Health

New pill could finally control stubborn high blood pressure

Results from the FigHTN Phase 2 clinical trial showed baxdrostat, a new medication that inhibits the production of the hormone aldosterone, lowered systolic blood pressure by about 5% when added to the existing medications taken by people with chronic kidney disease and who also have uncontrolled high blood pressure.
The analysis also found that baxdrostat lowered the loss of albumin in the urine, which is a marker of kidney and cardiovascular risk, by 55% compared to placebo, suggesting that this medication may help delay the progression of kidney disease .
These findings suggest the potential for baxdrostat to improve longer-term health outcomes like kidney and cardiovascular conditions and reduce the need for higher-cost care for people with uncontrolled high blood pressure and chronic kidney disease.

Adding the novel medication baxdrostat to standard care may help manage high blood pressure and delay the progression of kidney disease in people with chronic kidney disease and uncontrolled high blood pressure , according to preliminary research presented at the American Heart Association's Hypertension Scientific Sessions 2025. This study was simultaneously published in the Journal of the American Society of Nephrology.

Chronic kidney disease and high blood pressure are closely linked and, when not managed appropriately, can lead to serious outcomes such as heart attack, stroke, heart failure and progression to kidney failure. Aldosterone, a hormone produced by the adrenal glands, can play a role in both high blood pressure and chronic kidney disease. Aldosterone causes sodium to be retained, which increases water retention and blood pressure. Over time, an excess of the hormone can lead to stiffening and thickening of blood vessels, which can contribute to heart damage and cause scarring in the kidneys, thereby playing a role in both high blood pressure and chronic kidney disease.

"These findings are encouraging for people living with chronic kidney disease and high blood pressure, two conditions that often go hand-in-hand and create a dangerous cycle," said lead study author Jamie P. Dwyer, M.D., a professor of medicine in the division of nephrology and hypertension at University of Utah Health in Salt Lake City. "High blood pressure can worsen kidney function and declining kidney function can further elevate blood pressure, and these outcomes can be life-altering for patients."

The study was designed to find whether adding baxdrostat to standard care is safe and could help lower blood pressure in people who have both chronic kidney disease (serious enough that they are likely to develop kidney failure or require a transplant during their lifetime) and uncontrolled high blood pressure. Their blood pressure has remained high despite already taking either an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB), two medications that work on a group of hormones that act together to regulate blood pressure.

At the beginning of the study, participants had an average systolic (top number) blood pressure of 151 mm Hg despite treatment and evidence of kidney disease on laboratory testing. When the protein albumin was measured in the urine, the average level for participants was 714 mg/gm of creatinine; levels of 30 or higher may be a sign of chronic kidney disease. When a blood sample was used to measure the estimated glomerular filtration rate (eGFR, a key indicator of kidney function), the average level was 44mL/min/1.73. Levels that are persistently less than 60 suggest chronic kidney disease.

Of 195 initial study participants, 192 were randomized to begin treatment with low-dose (0.5 mg-1 mg) or high-dose baxdrostat (2 mg-4 mg) or a placebo in addition to standard care. Three people finished the study early due to adverse events, their own decision to leave the study or for other reasons.

After 26 weeks:

The average systolic blood pressure had fallen 8.1 mm Hg more in participants receiving either dose of baxdrostat than in those receiving the placebo, a reduction of about 5%.
High potassium levels in the blood, a known side effect of medications that block the renin-angiotensin-aldosterone system, occurred in 41% of participants on baxdrostat and 5% of those on placebo. Most cases were mild to moderate.
There were no deaths or unanticipated adverse events during the trial, however, 9% of participants taking baxdrostat and 3% of those in the placebo group experienced a serious adverse event.

In an exploratory analysis, the researchers looked at the amount of albumin lost in the urine, a type of protein that when found in the urine in high amounts is a predictor of cardiovascular and kidney disease. They found the urine albumin level was 55% lower in those taking baxdrostat than in those taking a placebo, comparable to the reduction seen with medications that delay the progression of kidney disease.

"The reduction in urine albumin gives us hope that baxdrostat may also help delay kidney damage. This potential is now being tested in two large Phase 3 trials to determine if baxdrostat delays the progression of kidney disease," said Dwyer.

