenome-wide significanceRNA sequencing dataKidney biopsyCommon genetic riskLiving donorsSubsequent sequelaeSerial evaluationFunctional annotationIntergenic regionAscending limbGene expressionSequencing dataRisk of AKIKidney biopsy tissueProximal tubular epithelial cellsMember 1 gene
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
2020
The Relationship Between Urine Uromodulin and Blood Pressure Changes: The DASH-Sodium Trial
Bakhoum CY, Anderson CAM, Juraschek SP, Rebholz CM, Appel LJ, Miller ER, Parikh CR, Obeid W, Rifkin DE, Ix JH, Garimella PS. The Relationship Between Urine Uromodulin and Blood Pressure Changes: The DASH-Sodium Trial. American Journal Of Hypertension 2020, 34: 154-156. PMID: 32856709, PMCID: PMC7951043, DOI: 10.1093/ajh/hpaa140.Peer-Reviewed Original ResearchConceptsSystolic blood pressureUrine uromodulinUromodulin levelsBlood pressureSodium dietSalt intakeDASH-Sodium trialHigh sodium dietHigh salt intakeHigh-salt dietSalt-induced hypertensionBlood pressure changesBody mass indexMultivariable linear regressionLoop of HenleHigher baseline levelsThick ascending limbFeeding periodGreater increaseSodium trialSalt dietDietary ApproachesMass indexRandomized trialsSBP change
2011
Renal outer medullary potassium channel knockout models reveal thick ascending limb function and dysfunction
Wang T. Renal outer medullary potassium channel knockout models reveal thick ascending limb function and dysfunction. Clinical And Experimental Nephrology 2011, 16: 49-54. PMID: 22038261, DOI: 10.1007/s10157-011-0495-0.Peer-Reviewed Original ResearchConceptsThick ascending limbIon transporter expressionRenal outer medullary potassium channelBartter's syndromeInward rectifier potassium channelPotassium channelsSmall-conductance K channelsROMK null miceMedullary thick ascending limbType II Bartter's syndromeSimilar phenotypeMammalian kidneyApical membraneK channelsROMK knockout miceKnockout modelsChannel activityChannel mutationsRenal functionLimb functionNull micePhysiological conditionsSalt wastingTransporter expressionPathophysiological conditions
2010
In vivo nuclear translocation of mineralocorticoid and glucocorticoid receptors in rat kidney: differential effect of corticosteroids along the distal tubule
Ackermann D, Gresko N, Carrel M, Loffing-Cueni D, Habermehl D, Gomez-Sanchez C, Rossier B, Loffing J. In vivo nuclear translocation of mineralocorticoid and glucocorticoid receptors in rat kidney: differential effect of corticosteroids along the distal tubule. American Journal Of Physiology. Renal Physiology 2010, 299: f1473-f1485. PMID: 20861076, DOI: 10.1152/ajprenal.00437.2010.Peer-Reviewed Original ResearchConceptsAldosterone-sensitive distal nephronThick ascending limbGlucocorticoid receptorLate distal convoluted tubuleLow-dose corticosterone replacementSegment-specific cellsNuclear translocationDietary NaCl loadingDistal convoluted tubuleKidneys of ratsDehydrogenase type 2Proximal tubule cellsAldosterone replacementMineralocorticoid selectivityPlasma aldosteroneCorticosteroid effectsCorticosterone replacementControl ratsDistal tubulesDistal nephronConvoluted tubulesNaCl loadingCorticosterone levelsAscending limbHigh dosesThe calcium-sensing receptor.
