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Albuminuria is Not an Appropriate Therapeutic Target in Patients with CKD: The Con View
1Renal Section, Veterans Affairs Pittsburgh Healthcare System and Departments of Medicine and Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania; and Linda.Fried@va.gov.
Insights
Albuminuria is a risk factor for kidney disease progression. However, current evidence does not support using albuminuria as a direct therapeutic target due to unproven benefits and potential harms.
Area of Science:
- Nephrology
- Pharmacology
Background:
- Albuminuria is a known risk factor for chronic kidney disease (CKD) progression.
- Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs) slow CKD progression, correlating with reduced albuminuria.
Purpose of the Study:
- To critically evaluate the hypothesis that albuminuria should be a therapeutic target for kidney disease.
- To assess the safety and efficacy of targeting albuminuria irrespective of the therapeutic mechanism.
Main Methods:
- Review of existing studies on ACEi and ARB therapies in kidney disease.
- Analysis of recent combination therapies targeting the renin-angiotensin system (RAS).
Main Results:
- Previous studies were not designed to isolate the effect of albuminuria reduction as a standalone therapeutic goal.
- Combining RAS therapies reduces albuminuria but lacks significant clinical benefit and increases adverse events.
- The causal relationship between albuminuria reduction and improved kidney outcomes remains unproven.
Conclusions:
- Albuminuria has not met the criteria to be accepted as a surrogate endpoint or therapeutic target in kidney disease.
- Further research is needed to establish the safety and efficacy of targeting albuminuria.
- The principle of 'first, do no harm' (primum non nocere) should guide treatment decisions.
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.
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