Angiotensin II (Ang II) blockade and restriction of dietary protein are thought to retard progression of renal disease primarily by reducing glomerular capillary pressure and thereby reducing injury to renal tissues. Relatively recent data suggest that both of these therapies may also act through pressure-independent mechanisms to reduce repair processes that follow tissue injury and which, if not self-limited, can continue to cause tissue fibrosis and organ failure. We review recent data suggesting that Ang II is a profibrotic molecule independent of blood pressure. Therapeutic actions of dietary restriction of total protein and restriction of the amino acid L-arginine that appear independent of pressure are also discussed. These effects are separated into those that reduce injury and those that reduce tissue repair. Finally, we ask whether the Ang II blockade or restriction of dietary protein could be more effective if they were aimed not only at limiting injury, but also at halting excessive repair.