Geibel JP. The calcium-sensing receptor. Journal Of Nephrology 2010, 23 Suppl 16: s130-5. PMID: 21170870.Peer-Reviewed Original ResearchConceptsCalcium-sensing receptorExtracellular environmentReceptor-targeted drugsThick ascending limbFiltered loadAscending limbNephron segmentsAmino acidsHandling of waterReceptorsImportant roleBasic physiologyImportant memberSalt absorptionRecent studiesDivalent ion concentrationSalinityCalciumIonic absorptionCaSR
2009
Chapter 14 Molecular Genetics of Magnesium Homeostasis
Asch W, Lifton R. Chapter 14 Molecular Genetics of Magnesium Homeostasis. 2009, 249-261. DOI: 10.1016/b978-0-12-449851-8.00014-0.Peer-Reviewed Original ResearchThick ascending limbParathyroid hormoneCalcium levelsLow serum magnesium levelsReturn of potassiumParathyroid hormone secretionSerum magnesium levelsLoop of HenlePotassium channel ROMKRenal magnesium transportAutosomal recessive disorderPTH secretionSevere hypomagnesemiaSerum magnesiumHormone secretionMagnesium replacementParathyroid cellsBartter's syndromeMagnesium levelsAscending limbChannel ROMKHypocalcemiaHypomagnesemiaSecondary hypocalcemiaCotransporter NKCC2
2008
Apoptosis of the Thick Ascending Limb Results in Acute Kidney Injury
Srichai MB, Hao C, Davis L, Golovin A, Zhao M, Moeckel G, Dunn S, Bulus N, Harris RC, Zent R, Breyer MD. Apoptosis of the Thick Ascending Limb Results in Acute Kidney Injury. Journal Of The American Society Of Nephrology 2008, 19: 1538-1546. PMID: 18495962, PMCID: PMC2488270, DOI: 10.1681/asn.2007101101.Peer-Reviewed Original ResearchConceptsAcute kidney injuryKidney injuryToxin-induced acute kidney injurySevere acute kidney injuryNovel transgenic mouse modelAdministration of gancyclovirIschemia/reperfusionBlood urea nitrogenTransgenic mouse modelToxin-induced injuryThick ascending limbHerpes simplex virus 1 thymidine kinase geneCreatinine levelsNeutrophil infiltrationAcute injuryControl miceInjury resultsMouse modelTransgenic miceUrea nitrogenProximal tubulesTAL cellsAscending limbInjuryTubular segmentsMouse model of type II Bartter's syndrome. I. Upregulation of thiazide-sensitive Na-Cl cotransport activity
Cantone A, Yang X, Yan Q, Giebisch G, Hebert SC, Wang T. Mouse model of type II Bartter's syndrome. I. Upregulation of thiazide-sensitive Na-Cl cotransport activity. American Journal Of Physiology. Renal Physiology 2008, 294: f1366-f1372. PMID: 18385266, DOI: 10.1152/ajprenal.00608.2007.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAmilorideAnimalsBartter SyndromeCation Transport ProteinsChloridesDisease Models, AnimalDiureticsEpithelial Sodium ChannelsFemaleFurosemideGlomerular Filtration RateHydrochlorothiazideLoop of HenleMaleMiceMice, Mutant StrainsPotassium Channels, Inwardly RectifyingPregnancySodiumSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1Up-RegulationConceptsThick ascending limbExcretion rateWhole kidney glomerular filtration rateKidney glomerular filtration rateFractional excretion rateFurosemide-induced incrementsGlomerular filtration rateType II Bartter's syndromeHyperprostaglandin E syndromeEffect of furosemideDistal nephron segmentsDistal convoluted tubuleExaggerated natriuresisROMK null miceNa excretionFiltration rateRenal saltAbsolute excretionBartter's syndromeE syndromeMouse modelClearance studiesConvoluted tubulesAscending limbNull miceMouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins
Wagner CA, Loffing-Cueni D, Yan Q, Schulz N, Fakitsas P, Carrel M, Wang T, Verrey F, Geibel JP, Giebisch G, Hebert SC, Loffing J. Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins. American Journal Of Physiology. Renal Physiology 2008, 294: f1373-f1380. PMID: 18322017, DOI: 10.1152/ajprenal.00613.2007.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsBartter SyndromeCarrier ProteinsCation Transport ProteinsDinoprostoneDisease Models, AnimalEpithelial Sodium ChannelsKidney Tubules, DistalKidney Tubules, ProximalLoop of HenleMiceMice, Mutant StrainsPotassium Channels, Inwardly RectifyingReverse Transcriptase Polymerase Chain ReactionSodiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSodium-Phosphate Cotransporter Proteins, Type IIaSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1Up-RegulationWaterConceptsThick ascending limbBartter's syndromeBartter-like phenotypeType II Bartter's syndromeWild-type miceAntenatal Bartter syndromeWild-type littermatesROMK null micePlasma aldosteroneMaternal polyhydramniosRenal sodiumVolume depletionRenal tubulopathyMouse modelSemiquantitative immunoblottingProximal tubulesAscending limbKidney homogenatesSyndromeHenle's loopNull miceDCT cellsWater transport proteinsCompensatory mechanismsMice
2007
Reversal of renal tubule transporter downregulation during severe leptospirosis with antimicrobial therapy.
