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Bernhard N Bohnert

Showing results (21-30 of 33) with videos related to

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Kidney & Blood Pressure Research|January 16, 2024
SGLT2 Inhibitors Decrease Overhydration and Proteasuria in Patients with Chronic Kidney Disease: A Longitudinal Observational StudyAnja Schork, Marie-Luise Eberbach, Bernhard N Bohnert, et al.
Transplant International : Official Journal of the European Society for Organ Transplantation|June 25, 2024
SGLT2 Inhibitors Correct Fluid Overload in Adult Kidney Transplant Recipients-A Prospective Observational StudyAnja Schork, Marie-Luise Eberbach, Ferruh Artunc, et al.
Pflugers Archiv : European Journal of Physiology|January 3, 2026
Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndromeDaniel Essigke, M Zaher Kalo, Lingsi Kong, et al.
Kidney International Reports|April 14, 2025
GFR is a Key Determinant of Red Blood Cell Survival in Anemia Associated With Progressive CKDRosi Bissinger, Lina Schaefer, Bernhard N Bohnert, et al.
Research Square|September 5, 2025
Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndromeDaniel Essigke, M Zaher Kalo, Lingsi Kong, et al.
Acta Physiologica (Oxford, England)|March 2, 2021
Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in miceDaniel Essigke, Alexandr V Ilyaskin, Matthias Wörn, et al.
American Journal of Physiology. Renal Physiology|August 23, 2021
Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na<sup>+</sup> channel in the mouse kidneyBernhard N Bohnert, Daniel Essigke, Andrea Janessa, et al.
Acta Physiologica (Oxford, England)|April 22, 2019
Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndromeBernhard N Bohnert, Sophie Daiminger, Matthias Wörn, et al.
Kidney International|October 19, 2017
Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndromeBernhard N Bohnert, Martina Menacher, Andrea Janessa, et al.
Acta Physiologica (Oxford, England)|May 27, 2020
Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndromeMengyun Xiao, Bernhard N Bohnert, Hande Aypek, et al.
Pageof 4

Showing results (21-30 of 33) with videos related to

Sort By:
Pageof 4
Kidney & Blood Pressure Research|January 16, 2024
SGLT2 Inhibitors Decrease Overhydration and Proteasuria in Patients with Chronic Kidney Disease: A Longitudinal Observational StudyAnja Schork, Marie-Luise Eberbach, Bernhard N Bohnert, et al.
Transplant International : Official Journal of the European Society for Organ Transplantation|June 25, 2024
SGLT2 Inhibitors Correct Fluid Overload in Adult Kidney Transplant Recipients-A Prospective Observational StudyAnja Schork, Marie-Luise Eberbach, Ferruh Artunc, et al.
Pflugers Archiv : European Journal of Physiology|January 3, 2026
Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndromeDaniel Essigke, M Zaher Kalo, Lingsi Kong, et al.
Kidney International Reports|April 14, 2025
GFR is a Key Determinant of Red Blood Cell Survival in Anemia Associated With Progressive CKDRosi Bissinger, Lina Schaefer, Bernhard N Bohnert, et al.
Research Square|September 5, 2025
Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndromeDaniel Essigke, M Zaher Kalo, Lingsi Kong, et al.
Acta Physiologica (Oxford, England)|March 2, 2021
Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in miceDaniel Essigke, Alexandr V Ilyaskin, Matthias Wörn, et al.
American Journal of Physiology. Renal Physiology|August 23, 2021
Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na<sup>+</sup> channel in the mouse kidneyBernhard N Bohnert, Daniel Essigke, Andrea Janessa, et al.
Acta Physiologica (Oxford, England)|April 22, 2019
Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndromeBernhard N Bohnert, Sophie Daiminger, Matthias Wörn, et al.
Kidney International|October 19, 2017
Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndromeBernhard N Bohnert, Martina Menacher, Andrea Janessa, et al.
Acta Physiologica (Oxford, England)|May 27, 2020
Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndromeMengyun Xiao, Bernhard N Bohnert, Hande Aypek, et al.
Pageof 4