Treating CKD Using Multiple Methods

EP: 1.Getting to Know CKD

EP: 2.Populations That Develop CKD

EP: 3.Unmet Needs in CKD Therapy

EP: 4.CKD Health Disparities and Their Consequences

EP: 5.Recognizing the Economic Burden of CKD

EP: 6.Acknowledging the Economic and Clinical Burdens of CKD and CVD

EP: 7.Screening for CKD

EP: 8.Preventing CKD Underdiagnosis

EP: 9.Treatment Goals for Patients With CKD

EP: 10.Blood Pressure Management Within the CKD Treatment Landscape

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EP: 11.Treating CKD Using Multiple Methods

EP: 12.The Role of MRAs in CKD and CV Treatment

EP: 13.Using Published Data to Consider SGLT2 Inhibitors and MRAs in CKD Management

EP: 14.Combination Therapy and Payer Perspective on CKD Therapies

EP: 15.Continued Health Disparities Seen in Practice

EP: 16.Closing Thoughts on CKD Management

Ryan Haumschild, PharmD, MS, MBA: As we look at the treatment of CKD [chronic kidney disease], we have to think about glycemic control in the role of SGLT2 inhibitors. Also, how do we focus and treat inflammation in fibrosis? Dr Feldman, I’d love to hear your thoughts on those 2 points.

Jeffrey Feldman, MD: I have to pivot to Dr Agarwal and his studies with the finerenone portfolio. If you have somebody with CKD, albuminuria, and they’re diabetic, and even if they aren’t diabetic now with certain SGLT2 inhibitors, those are first-line drugs. The data are clear. The adverse effect profile is good, so [I’d choose] SGLT2 inhibitors.

If you look at mechanisms of chronic kidney disease and neurohumoral mechanisms, there’s inflammation, fibrosis, and the third part of the triangle is metabolic. The SGLT2 inhibitor may have an effect on metabolic glycemic control, and there are a lot of pleiotropic effects that people talk about that SGLT2 inhibitors do for metabolic effects. They have the neurohumoral effect in the kidney and the heart. You could have a 6-hour symposium with 400 different experts telling you how they work in the kidney and the heart. As a community nephrologist, [I’ve seen that] they work. I’ve taken people off diuretics as I’m putting them on SGLT2 inhibitors, and they probably have heart failure and they have a little edema, and they feel much better. The pathophysiologic effects and the effects on SGLT2 inhibitors are real.

The next question is that you’re still left with inflammation and fibrosis. During the first rollout of finerenone, they talked about how mineralocorticoid receptor antagonists [MRAs] work and where they work. Dr Agarwal is an expert on this. They work in the heart, the kidney, the vasculature, and the immune system. There are a lot of things going on, particularly in the immune system, that you can show with basic science that the mineralocorticoid antagonist—particularly a specific with high affinity, finerenone—blocks inflammation and scarring.

As alluded to earlier, SGLT2 inhibitors have an effect for cardiovascular disease. They start pretty early because they work by one mechanism, and then we have another mechanism, which is inflammation and scarring. The combination of finerenone with SGLT2 inhibitors blocks 3, because you get the metabolic effects. Later, within the first 4 months, you get a 30% reduction with finerenone, with UACR [urine albumin-to-creatinine ratio] showing an effect within 4 months, and the curves for protection start separating after 6 months to a year depending on whether you’re looking at cardiovascular outcomes or renal outcomes. In my toolbox, you need both MRA antagonists and SGLT2 inhibitors to slow the progression. The goal is to slow the progression of loss of renal function. If the renal function is better and you aren’t in stage 3B or 4, there are fewer cardiovascular outcomes, and probably more dreaded is heart failure. That’s how I look at it when I’m seeing my patients.

Transcript edited for clarity.