Key result
Oral N-acetyl-D-mannosamine reduces proteinuria by over 40%, and intravenous recombinant mutated human Angptl4 reduces proteinuria by up to 65% in experimental models of glomerular disease.
Why the study?
Do Angptl4-based therapeutics (ManNAc or recombinant mutant Angptl4) reduce proteinuria in experimental models of glomerular disease?
Population
Experimental models of glomerular disease and human minimal change disease/nephrotic syndrome
Design
Review
Authors
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Hypothesis-generating for Angptl4-based agents in glomerular disease; prospective human trials needed before clinical adoption.
Do Angptl4-based therapeutics (ManNAc or recombinant mutant Angptl4) reduce proteinuria in experimental models of glomerular disease?
Angptl4-based therapeutics, including ManNAc and recombinant mutant Angptl4, represent promising novel, mechanism-based treatments for reducing proteinuria in chronic kidney disease.
Chugh et al. (2014) conducted a review in Proteinuria and kidney disease. Angiopoietin-like 4 based therapeutics (N-acetyl-D-mannosamine and recombinant Angptl4 mutants) was evaluated. Oral N-acetyl-D-mannosamine reduces proteinuria by over 40%, and intravenous recombinant mutated human Angptl4 reduces proteinuria by up to 65% in experimental models of glomerular disease.