Das Klinikum

Dr. med. Daniel Essigke

Dr. med. Daniel Essigke

Arzt in Weiterbildung

Sektion für Nieren- und Hochdruckkrankheiten

Kontakt

Telefonnummer: 07071 29-83172

E-Mail-Adresse: daniel.essigke@med.uni-tuebingen.de

Klinik / Institut / Zentrum

  • Abstractpreis der Deutschen Gesellschaft für Nephrologie bei der 10. Jahrestagung 2018
  • Abstractpreis der Deutschen Gesellschaft für Nephrologie bei der 12. Jahrestagung 2020
  • Essigke D, Bohnert BN, Janessa A, Wörn M, Omage K, Kalbacher H, Birkenfeld AL, Bugge TH, Szabo R, Artunc F. Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity. Pflugers Arch. 2022 Jun;474(6):613-624. doi: 10.1007/s00424-022-02682-y. Epub 2022 Mar 21. PMID: 35312839; PMCID: PMC9117342.
  • Essigke D, Ilyaskin AV, Wörn M, Bohnert BN, Xiao M, Daniel C, Amann K, Birkenfeld AL, Szabo R, Bugge TH, Korbmacher C, Artunc F. Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice. Acta Physiol (Oxf). 2021 May;232(1):e13640. doi: 10.1111/apha.13640. Epub 2021 Mar 11. PMID: 33650216; PMCID: PMC8159854.
  • Bohnert BN, Essigke D, Janessa A, Schneider JC, Wörn M, Kalo MZ, Xiao M, Kong L, Omage K, Hennenlotter J, Amend B, Birkenfeld AL, Artunc F. Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na+ channel in the mouse kidney. Am J Physiol Renal Physiol. 2021 Oct 1;321(4):F480-F493. doi: 10.1152/ajprenal.00199.2021. Epub 2021 Aug 23. PMID: 34423678.
  • Bissinger R, Nemkov T, D Alessandro A, Grau M, Dietz T, Bohnert BN, Essigke D, Wörn M, Schaefer L, Xiao M, Beirne JM, Kalo MZ, Schork A, Bakchoul T, Omage K, Kong L, Gonzalez-Menendez I, Quintanilla-Martinez L, Fehrenbacher B, Schaller M, Dhariwal A, Birkenfeld AL, Grahammer F, Qadri SM, Artunc F. Proteinuric chronic kidney disease is associated with altered red blood cell lifespan, deformability and metabolism. Kidney Int. 2021 Sep 16:S0085-2538(21)00858-9. doi: 10.1016/j.kint.2021.08.024. Epub ahead of print. PMID: 34537228.
  • Xiao M, Bohnert BN, Aypek H, Kretz O, Grahammer F, Aukschun U, Wörn M, Janessa A, Essigke D, Daniel C, Amann K, Huber TB, Plow EF, Birkenfeld AL, Artunc F. Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome. Acta Physiol (Oxf). 2021 Jan;231(1):e13512. doi: 10.1111/apha.13512. Epub 2020 Jun 10. PMID: 32455507; PMCID: PMC7688481.F
  • Bohnert BN, Daiminger S, Wörn M, Sure F, Staudner T, Ilyaskin AV, Batbouta F, Janessa A, Schneider JC, Essigke D, Kanse S, Haerteis S, Korbmacher C, Artunc F. Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndrome. Acta Physiol (Oxf). 2019 Dec;227(4):e13286. doi: 10.1111/apha.13286. Epub 2019 May 20. PMID: 31006168.
  • Haerteis S, Schork A, Dörffel T, Bohnert BN, Nacken R, Wörn M, Xiao M, Essigke D, Janessa A, Schmaier AH, Feener EP, Häring HU, Bertog M, Korbmacher C, Artunc F. Plasma kallikrein activates the epithelial sodium channel in vitro but is not essential for volume retention in nephrotic mice. Acta Physiol (Oxf). 2018 Sep;224(1):e13060. doi: 10.1111/apha.13060. Epub 2018 Mar 25. PMID: 29489063.
  • Publikationen