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1. Amiloride versus furosemide for the treatment of edema in patients with nephrotic syndrome: A pilot study (AMILOR).

2. SGLT2 Inhibitors Correct Fluid Overload in Adult Kidney Transplant Recipients-A Prospective Observational Study.

3. SGLT2 Inhibitors Decrease Overhydration and Proteasuria in Patients with Chronic Kidney Disease: A Longitudinal Observational Study.

5. Two cases of severe vitamin D 3 intoxication treated with therapeutic plasma exchange and high cut-off hemodialysis.

6. Rodent models to study sodium retention in experimental nephrotic syndrome.

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

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

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

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

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

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

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

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

18. Proteasuria in nephrotic syndrome-quantification and proteomic profiling.

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

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

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

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

24. Proteasuria-The impact of active urinary proteases on sodium retention in nephrotic syndrome.

25. Plasma kallikrein activates the epithelial sodium channel in vitro but is not essential for volume retention in nephrotic mice.

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

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

28. Impact of phosphorus restriction and vitamin D-substitution on secondary hyperparathyroidism in a proteinuric mouse model.

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