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
2021
Determinants and Outcomes Associated With Urinary Calcium Excretion in Chronic Kidney Disease
Liu J, Tio M, Verma A, Schmidt I, Ilori T, Knauf F, Mc Causland F, Waikar S. Determinants and Outcomes Associated With Urinary Calcium Excretion in Chronic Kidney Disease. The Journal Of Clinical Endocrinology & Metabolism 2021, 107: e281-e292. PMID: 34390334, PMCID: PMC8684460, DOI: 10.1210/clinem/dgab574.Peer-Reviewed Original ResearchConceptsUrinary calcium excretionChronic kidney diseaseEnd-stage kidney diseaseCalcium excretionKidney diseaseChronic Renal Insufficiency Cohort (CRIC) StudyIncident end-stage kidney diseaseLevel of CKDSelf-identified black raceAtherosclerotic cardiovascular disease eventsSerum parathyroid hormoneCardiovascular disease eventsAdverse clinical eventsAdverse clinical outcomesStage kidney diseaseBaseline eGFRCKD progressionUrinary sodiumCause mortalityCohort studyLoop diureticsThiazide diureticsClinical outcomesParathyroid hormoneVascular calcification
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
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 functionChallenges to hypertension and diabetes management in rural Uganda: a qualitative study with patients, village health team members, and health care professionals
Chang H, Hawley NL, Kalyesubula R, Siddharthan T, Checkley W, Knauf F, Rabin TL. Challenges to hypertension and diabetes management in rural Uganda: a qualitative study with patients, village health team members, and health care professionals. International Journal For Equity In Health 2019, 18: 38. PMID: 30819193, PMCID: PMC6394065, DOI: 10.1186/s12939-019-0934-1.Peer-Reviewed Original ResearchConceptsHealth care professionalsVillage health team membersHealth team membersCare professionalsRural UgandaPrevalence of hypertensionCommunity health workersIndividual health care professionalsUgandan health care systemHealth care systemLifestyle factorsDiabetes careDM managementHealth workersHypertensionPatientsNakaseke districtHealth system reformPreventable aspectsMedication accessibilityCare systemLack of awarenessRural settingsPotential roleDiabetes
2018
Characterization of renal NaCl and oxalate transport in Slc26a6−/− mice
Knauf F, Velazquez H, Pfann V, Jiang Z, Aronson PS. Characterization of renal NaCl and oxalate transport in Slc26a6−/− mice. American Journal Of Physiology. Renal Physiology 2018, 316: f128-f133. PMID: 30427220, PMCID: PMC6383200, DOI: 10.1152/ajprenal.00309.2018.Peer-Reviewed Original ResearchConceptsWild-type miceNaCl homeostasisBlood pressureProximal tubulesFree-flow micropuncture studiesSurface proximal tubulesLow-salt dietMean blood pressureLower blood pressureUrine flow rateLack of effectFurosemide infusionNet renal secretionSodium excretionUrine oxalateFractional excretionMicropuncture studiesNaCl deliveryRenal secretionApical membrane ClExchanger SLC26A6MiceRenal NaClNaCl transportHomeostasis
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