"These new findings are reassuring that this new class of antihypertensive medications are likely to have both kidney- and cardio-protective benefits and to be safe and effective for broad patient populations," said Jordana B. Cohen, M.D., M.S.C.E., immediate past chair of the American Heart Association's Hypertension and Kidney Cardiovascular Science Committee. "Patients with chronic kidney disease were historically often excluded from drug studies. It is particularly reassuring to know that patients with chronic kidney disease, who have very high rates of hypertension and elevated renin-angiotensin aldosterone activity, were represented in their own study, tolerated the medication well, and had both blood pressure and albuminuric benefits. This medication class could be a game changer in the management of hypertension in this patient group." Cohen, who was not involved in this study, is deputy director and associate professor of medicine and epidemiology in the Perelman School of Medicine at the University of Pennsylvania.

Study details, background and design:

The study included 195 people with an average age of 66 years. Of the participants, 32% were women, 40% were non-Hispanic white and 80% had Type 2 diabetes. The study was conducted at 71 sites in the United States. Three participants were not randomized or included in the final analysis.
All participants had uncontrolled high blood pressure (systolic blood pressure of 140 mm Hg or higher, or 130 mm Hg or higher for people with Type 2 diabetes ) despite taking the maximum tolerated dose of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker among their medications, with average systolic blood pressure of 151.2 mm Hg at the start of the study.
All participants also had chronic kidney disease but were not in kidney failure (eGFR of 25-75 mL/min/1.73, average eGFR of 44 mL/min/1.73 at the start of the study; and urine albumin-creatinine ratio of 100 mg/g or higher, average of 713.8 at the start of the study).
The 192 participants were randomized to one of the three treatment groups: low-dose baxdrostat (0.5 mg/day, increasing to 1 mg/day after two weeks); high-dose baxdrostat (2 mg/day, increasing to 4 mg/day after two weeks); or a placebo.
After 26 weeks, blood pressure and kidney function tests were repeated, and the primary analysis compared changes in systolic blood pressure among the three groups. Adverse events were also reported for each of the three treatment groups.
Baxdrostat is in a class of medications that inhibit the production of aldosterone and are being tested for their ability to treat conditions such as high blood pressure, chronic kidney disease and heart failure. Baxdrostat is not approved for any use by the U.S. Food and Drug Administration.

Co-authors and their disclosures and funding sources are listed in the abstract. The study was funded by AstraZeneca, developer of baxdrostat.

Note: The study featured in this news release is a research abstract. Abstracts presented at the American Heart Association's scientific meetings are not peer-reviewed, and the findings are considered preliminary until published as a full manuscript in a peer-reviewed scientific journal.

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Scientists reveal green tea’s fat-burning secret

Green tea is an ancient beverage recognized for its medicinal and antioxidant properties. It has been widely studied for its beneficial effects on metabolic diseases, such as obesity and type 2 diabetes. Recent studies funded by FAPESP have deepened our understanding of the mechanisms of action of this infusion and revealed that green tea treatment reduced weight and significantly improved glucose sensitivity and insulin resistance in obese mice. These results reinforce the potential relevance of the beverage as an adjunct in the treatment of obesity in humans.

Rosemari Otton led the studies from the Interdisciplinary Graduate Program in Health Sciences at Cruzeiro do Sul University in São Paulo, Brazil. The scientist, who has dedicated more than 15 years to green tea research, explains that her initial motivation came from curiosity about the truth behind the popular belief that the drink aids in weight loss. The results of her most recent study were published in the journal Cell Biochemistry & Function.

To study the effects of green tea on obesity, the research team fed mice a high-calorie diet for four weeks, with both fat and what they call a "cafeteria diet," which mimics the Western diet. "We give them chocolate, filled cookies, dulce de leche, condensed milk... In other words, the same type of food that many people consume on a daily basis," says Otton.

After this initial phase, the animals underwent the green tea experiment for another 12 weeks. During this period, they continued on the high-calorie diet, but some of them began receiving standardized green tea extract at a dose of 500 mg per kilogram of body weight, administered intragastrically (via gavage).

