Markers of hypercortisolism and primary aldosteronism may co-occur in patients with resistant hypertension, MOMENTUM analysis shows
Presenter: Lance A. Sloan, MD, MSE, Texas Institute for Kidney and Endocrine Disorders, Lufkin, TX
Co-secretion of cortisol and aldosterone in individuals with resistant hypertension: results from the MOMENTUM trial. Presented April 24, 2026.
Among patients with resistant hypertension, a substantial proportion have biochemical markers of endogenous hypercortisolism, primary aldosteronism, or both, results of a large, observational, multicenter study suggest.
Evidence of hypercortisolism was found in approximately 27% of patients with resistant hypertension in the MOMENTUM study, results of which were presented at AACE 2026. Markers of primary aldosteronism were seen in approximately 18% of the participants.
Roughly 4% of participants had markers for both of these conditions, suggesting that concurrent screening for both conditions should be considered in this population, according to investigator Lance A. Sloan, MD.
“When they're on multiple medications and you're not seeing the kind of blood pressure control you normally would see, maybe you should be looking for a secondary cause,” Dr. Sloan said in an interview. “Hyperaldosteronism is one, but we're seeing just as much hypercortisolism.”
The Endocrine Society now recommends screening every patient with hypertension for primary aldosteronism, a broader stance than their prior focus on resistant cases, Sloan said.
Multicenter study
MOMENTUM is a multicenter observational study that enrolled adults with resistant hypertension, defined by American Heart Association criteria. Eligible participants had systolic blood pressure at or above 130 mm Hg while taking three or more antihypertensive drugs from different classes with at least one being a diuretic, or while taking four or more agents regardless of blood pressure.
Investigators screened participants for endogenous hypercortisolism using a 1-mg overnight dexamethasone suppression test, defining a positive result as a posttest cortisol above 1.8 μg/dL with a documented dexamethasone level of 140 ng/dL or higher. Aldosterone levels, aldosterone-to-renin ratio, and plasma renin activity were documented as markers of primary aldosteronism.
Marker prevalence
Among the 1,086 participants screened, 297 met criteria for hypercortisolism, yielding an overall prevalence of 27.3%.
Primary aldosteronism marker prevalences were similar in the overall cohort and in the subset with hypercortisolism. According to results presented in abstract form, plasma renin activity was suppressed (below 0.6 ng/mL/h) in 29.7% of all participants and in 26.6% of those with hypercortisolism, while aldosterone above 10 ng/dL was found in 54.7% and 57.6%, respectively.
Approximately 18% of participants (196 of 1,086) showed evidence of primary aldosteronism, using the combined criterion of plasma renin activity below 1.0 ng/mL/h and aldosterone above 10 ng/dL, Dr. Sloan reported in an oral presentation at the AACE meeting.
Using that same combined criterion, 43 participants in MOMENTUM, or approximately 4%, had evidence of both hyperaldosteronism and hypercortisolism, he added.
“We couldn't find a mechanism for one causing the other,” Dr. Sloan said in the interview. “They're really separate, but you should be checking for both in people with resistant hypertension.”
The MOMENTUM analysis did not include a treatment phase. Dr. Sloan said a follow-up study is planned that will replicate the screening protocol in resistant hypertension and add treatment for participants who screen positive for hypercortisolism.
Disclosures
Lance A. Sloan, MD, MSE, reported serving as an investigator, advisor, and educational speaker for Corcept Therapeutics, which supported the trial. He also reported speaking engagements with Xeris Biopharma.
References
Sloan LA, Aroda VR, Bhatt DL, et al. Co-secretion of cortisol and aldosterone in individuals with resistant hypertension: results from the MOMENTUM trial. Endocr Pract 2026; 32(suppl). https://doi.org/10.1016/j.eprac.2026.03.013