March 17, 2026

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Ozempic and other new diabetes drugs revolutionize kidney treatment

Three types of diabetes medication are improving the outlook for patients with kidney disease

By Tara Haelle edited by Lauren Gravitz

Chiara Vercesi

This article is part of “Innovations In: Kidney Disease,” an editorially independent special report that was produced with financial support from Vertex.

More than one in seven people in the U.S. have chronic kidney disease, which was the ninth-leading cause of death worldwide in 2023. But until recently, just one class of drugs—called renin-angiotensin system (RAS) inhibitors—had been shown to slow progression of the illness, and even those medications were only modestly effective.

For decades researchers have been investigating whether other types of medications can treat the ailment. Because kidney health is inextricably intertwined with other conditions, particularly diabetes and cardiovascular disease, it seemed possible that drugs developed for those issues might also be useful for halting kidney deterioration. Medications known as GLP-1 receptor agonists—including the blockbuster drug Ozempic—were first developed for type 2 diabetes and have since gained prominence for treating obesity and cardiovascular disease. These drugs also have begun to revolutionize treatment for chronic kidney disease.

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They’re not the only ones. A drug called finerenone, part of a drug class called mineralocorticoid receptor antagonists (MRAs), and another group of medications, inhibitors of a protein called SGLT2, also have shown success in preserving kidney function. Despite their similarities, however, each of these drug groups works differently. Today kidney specialists believe it’s possible that combined treatment with all three types, together with RAS inhibitors, could add decades to the lives of people with chronic kidney disease. Because kidney patients also often have heart problems, diabetes and obesity, the drugs have a chance of treating multiple conditions.

“For the first time there’s a realistic prospect of actually stopping kidney disease progression,” says Maarten Taal, a nephrologist at the University of Nottingham in England. And the combinations raise hope of a day when the disease could actually be reversed, he says. “That’s why these drugs are game changers, and the fact that they each work by a completely different mechanism implies that they will have an additive effect because they’re not all doing the same thing.”

Researchers began to identify the mechanisms that drive progressive kidney damage in the 1980s. No matter the cause—diabetes, high blood pressure, glomerulonephritis, autoimmune conditions, or something else—all kidney disease progresses over time, so scientists hypothesized that there must be common underlying processes. If they could find and inhibit those things, they could build therapies to treat a broad range of kidney diseases, Taal says. They discovered that a hormone called angiotensin was a “master regulator of the whole process,” he says. Angiotensin can constrict blood flow, prompt people to increase salt and water intake, and retain more of those substances in their kidneys. It is often overactive in people with kidney disease. Scientists therefore developed RAS inhibitors that curb the production of angiotensin or its actions in the kidneys.

RAS inhibitors can reduce the risk of kidney disease by 15 to 50 percent, but they aren’t enough. “Although they slowed progression, they didn’t halt it,” Taal says, and they didn’t work in everyone.

Scientists returned to the drawing board, but success remained elusive. “We had 15 years during which there was just no progress. All sorts of other therapies were tried and found ineffective,” Taal says. Nothing seemed to work.

Then, in 2019, results of a trial of an SGLT2 inhibitor drug called canagliflozin were presented at a conference. They were impressive enough that audience members stood up and clapped. The medication, initially approved in 2013 for type 2 diabetes, was the first SGLT2 inhibitor shown to protect the kidneys. The trial showed those who took the drug had much lower levels of creatinine protein in the blood (a sign of kidney damage). Death from renal or cardiovascular causes was also reduced, as was end-stage kidney disease, which meant fewer people needed dialysis or transplants. “The trial was stopped early because of its benefit,” Taal says.

All the participants in that trial had type 2 diabetes.