Spichler A, Ko AI, Silva EF, De Brito T, Silva AM, Athanazio D, Silva C, Seguro A. Reversal of renal tubule transporter downregulation during severe leptospirosis with antimicrobial therapy. American Journal Of Tropical Medicine And Hygiene 2007, 77: 1111-9. PMID: 18165532, DOI: 10.4269/ajtmh.2007.77.1111.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcysteineAmpicillinAnimalsAnti-Bacterial AgentsAntigens, BacterialCricetinaeDown-RegulationFemaleFree Radical ScavengersGene Expression ProfilingGene Expression RegulationKidneyLiverMesocricetusSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1ThiobarbituratesWeil DiseaseConceptsSevere leptospirosisAntimicrobial therapyN-acetylcysteineSerum thiobarbituric acidEvidence of benefitThick ascending limbNKCC2 transportersRenal involvementRenal expressionTubular dysfunctionAntioxidant therapyInfected hamstersTubular defectsNAC effectAscending limbAmpicillin treatmentRenal transportersTherapyTarget tissuesLeptospiral antigensAMP treatmentType 3Reduced levelsTransporter downregulationNormal expressionFunctional BSND Variants in Essential Hypertension*
Sile S, Gillani NB, Velez DR, Vanoye CG, Yu C, Byrne LM, Gainer JV, Brown NJ, Williams SM, George AL. Functional BSND Variants in Essential Hypertension*. American Journal Of Hypertension 2007, 20: 1176-1182. PMID: 17954364, DOI: 10.1016/j.amjhyper.2007.07.003.Peer-Reviewed Original ResearchConceptsThick ascending limbControl populationNormotensive control populationSodium chloride reabsorptionClC-Kb chloride channelsBlood pressure regulationLogistic regression analysisRenal salt reabsorptionChloride channelsNormotensive populationEssential hypertensionChloride reabsorptionHomogenous cohortStudy populationHypertensionAscending limbGhanaian subjectsSalt reabsorptionHispanic subjectsClC-KbCaucasian populationPartial lossSingle nucleotide polymorphismsRegression analysisRare variants
2006
The connecting tubule is the main site of the furosemide-induced urinary acidification by the vacuolar H+-ATPase
Kovacikova J, Winter C, Loffing-Cueni D, Loffing J, Finberg K, Lifton R, Hummler E, Rossier B, Wagner C. The connecting tubule is the main site of the furosemide-induced urinary acidification by the vacuolar H+-ATPase. Kidney International 2006, 70: 1706-1716. PMID: 16985514, DOI: 10.1038/sj.ki.5001851.Peer-Reviewed Original ResearchMeSH KeywordsAcid-Base EquilibriumAmilorideAnimalsDiureticsEpithelial Sodium ChannelsFurosemideGene Expression RegulationGene Expression Regulation, EnzymologicHydrochlorothiazideHydrogen-Ion ConcentrationKidney Tubules, CollectingKidney Tubules, DistalMetabolic Clearance RateMiceMice, KnockoutNephronsProton-Translocating ATPasesWater-Electrolyte BalanceConceptsUrinary acidificationRenal clearance experimentsEffect of furosemideNormal urinary acidificationLumen-negative voltageNet acid excretionThick ascending limbFinal urinary acidificationKidney-specific inactivationENaC channelsClearance experimentsAcid excretionMouse modelAscending limbFurosemideDuct cellsProton secretionMiceExact localizationReabsorptionMain siteB1 subunitAlpha subunitTubulesFunctional expressionCFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney
