Abstract
Albuminuria is a risk factor for progression of kidney disease. Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers slow the progression to ESRD, an effect that is correlated with reduction in albuminuria. This has led to the hypothesis that albuminuria should be a target for therapy. This work argues that there are issues with this hypothesis. The previously reported studies were not designed to test the hypothesis that achieving a specific albuminuria target would be beneficial in and of itself irrespective the mechanism used to achieve that goal. One cannot assume that the beneficial effect observed was causally related to the effect on albuminuria or that it would extend to other interventions. Most importantly, it is not known if the approach of maximizing therapy to reduce proteinuria is safe. Recent studies have shown that combining renin-angiotensin system therapies decreases albuminuria without significant clinical benefit but with increased risk of adverse events. More studies are needed, but at this time, albuminuria has not jumped the hurdle needed to be accepted as a surrogate end point or target for treatment. Primum non nocere, first do no harm.