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Senior Health Secrets · Jul 22, 2026

A New Kidney Trial Just Changed the Conversation

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Senior Health Secrets · Senior Health Secrets

The last article on kidney function was about the test. Specifically, the gap between what creatinine measures and what cystatin C catches, and how that gap leaves people believing their kidneys are fine when they aren’t.

A lot of you wrote back after that article. The details varied, but the pattern was familiar: Stage 2 or Stage 3 CKD, numbers that had barely moved, and another appointment ending with “we’ll check again next year.”

No discussion of treatment. Just monitoring.

Now there’s something new to discuss.

It isn’t a breakthrough, and it won’t apply to everyone with CKD.

For years, ACE inhibitors and ARBs were the main medications used to slow progression in many forms of non-diabetic CKD.

Then SGLT2 inhibitors changed things. Large trials found meaningful kidney benefits in people with CKD whether or not they had diabetes.DAPA-CKD included nearly 1,400 participants without diabetes. EMPA-KIDNEY included over 3,500.

FIND-CKD asked a different question: could finerenone, a nonsteroidal mineralocorticoid receptor antagonist already approved for diabetic kidney disease, also slow decline in people without diabetes?

1,584 adults with non-diabetic CKD across 24 countries. All were receiving a stable, maximally tolerated ACE inhibitor or ARB. Only about 17% were also taking an SGLT2 inhibitor at baseline.

So FIND-CKD tells us far more about adding finerenone to an ACE inhibitor or ARB than it does about adding it to a fuller modern regimen that already includes an SGLT2 inhibitor.

FIND-CKD was the first Phase III trial of finerenone in non-diabetic CKD, and it met its primary endpoint.

Finerenone slowed the annual rate of kidney function decline by 0.7 mL/min/1.73 m² per year compared with placebo.

Modest, yes. I want to be honest about that, because the headlines haven’t been.

But kidney decline accumulates. A slower rate may matter considerably to someone already approaching Stage 4, while meaning much less to someone whose kidney function is higher and has remained stable for years.

The study followed participants for 32 months. We cannot take the annual difference, multiply it across five or ten years, and assume the benefit would continue unchanged.

The combined kidney and cardiovascular endpoint was lower with finerenone, with a hazard ratio of 0.77.

I would be more cautious with this result. The confidence interval only just excluded no effect, and neither the kidney-only nor the cardiovascular-only result was conclusive on its own.

The combined outcome was lower. We just cannot say confidently which component drove the difference.

Bayer, which manufactures finerenone, funded the trial. The study was randomized and used a prespecified primary endpoint. Readers should still know who paid for it.

But the people enrolled were not representative of everyone with Stage 3 CKD.

Participants needed an eGFR from 25 to less than 90, persistent albuminuria with a UACR between 200 and 3,500 mg/g, stable ACE inhibitor or ARB treatment, and potassium no higher than 4.8 mmol/L at screening. Several kidney conditions were excluded, as were people recently requiring immunosuppressive treatment.

So no, this is not evidence for every person with Stage 3 CKD.

If you have non-diabetic CKD with persistent albuminuria and an eGFR between 25 and 90, FIND-CKD may be worth discussing at your next appointment. If you have Stage 3 CKD without significant albuminuria, these findings do not directly apply to you.

Finerenone is not currently FDA-approved specifically for non-diabetic CKD. A physician can legally prescribe an approved medication off-label, but that doesn’t mean every physician will consider it appropriate or that insurance will cover it. Until the indication and clinical guidelines are updated, access may remain inconsistent.

The drug also carries a real risk of elevated potassium. In the trial, hyperkalemia occurred in 17% of participants receiving finerenone and 13.3% receiving placebo. It led to stopping the medication in 1.5% of the finerenone group and 0.1% of the placebo group. Potassium and kidney function monitoring are part of the treatment, not optional extras.

Blood pressure still matters. So do ACE inhibitors or ARBs when appropriate, SGLT2 inhibitors for eligible patients, albuminuria management, and avoiding medications that can damage the kidneys. KDIGO is currently updating its CKD guidance specifically because new evidence is emerging for SGLT2 inhibitors, GLP-1 therapies, and nonsteroidal mineralocorticoid receptor antagonists in CKD without diabetes.

Cystatin C serves a different purpose. It may give you a better estimate of kidney function. It does not slow the disease.

The average participant in this trial had an eGFR of 47. Stage 3 CKD.

Most people with Stage 3 non-diabetic CKD are managed in primary care. Not by a nephrologist.

And that creates a delay. Kidney specialists are more likely to encounter this evidence early, while the patients who might qualify may not see one for months.

The trial does not fix that. But it gives you something specific to raise at your next appointment.

If you have non-diabetic CKD with persistent albuminuria and an eGFR between 25 and 90, bring the FIND-CKD trial to your next appointment.

Heerspink HJL, et al. Finerenone in Persons with Chronic Kidney Disease without Diabetes. New England Journal of Medicine. Published June 4, 2026. DOI: 10.1056/NEJMoa2604625.

Ask these two questions:

“Does the FIND-CKD trial apply to my type of kidney disease, and could finerenone eventually be appropriate for me?”

“Is there anything in my current treatment plan that should be reviewed given the new evidence in non-diabetic CKD?”

If it’s unclear whether the trial applies to your situation, or if your albuminuria is substantial, ask whether a nephrology referral would be useful. You don’t need to wait until Stage 4 or 5 to have that conversation.

Heerspink HJL, et al. Finerenone in Persons with Chronic Kidney Disease without Diabetes. New England Journal of Medicine. Published June 4, 2026. DOI: 10.1056/NEJMoa2604625.

Heerspink HJL, Stefansson BV, Correa-Rotter R, et al. Dapagliflozin in patients with chronic kidney disease. New England Journal of Medicine. 2020;383(15):1436-1446. PMID: 32970396. (DAPA-CKD)

The EMPA-KIDNEY Collaborative Group. Empagliflozin in patients with chronic kidney disease. New England Journal of Medicine. 2023;388(2):117-127. PMID: 36331190. (EMPA-KIDNEY)

Shlipak MG, Matsushita K, Arnlov J, et al. Cystatin C versus creatinine in determining risk based on kidney function. New England Journal of Medicine. 2013;369(10):932-943. PMID: 24004120.

Medical Disclaimer: This article is for educational purposes only and does not constitute medical advice. It does not replace individualized guidance from a qualified health professional. Consult your physician or nephrologist before making any changes to your medications or treatment plan.

Stay independent. Stay capable.

Published July 2026 | Senior Health Secrets
Evidence-based health research for seniors.

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