Key result
Endothelium-dependent relaxation was significantly reduced in MWF rats compared to LEW or FHH rats (p < 0.05), indicating that proteinuria alone is insufficient to cause endothelial dysfunction.
Population
26-week-old inbred rat strains with genetic proteinuria and without proteinuric renal disease
Comparison
Munich Wistar Fromter and fawn-hooded… vs Lewis (LEW) rats without proteinuric renal disease
Design
Preclinical
Authors
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Proteinuria alone may not drive endothelial dysfunction; leaves open strain-specific factors as mediators in renal disease models.
p-value: p=<0.05
Proteinuria alone does not universally cause endothelial dysfunction, indicating that additional strain-specific deleterious factors are required for vascular damage in renal disease.
Ulu et al. (2009) studied Proteinuria-associated endothelial dysfunction. Genetic proteinuria (MWF and FHH strains) vs. Lewis (LEW) rats without proteinuric renal disease was evaluated on Aortic endothelial function (endothelium-dependent relaxation) (p=<0.05). Endothelium-dependent relaxation was significantly reduced in MWF rats compared to LEW or FHH rats (p < 0.05), indicating that proteinuria alone is insufficient to cause endothelial dysfunction.
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