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 changesTransplantation
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 strategyExcretion
2019
Tumor 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 domain
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