The Value of Albuminuria in Heart Failure Risk Assessment, with Javed Butler, MD, MBA

Albuminuria, measured as the urine albumin-to-creatinine ratio (UACR), is drawing renewed attention in cardiology as a marker that sits at the intersection of kidney and cardiovascular risk.

It rises before the glomerular filtration rate declines, making it an early signal of chronic kidney disease, and it also reflects systemic vascular endothelial dysfunction. Together, those properties position UACR as both an indirect cardiovascular risk factor, through chronic kidney disease, and a direct marker of vascular disease.

The clinical case for measuring UACR in patients with or at risk for heart failure parallels how cardiology absorbed lipids and blood pressure into routine practice. The therapies prescribed for early chronic kidney disease, including MRAs, SGLT2 inhibitors, GLP-1 receptor agonists, and ACE inhibitors, lower UACR and reduce the risk of developing heart failure. That overlap is an argument for folding UACR into routine risk assessment now, even before guideline-directed targets are established.

A more difficult question for cardiology is whether therapy should be titrated to a UACR goal. In the most recent 2026 AHA/ACC/ADA/ASN Guideline for the Prevention, Detection, Evaluation, and Management of Cardiovascular-Kidney-Metabolic Syndrome, the organizations endorse both eGFR and UACR testing for characterizing chronic kidney disease and guiding treatment decisions. The nephrology community has adopted a target of a 30% reduction in UACR, but those trials have not been conducted in cardiology. Because there is no physiologic floor for albuminuria, unlike cholesterol, an open question remains whether a 30% reduction is sufficient or whether clinicians should drive UACR as low as possible. Many patients retain persistent albuminuria despite standard combination therapy.^1,2

In an interview at the 10th Annual Heart in Diabetes Meeting, Javed Butler, MD, MPH, MBA, president of the Baylor Scott & White Research Institute and a heart failure trialist, discussed whether albuminuria warrants a conceptual shift in heart failure risk assessment, when to act on an elevated UACR, and whether it could become a therapeutic monitoring target in future trials.

Q&A: Javed Butler, MD, MBA, on the Evolving Role of Albuminuria

HCPLive: Does the emerging evidence justify a conceptual shift in how we approach heart failure and albuminuria measurement in these patients? And if so, do you agree this should be included in routine risk assessment in heart failure?

Javed Butler, MD, MBA: The challenge that always comes up is risk factor versus risk marker. We have a lot of risk factors in cardiology, so how do we decide which tests to add? Historically, remember that at one point cardiologists had nothing to do with lipids. It was an endocrine disease until we found that lipids were associated with cardiovascular outcomes, and that lipid modulation was associated with improved outcomes, and now it is bread-and-butter cardiology. Hypertension used to be a nephrology disease, and now you obviously cannot go to a cardiologist's office and not get your blood pressure checked.

So if you look at the data with UACR, the reason it modulates cardiovascular risk is, one, that it is an earlier marker of chronic kidney disease, even before the GFR goes down; and two, that it is a marker of systemic vascular endothelial dysfunction. Hence it is a risk factor for cardiovascular disease indirectly, through CKD, and directly, as a marker of vascular disease. In my opinion, at least, the data are strong enough that when UACR goes up and you start giving the therapies you would give to patients with early CKD, all of those therapies reduce the risk of developing heart failure. For that reason alone, cardiology should do it now.

What if you already have heart failure and you are going to give heart failure therapies? Do you still need to do it? Now we are not talking about the risk going up, but about whether therapy should be targeted to UACR. You give somebody standard therapy and you measure the UACR, but it is still high. Should you then give even higher doses or add more medication? That part of the equation we have not solved just yet. But in terms of identifying high-risk patients and early targeting of comprehensive therapy, I think the data are pretty much there that UACR is a good marker, and I think the cardiology community will, hopefully, be embracing it.

HCPLive: When we talk about albuminuria, do you think the heart failure framework should begin treating it as early as possible? Or, in the absence of a guideline-directed approach, is this more of a fundamental limitation?

Javed Butler, MD, MBA: Let's break it down into a few component pieces. If you do not have heart failure, you are in general cardiology practice, and you are completely asymptomatic and otherwise doing well, you should check your hemoglobin A1C; if it is elevated, you need to be treated for diabetes. You should measure cholesterol; if it is elevated, you should be treated for dyslipidemia. I think you should develop the same mindset that you should check the UACR, and if it is elevated, you have CKD, and it needs to be treated with appropriate therapy to reduce cardiovascular risk. That is one bucket, about prevention.

The second bucket is the heart failure patient. Even if you adjust for other risk factors, if the UACR is substantially elevated, then close follow-up and aggressive management are important.

But the third part, which you are specifically asking about, is probably the most important question: whether, as with lipids, we should titrate therapy to a target. With lipids, we have the LDL, we start therapy, but we do not stop there; we titrate therapy to get the lipid to a certain level. Should we be titrating therapy to get UACR to a certain level? There is a lot of interest in it. In the nephrology community, they have set a target of a 30% reduction in UACR. We have not done those trials in cardiology just yet.

HCPLive: If albuminuria is both predictive and modifiable, do you foresee it becoming a core therapeutic monitoring target in future heart failure trials? And if so, why or why not?

Javed Butler, MD, MBA: Here is my best prediction. The nephrology community right now is a little bit divided over whether everybody should get all the therapies, or whether, if somebody responds very favorably to UACR reduction with, say, two medicines, you really need the third or the fourth. In the cardiology community, we have a slightly different orientation right now, in that pretty much everybody believes in combination therapy. The combination therapy we give to patients includes MRA, SGLT2 inhibitor, aldosterone synthase inhibitor (possibly coming down the pike), GLP-1 receptor agonist (possibly coming down the pike), and ACE inhibitors, and all of these therapies reduce UACR. So if you go with the target of a 30% reduction, I think with standard therapy you will probably find that most patients get there anyway, and that this becomes a moot point.

The question that comes up is that, unlike cholesterol, where a certain degree of cholesterol is needed for us to live, UACR is different. For cholesterol, the right number is not zero; it is quite low, but not zero. For UACR, there is no right number. You should not be leaking protein at all. So should we be satisfied with a 30% reduction in UACR, or should we really try to drive it as far down as possible? That science has not been done. I can bet you that even on standard therapy, there are a lot of patients who have a substantial reduction but still have persistent albuminuria, and what to do about that is maybe something we should work on for the next 10 years.

This transcript has been edited for grammar and clarity using artificial intelligence tools.

References:

1. Butler J, Jamil A, Cherney DZI, Jafar TH, Testani JM, Khan MS. Albuminuria and heart failure. Eur Heart J. Published online June 12, 2026. doi:10.1093/eurheartj/ehag426

2. Writing Committee Members, Ndumele CE, Rodriguez F, et al. 2026 AHA/ACC/ADA/ASN Guideline for the Prevention, Detection, Evaluation, and Management of Cardiovascular-Kidney-Metabolic Syndrome: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. Published online June 9, 2026. doi:10.1161/CIR.0000000000001453