Lu M, Leng Q, Egan ME, Caplan MJ, Boulpaep EL, Giebisch GH, Hebert SC. CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney. Journal Of Clinical Investigation 2006, 116: 797-807. PMID: 16470247, PMCID: PMC1361349, DOI: 10.1172/jci26961.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCurcuminCyclic AMP-Dependent Protein KinasesCystic Fibrosis Transmembrane Conductance RegulatorHydrogen-Ion ConcentrationKidneyMiceMice, Inbred C57BLMice, Inbred CFTRMice, TransgenicMutationOocytesPatch-Clamp TechniquesPotassium Channels, Inwardly RectifyingXenopus laevisConceptsFunctional switchCystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channelATP sensitivityEffects of CFTRThick ascending limbPotential physiological rolePKA activityRenal K channelsCystic fibrosisPhysiological roleSecretory channelsK channelsRenal tubule epithelial cellsApical membraneCFTRDeltaF508 mutationDistal nephron segmentsCl- channelsK homeostasisTubule epithelial cellsEpithelial cellsTAL cellsPotassium channelsK handlingGlibenclamide sensitivity
2005
Immunolocalization of anion transporter Slc26a7 in mouse kidney
Dudas PL, Mentone S, Greineder CF, Biemesderfer D, Aronson PS. Immunolocalization of anion transporter Slc26a7 in mouse kidney. American Journal Of Physiology. Renal Physiology 2005, 290: f937-f945. PMID: 16263805, DOI: 10.1152/ajprenal.00197.2004.Peer-Reviewed Original ResearchConceptsThick ascending limbMouse kidneyProximal tubulesAscending limbThick ascending limb cellsLoop of HenleProximal tubule cellsSimilar staining patternExpression of SLC26A7Recent studiesTubule cellsNull miceNephron segmentsRat kidneyKidneyDifferent epitopesStaining patternMonoclonal antibodiesAntibodiesApical membrane transportersLimb cellsCOS-7 cellsImmunofluorescence microscopyLimbBasolateral surface
2003
ROMK is required for expression of the 70-pS K channel in the thick ascending limb
Lu M, Wang T, Yan Q, Wang W, Giebisch G, Hebert SC. ROMK is required for expression of the 70-pS K channel in the thick ascending limb. American Journal Of Physiology. Renal Physiology 2003, 286: f490-f495. PMID: 14600033, DOI: 10.1152/ajprenal.00305.2003.Peer-Reviewed Original ResearchConceptsThick ascending limbBartter's syndromeK dietK channelsAscending limbChannel activityApical K channelsFunctional expressionHypokalemic alkalosisTAL cellsNull miceSK activityHeterozygous miceHeterogeneous disorderMicePotassium recyclingROMKFunction mutationsSyndromeCritical subunitApical conductanceSalt absorptionLimbDietExpressionShort-term Stimulation of the Renal Na-K-Cl Cotransporter (NKCC2) by Vasopressin Involves Phosphorylation and Membrane Translocation of the Protein*
Giménez I, Forbush B. Short-term Stimulation of the Renal Na-K-Cl Cotransporter (NKCC2) by Vasopressin Involves Phosphorylation and Membrane Translocation of the Protein*. Journal Of Biological Chemistry 2003, 278: 26946-26951. PMID: 12732642, DOI: 10.1074/jbc.m303435200.Peer-Reviewed Original ResearchConceptsNa-K-Cl cotransporterRenal Na-K-Cl cotransporterCell membrane compartmentsRegulatory threonineMembrane compartmentsAntidiuretic hormone vasopressinPhosphospecific antibodiesMembrane translocationAmino terminusCytoplasmic vesiclesNKCC2 phosphorylationShort-term activationApical membranePhosphorylationTerm activationHormone vasopressinShort-term stimulationThick ascending limbProteinTranslocationCotransporterNKCC2ActivationAscending limbMorphometric analysis
