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Proteasuria—The impact of active urinary proteases on sodium retention in nephrotic syndrome

Acta Physiologica, 2019-04, Vol.225 (4), p.e13249-n/a

2019

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Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndrome

Kidney international, 2018-01, Vol.93 (1), p.159-172

2018

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79-year-old female patient with nephrotic-range proteinuria

Deutsche medizinische Wochenschrift (1946), 2022-04, Vol.147 (7), p.377

2022

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Renal effects of the serine protease inhibitor aprotinin in healthy conscious mice

Acta pharmacologica Sinica, 2022-01, Vol.43 (1), p.111-120

2022

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SGLT2 inhibitors decrease overhydration and proteasuria in patients with chronic kidney disease: a longitudinal observational study

Kidney & blood pressure research, 2024-01, p.1-1

2024

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Overhydration Measured by Bioimpedance Spectroscopy and Urinary Serine Protease Activity Are Risk Factors for Progression of Chronic Kidney Disease

Kidney & blood pressure research, 2020-12, Vol.45 (6), p.955-968

2020

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Essential role of DNA-PKcs and plasminogen for the development of doxorubicin-induced glomerular injury in mice

Disease models & mechanisms, 2021-09, Vol.14 (9)

2021

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Rodent models to study sodium retention in experimental nephrotic syndrome

Acta Physiologica, 2022-07, Vol.235 (3), p.e13844-n/a

2022

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Impact of Phosphorus Restriction and Vitamin D-Substitution on Secondary Hyperparathyroidism in a Proteinuric Mouse Model

Kidney & blood pressure research, 2015-01, Vol.40 (2), p.153-165

2015

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Rebuttal to editorial: Sodium retention by uPA in nephrotic syndrome?

Acta Physiologica, 2020-04, Vol.228 (4), p.e13427-n/a

2020

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Organ Donation From a Brain Dead Donor With Vaccine-induced Immune Thrombotic Thrombocytopenia After Ad26.COV2.S: The Risk of Organ Microthrombi

Transplantation, 2022-03, Vol.106 (3), p.e178

2022

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Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin

Journal of visualized experiments, 2018-05 (135)

2018

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The Case | A 74-year-old liver transplant recipient with nephrotic-range proteinuria

Kidney international, 2021-04, Vol.99 (4), p.1031-1032

2021

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Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice

Pflügers Archiv, 2022-02, Vol.474 (2), p.217-229

2022

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Proteasuria in nephrotic syndrome–quantification and proteomic profiling

Journal of proteomics, 2021-01, Vol.230, p.103981, Article 103981

2021

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Two cases of severe vitamin D3 intoxication treated with therapeutic plasma exchange and high cut-off hemodialysis

Journal of nephrology, 2023-06, Vol.36 (5), p.1461-1467

2023

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Urokinase‐type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)‐mediated sodium retention in experimental nephrotic syndrome

Acta Physiologica, 2019-12, Vol.227 (4), p.e13286-n/a

2019

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Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na + channel in the mouse kidney

American journal of physiology. Renal physiology, 2021-10, Vol.321 (4), p.F480-F493

2021

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Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome

Acta Physiologica, 2021-01, Vol.231 (1), p.e13512-n/a

2021

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Zymogen‐locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice

Acta Physiologica, 2021-05, Vol.232 (1), p.e13640-n/a

2021

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Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity

Pflügers Archiv, 2022-06, Vol.474 (6), p.613-624

2022

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Retrobulbar Sinus Injection of Doxorubicin is More Efficient Than Lateral Tail Vein Injection at Inducing Experimental Nephrotic Syndrome in Mice: A Pilot Study

Laboratory animals (London), 2019-12, Vol.53 (6), p.564-576

2019

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First person – Bernhard N. Bohnert

Disease models & mechanisms, 2021-09, Vol.14 (9)

2021

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The authors reply

Kidney international, 2022-03, Vol.101 (3), p.649-650

2022

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Proteasuria—The impact of active urinary proteases on sodium retention in nephrotic syndrome

Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndrome

79-year-old female patient with nephrotic-range proteinuria

Renal effects of the serine protease inhibitor aprotinin in healthy conscious mice

SGLT2 inhibitors decrease overhydration and proteasuria in patients with chronic kidney disease: a longitudinal observational study

Overhydration Measured by Bioimpedance Spectroscopy and Urinary Serine Protease Activity Are Risk Factors for Progression of Chronic Kidney Disease

Essential role of DNA-PKcs and plasminogen for the development of doxorubicin-induced glomerular injury in mice

Rodent models to study sodium retention in experimental nephrotic syndrome

Impact of Phosphorus Restriction and Vitamin D-Substitution on Secondary Hyperparathyroidism in a Proteinuric Mouse Model

Rebuttal to editorial: Sodium retention by uPA in nephrotic syndrome?

Organ Donation From a Brain Dead Donor With Vaccine-induced Immune Thrombotic Thrombocytopenia After Ad26.COV2.S: The Risk of Organ Microthrombi

Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin

Proteinuric chronic kidney disease is associated with altered red blood cell lifespan, deformability and metabolism

The Case | A 74-year-old liver transplant recipient with nephrotic-range proteinuria

Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice

Proteasuria in nephrotic syndrome–quantification and proteomic profiling

Two cases of severe vitamin D3 intoxication treated with therapeutic plasma exchange and high cut-off hemodialysis

Urokinase‐type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)‐mediated sodium retention in experimental nephrotic syndrome

Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na + channel in the mouse kidney

Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome

Zymogen‐locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice

Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity

Retrobulbar Sinus Injection of Doxorubicin is More Efficient Than Lateral Tail Vein Injection at Inducing Experimental Nephrotic Syndrome in Mice: A Pilot Study

First person – Bernhard N. Bohnert

The authors reply

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