In patients with renal diseases characterized by proteinuria, the initial insult to the kidney is usually followed by a progressive decline in the glomerular filtration rate. This decline has been thought to be due to changes in renal hemodynamics initiated by the loss of nephrons.¹ When renal mass is reduced in rats, the remaining nephrons undergo sudden hypertrophy, with a concomitant lowering of arteriolar resistance and an increase in glomerular plasma flow.²,³ Afferent arteriolar tone decreases more than efferent arteriolar tone, and therefore, the hydraulic pressure in glomerular capillaries rises⁴ and the amount of filtrate formed by each nephron . . .