2002
Cyclooxygenase-2 inhibitor blocks expression of mediators of renal injury in a model of diabetes and hypertension1
Cheng HF, Wang CJ, Moeckel GW, Zhang MZ, Mckanna JA, Harris RC. Cyclooxygenase-2 inhibitor blocks expression of mediators of renal injury in a model of diabetes and hypertension1. Kidney International 2002, 62: 929-939. PMID: 12164875, DOI: 10.1046/j.1523-1755.2002.00520.x.Peer-Reviewed Original ResearchConceptsCOX-2 expressionCOX-2 inhibitorsDiabetic groupRenal injuryDiabetic ratsImmunoreactive COX-2 expressionCortical thick ascending limbSelective COX-2 inhibitorsSystolic blood pressureModel of diabetesVascular endothelial growth factorDevelopment of glomerulosclerosisCOX-2 inhibitionThick ascending limbEndothelial growth factorMesangial sclerosis indexTubulointerstitial injuryDiabetic nephropathyBlood pressureChronic treatmentSubtotal nephrectomySclerosis indexBlood glucoseMacula densaRenal cortexAbsence of Small Conductance K+ Channel (SK) Activity in Apical Membranes of Thick Ascending Limb and Cortical Collecting Duct in ROMK (Bartter's) Knockout Mice*
Lu M, Wang T, Yan Q, Yang X, Dong K, Knepper MA, Wang W, Giebisch G, Shull GE, Hebert SC. Absence of Small Conductance K+ Channel (SK) Activity in Apical Membranes of Thick Ascending Limb and Cortical Collecting Duct in ROMK (Bartter's) Knockout Mice*. Journal Of Biological Chemistry 2002, 277: 37881-37887. PMID: 12130653, PMCID: PMC4426997, DOI: 10.1074/jbc.m206644200.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsBartter SyndromeBase SequenceCell MembraneDisease Models, AnimalDNA PrimersGene Expression RegulationGenotypeHumansKidneyKidney CortexKidney Tubules, CollectingMiceMice, KnockoutPotassium ChannelsPotassium Channels, Calcium-ActivatedPotassium Channels, Inwardly RectifyingPotassium ChlorideSmall-Conductance Calcium-Activated Potassium ChannelsSurvival AnalysisConceptsThick ascending limbSK channel activityROMK null miceBartter's syndromeNull miceSK channelsAscending limbChannel activityExtracellular volume depletionROMK geneCortical collecting ductsWild-type littermatesAbsorption/secretionROMK knockout miceNull mice exhibitPatch-clamp analysisSmall conductanceSignificant hydronephrosisRenal morphologyVolume depletionKnockout miceMice exhibitSyndromeCollecting ductsNaCl reabsorptionGlucagon Acutely Inhibits but Chronically Activates Na+/H+ Antiporter 3 Activity in OKP Cells
Amemiya M, Kusano E, Muto S, Tabei K, Ando Y, Alpern RJ, Asano Y. Glucagon Acutely Inhibits but Chronically Activates Na+/H+ Antiporter 3 Activity in OKP Cells. Experimental Nephrology 2002, 10: 26-33. PMID: 11803202, DOI: 10.1159/000049895.Peer-Reviewed Original ResearchConceptsNHE3 protein abundanceOKP cellsNHE3 activityCell pH recoveryRat renal proximal tubulesDibutyryl cAMPThick ascending limbRenal proximal tubulesWestern blot analysisM dibutyryl-cAMPChronic activationPKA-dependent pathwayProximal tubulesAscending limbGlucagonSurface membraneAcid loadNHE3 mRNAProtein abundancePH recoveryExchanger 3Independent mechanismsSignificant increaseBlot analysisP cells
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply