2023
Strikingly conserved gene expression changes of polyamine regulating enzymes among various forms of acute and chronic kidney injury
Sieckmann T, Schley G, Ögel N, Kelterborn S, Boivin F, Fähling M, Ashraf M, Reichel M, Vigolo E, Hartner A, Lichtenberger F, Breiderhoff T, Knauf F, Rosenberger C, Aigner F, Schmidt-Ott K, Scholz H, Kirschner K. Strikingly conserved gene expression changes of polyamine regulating enzymes among various forms of acute and chronic kidney injury. Kidney International 2023, 104: 90-107. PMID: 37121432, DOI: 10.1016/j.kint.2023.04.005.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryKidney injuryKidney pathologyExperimental kidney injuryChronic kidney injuryUnilateral ureteral obstructionForms of injuryPolyamine synthesisCyclosporine treatmentArterial hypertensionKidney transplantationUreteral obstructionKidney levelsTissue injuryTubular castsHealthy kidneysHomeostasis contributesInjuryKidneyExperimental modelKidney cell linePutrescine contentReduced expressionGene expression changesTransplantationSLC26A1 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
2019
P2X7 Receptor Stimulation Is Not Required for Oxalate Crystal-Induced Kidney Injury
Luz H, Reichel M, Unwin R, Mutig K, Najenson A, Tonner L, Eckardt K, Tam F, Knauf F. P2X7 Receptor Stimulation Is Not Required for Oxalate Crystal-Induced Kidney Injury. Scientific Reports 2019, 9: 20086. PMID: 31882798, PMCID: PMC6934555, DOI: 10.1038/s41598-019-56560-2.Peer-Reviewed Original ResearchConceptsIL-1ß releaseDendritic cellsKidney failureP2X7 receptorBone marrowNLRP3/CASPP2X7 receptor signalingProgressive kidney diseaseSuitable therapeutic targetProgressive kidney failureMonosodium urate crystalsHuman peripheral bloodKidney injuryRenal inflammationRenal injuryTubular damageWT miceIL-1ßKidney diseasePeripheral bloodCytokine releasePlasma creatinineMurine bone marrowInterleukin-1betaInflammasome activationTumor necrosis factor stimulates fibroblast growth factor 23 levels in chronic kidney disease and non-renal inflammation
Egli-Spichtig D, Imenez Silva P, Glaudemans B, Gehring N, Bettoni C, Zhang M, Pastor-Arroyo E, Schönenberger D, Rajski M, Hoogewijs D, Knauf F, Misselwitz B, Frey-Wagner I, Rogler G, Ackermann D, Ponte B, Pruijm M, Leichtle A, Fiedler G, Bochud M, Ballotta V, Hofmann S, Perwad F, Föller M, Lang F, Wenger R, Frew I, Wagner C. Tumor necrosis factor stimulates fibroblast growth factor 23 levels in chronic kidney disease and non-renal inflammation. Kidney International 2019, 96: 890-905. PMID: 31301888, DOI: 10.1016/j.kint.2019.04.009.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsCell LineCohort StudiesDisease Models, AnimalFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsHumansInflammatory Bowel DiseasesInterleukin-10KidneyMaleMiceMice, TransgenicMiddle AgedNuclear Receptor Subfamily 4, Group A, Member 2Primary Cell CultureRenal Insufficiency, ChronicTumor Necrosis Factor-alphaConceptsChronic kidney diseaseTumor necrosis factorPlasma FGF23Kidney diseaseFGF23 expressionFGF23 levelsNecrosis factorGrowth factor 23 levelsFibroblast growth factor 23Inflammatory cytokines tumor necrosis factorCytokines tumor necrosis factorInflammatory bowel diseaseGrowth factor 23Normal kidney functionIL10-deficient micePopulation-based cohortAntibody-mediated neutralizationOrphan nuclear receptor Nurr1Nuclear receptor Nurr1Cause mortalityRenal inflammationTNF neutralizationBowel diseaseFactor 23Kidney function
2016
Oxalate, 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 domainLoss 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) geneHyperoxaluriaPatientsOxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice
Mulay SR, Eberhard JN, Pfann V, Marschner JA, Darisipudi MN, Daniel C, Romoli S, Desai J, Grigorescu M, Kumar SV, Rathkolb B, Wolf E, Hrabě de Angelis M, Bäuerle T, Dietel B, Wagner CA, Amann K, Eckardt KU, Aronson PS, Anders HJ, Knauf F. Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice. American Journal Of Physiology. Renal Physiology 2016, 310: f785-f795. PMID: 26764204, PMCID: PMC5504458, DOI: 10.1152/ajprenal.00488.2015.Peer-Reviewed Original ResearchConceptsC57BL/6 miceChronic kidney disease researchOxalate-rich dietChronic kidney diseaseFemale C57BL/6 miceArterial hypertensionCardiovascular complicationsKidney disease researchAtubular glomeruliInterstitial inflammationRenal histologyTubular damageKidney diseaseCardiac fibrosisMetabolic acidosisNormochromic anemiaTissue involvementHistological changesHuman CKDCKDExperimental animalsComplicationsInducible modelControl dietFibrosis
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
Sat1 is dispensable for active oxalate secretion in mouse duodenum
Ko N, Knauf F, Jiang Z, Markovich D, Aronson PS. Sat1 is dispensable for active oxalate secretion in mouse duodenum. American Journal Of Physiology - Cell Physiology 2012, 303: c52-c57. PMID: 22517357, PMCID: PMC3404526, DOI: 10.1152/ajpcell.00385.2011.Peer-Reviewed Original ResearchConceptsCalcium oxalate stonesMouse duodenumOxalate secretionOxalate stonesIntestinal oxalate secretionIntestinal oxalate transportSecretory fluxSAT1 expressionDisulfonic stilbene DIDSDuodenumTransporter 1SecretionMiceHyperoxalemiaBasolateral solutionHyperoxaluriaBasolateral transportersBicarbonate productionOxalate transportBasolateral membraneSAT1Apical membraneComplete removalMedium concentration
2011
Net Intestinal Transport of Oxalate Reflects Passive Absorption and SLC26A6-mediated Secretion
Knauf F, Ko N, Jiang Z, Robertson WG, Van Itallie CM, Anderson JM, Aronson PS. Net Intestinal Transport of Oxalate Reflects Passive Absorption and SLC26A6-mediated Secretion. Journal Of The American Society Of Nephrology 2011, 22: 2247-2255. PMID: 22021714, PMCID: PMC3250206, DOI: 10.1681/asn.2011040433.Peer-Reviewed Original Research
2001
Identification of a chloride-formate exchanger expressed on the brush border membrane of renal proximal tubule cells
Knauf F, Yang C, Thomson R, Mentone S, Giebisch G, Aronson P. Identification of a chloride-formate exchanger expressed on the brush border membrane of renal proximal tubule cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2001, 98: 9425-9430. PMID: 11459928, PMCID: PMC55437, DOI: 10.1073/pnas.141241098.Peer-Reviewed Original ResearchMeSH Keywords4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAmino Acid SequenceAnimalsAntiportersBase SequenceCloning, MolecularCOS CellsDNA PrimersDNA, ComplementaryFemaleKidney Tubules, ProximalMiceMice, Inbred C57BLMicroscopy, FluorescenceMicrovilliMolecular Sequence DataSodium-Phosphate Cotransporter Proteins, Type IIaXenopus laevis