Key result
Intravenous dipyridamole acutely decreased urinary protein loss and filtration fraction in salt-depleted patients with nephrotic syndrome, suggesting efferent vasodilation.
Why the study?
Does intravenous dipyridamole reduce proteinuria and alter renal hemodynamics in salt-depleted patients with nephrotic syndrome?
Does intravenous dipyridamole reduce proteinuria and alter renal hemodynamics in salt-depleted patients with nephrotic syndrome?
Intravenous dipyridamole acutely reduces proteinuria in nephrotic syndrome, likely mediated by efferent vasodilation and decreased intraglomerular capillary pressure.
We studied the acute antiproteinuric and renal hemodynamic effect of dipyridamole 30-60 mg intravenously in 13 salt-depleted patients with the nephrotic syndrome of different etiology. Whereas mean arterial pressure did not change, a small fall in glomerular filtration rate with a concomitant fall in filtration fraction and a decrease in urinary protein loss occurred. The fall in filtration fraction was positively correlated with the fall in proteinuria. This suggests that the antiproteinuric effect of dipyridamole is at least partly due to an efferent vasodilation with a fall in intraglomerular capillary pressure.
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Jong et al. (2008) studied Nephrotic syndrome (n=13). Dipyridamole was evaluated on Acute antiproteinuric and renal hemodynamic effect. Intravenous dipyridamole acutely decreased urinary protein loss and filtration fraction in salt-depleted patients with nephrotic syndrome, suggesting efferent vasodilation.
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