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 ResearchConceptsIL-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
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 strategyExcretionAuthors’ Reply: Calcium-Based Phosphate Binders and Plasma Oxalate Concentration in Dialysis Patients
Pfau A, Knauf F. Authors’ Reply: Calcium-Based Phosphate Binders and Plasma Oxalate Concentration in Dialysis Patients. Journal Of The American Society Of Nephrology 2022, 33: 1428-1428. PMID: 35500939, PMCID: PMC9257799, DOI: 10.1681/asn.2022030359.Peer-Reviewed Original Research
2020
Stiripentol fails to lower plasma oxalate in a dialysis-dependent PH1 patient
Kempf C, Pfau A, Holle J, Müller-Schlüter K, Bufler P, Knauf F, Müller D. Stiripentol fails to lower plasma oxalate in a dialysis-dependent PH1 patient. Pediatric Nephrology 2020, 35: 1787-1789. PMID: 32418144, PMCID: PMC7385015, DOI: 10.1007/s00467-020-04585-5.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseChronic kidney diseaseLactate dehydrogenase 5Urinary oxalateAdvanced chronic kidney diseaseAnti-convulsive drugsMultisystemic metabolic disorderLiver-kidney transplantationMajority of patientsCurrent standard treatmentTreatment of childrenHyperoxaluria type 1Anuric infantsPH patientsUox excretionRenal diseaseDravet syndromeKidney diseasePrimary hyperoxaluriaCompassionate useStandard treatmentPlasma concentrationsMetabolic disordersPromising drugEarly infancy
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 activation
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
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