"It's a method that ensures they all receive the exact dose we want to study. If we put it in water, for example, we'd have no way of knowing how much the animal actually ingested," says the researcher. For humans, this amount would be equivalent to consuming about 3 grams of green tea per day, or three cups.

However, according to the researcher, not all commercial green tea meets the necessary quality standards. "Ready-made tea bags do not always guarantee the quantity or quality of the compounds. The ideal for consumption would be to use standardized green tea extract, like those found in compounding pharmacies. This is a concentrated way of using the plant, with a guarantee of the presence of flavonoids, which are the health-beneficial compounds present in the green tea plant," Otton points out.

One methodological difference in the study was the controlled room temperature. The animals were kept in a thermoneutral environment (28 °C) throughout the experiment. Animal facilities generally maintain an average temperature of 22 °C, which represents chronic cold for mice.

"Excessive cold activates compensatory regulatory mechanisms in the animals' bodies, causing them to expend more energy to stay warm. This can mask the real effects of any substance," explains the researcher. "If the animals are in a colder environment, the effect of the tea is enhanced by the activation of energy expenditure due to the cold. But by maintaining thermoneutrality, we were able to see the effects of green tea in a 'clean' way, without environmental interference," she explains.

A previous study published in August 2022 in the European Journal of Nutrition found that obese mice treated with green tea experienced a reduction of up to 30% in body weight. "If a person loses 5% to 10% of their body weight, that's already a lot. So this result in animals is very significant," says the professor.

Muscular effect

Another highlight of the most recent study was the preservation of muscle morphology. Obesity typically causes a reduction in muscle fiber diameter, but green tea prevented this muscle atrophy. "One way to assess muscle function is to look at fiber diameter. If it increases, we have more active muscle components. Green tea managed to maintain this diameter, showing that it protects muscle against the harmful effects of obesity," Otton explains.

In addition to morphological data, the researchers evaluated the expression of genes related to glucose metabolism. Treatment with green tea increased the expression of Insr, Irs1, Glut4, Hk1, and Pi3k - genes that are important for glucose uptake and use in muscles. The activity of lactate dehydrogenase (LDH), an enzyme that is essential for glucose metabolism, was also restored.

According to Otton, there is evidence indicating that green tea does not affect the weight of lean animals, suggesting that it acts selectively against excess body fat. "It makes obese animals lose weight but keeps lean animals at a balanced weight. This shows that the tea seems to need an environment with excess nutrients to act, which supports the hypothesis that it acts directly on fat cells."

Another aspect investigated by the team was the action of the compounds in isolation. "Green tea is a complex matrix with dozens of bioactive compounds. We've tried to separate these compounds and study their effects individually, but the whole extract is always more effective. There's a synergy between the compounds that we can't reproduce when they're isolated," she says.

According to the scientist, one hypothesis explaining the mechanism by which green tea affects obesity involves adiponectin, a protein produced by adipocytes that has anti-inflammatory and metabolic regulation functions. "We conducted a study with adiponectin-knockout mice, meaning they don't produce it. And in these animals, green tea had no effect. This suggests that adiponectin is a key player in the mechanism of action of the tea," she comments.

Real-life effects

Despite the encouraging results of the mouse study, Otton points out that it is not yet possible to determine a safe and effective dose of green tea for humans. This is mainly due to the variability of the extracts and the fact that each person behaves differently. "The ideal is chronic consumption, as we see in Asian countries. In Japan, for example, people consume green tea every day, throughout their lives, and obesity rates are low. But this is different from drinking tea for five months and expecting a miraculous weight loss effect," she ponders.

The researcher argues that natural and accessible treatments should gain ground in the fight against obesity, especially as alternatives to expensive medications that often have side effects. "The idea is to have safe, natural, effective, and high-quality compounds. The Camellia sinensis plant offers this. We're still studying all the compounds involved, but there's no doubt that green tea, as a plant matrix rich in flavonoids, has important therapeutic potential."

The researcher emphasizes that science always seeks to develop practical solutions. "What we see in animals doesn't always reproduce in humans. But if we want to make this translation to real life, we need to think about all the details, such as ambient temperature. It's these precautions that increase the validity of our data. We're far from having all the answers, but we're getting closer and closer."

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