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CLINICAL STATEMENTS AND GUIDELINES Circulation. 2025;152:e114–e218. DOI: 10.1161/CIR.0000000000001356 September 16, 2025 e139 angiotensin-converting enzyme inhibitors (ACEis) and angiotensin receptor blockers (ARBs) may stimulate renin and suppress aldosterone4; thiazidetype, loop diuretics, MRA, and potassium-sparing diuretics can stimulate both renin and aldosterone.4 Throughout this guideline, we use the term thiazidetype diuretic to collectively refer to hydrochloro thiazide (HCTZ), chlorthalidone, and indapamide. Although the literature traditionally differentiates these medications based on their chemical struc tures, categorizing HCTZ as a thiazide-type diuretic because it possesses a benzothiadiazine ring and categorizing chlorthalidone and indapamide as thiazide-like diuretics because they lack this ring (yet remain closely related sulfonamide deriva tives), the interchangeability of thiazide-type and -like agents remains a debated topic. For simplic ity and to minimize confusion, in this guideline we have chosen to group them under a single term. In most settings, it is acceptable for clinicians to choose among these agents for treatment. We rec ognize that there are differences in potency and half-life between these agents that may be relevant in some situations, particularly in the management of resistant hypertension (Section 5.6, “Resistant Hypertension”). Initial screening for primary aldo steronism can typically be interpreted in the con text of most medications that affect renin and aldosterone. If screening results are negative or borderline in patients in whom there is a high level of suspicion for primary aldosteronism and confir mation of the diagnosis will change management, potentially interfering medications may be tempo rarily substituted with noninterfering medications (ie, nondihydropyridine calcium channel blockers [CCBs], vasodilators, peripheral alpha-blockers, and potentially dihydropyridine CCB21) for at least 2 to 4 weeks prior to repeat testing. 5. The diagnosis of primary aldosteronism may require an aldosterone suppression test such as an intrave nous (IV) saline suppression test or oral salt-loading test.4 If the diagnosis of primary aldosteronism is confirmed and the patient agrees that surgery would be desirable, the patient is referred for an adrenal venous sampling procedure to determine whether the increased aldosterone production is unilateral or bilat eral in origin. If unilateral excess aldosterone produc tion is documented on adrenal venous sampling, the patient is referred for unilateral laparoscopic adrenal ectomy.4,22 If the patient has bilaterally increased aldo sterone secretion on adrenal venous sampling, is not a surgical candidate, or is not interested in pursuing surgery, the patient is treated with an MRA (eg, spi ronolactone or eplerenone).4 If primary aldosteronism is confirmed, imaging of the adrenal glands should be considered, even if treatment will be with medica tion, to exclude a large adrenal mass that may require adrenalectomy if features suggestive of malignancy are present (size >4 cm, imaging characteristics).23 Treating primary aldosteronism, either with an MRA or unilateral adrenalectomy, if indicated, is associ ated with resolution of hypokalemia, lower BP, fewer number of antihypertensive medications required, and improved parameters of impaired cardiac and kidney function.4,12,13 Meta-analysis of observational data suggests that adrenalectomy may be associated with lower risk of MACE and all-cause mortality compared with medical therapy.22 3.2.3.2 Renal Artery Stenosis Recommendations for Renal Artery Stenosis References that support recommendations are summarized in the Evidence Table. COR LOE Recommendations 1 A 1 In adults with hypertension and atherosclerotic renal artery stenosis, medical therapy is recommended to reduce kidney and CVD morbidity and mortality.1–3 2a C-EO 2 In adults with hypertension and atherosclerotic renal artery stenosis for whom medical management has failed (eg, resistant hypertension, worsening kidney function, and/or acute HF), it is reasonable to refer patients for revascularization by percutaneous renal artery angioplasty and/or stent placement. 2b C-LD 3 In adults with hypertension and nonatheroscle rotic renal artery stenosis, including fibromuscular dysplasia, it may be reasonable to refer patients for revascularization by percutaneous renal artery angioplasty.4 Synopsis Renal artery stenosis refers to a narrowing of the renal artery that can result in a hemodynamically significant re striction of blood flow, usually by >75%. Atherosclerotic disease (90%) is the most common cause of renal artery stenosis, whereas nonatherosclerotic disease, of which fi bromuscular dysplasia is the most common, is much less prevalent and tends to occur in younger, otherwise health ier patients with a predilection for women.5 Atherosclerotic renovascular disease may be present in 14% to 40% of adults with hypertension; however, only a small fraction (0.1%-5%) is considered to be hemodynamically signifi cant to result in renovascular hypertension.6 With the ad vent of endovascular procedures to restore blood flow, the risk for postprocedure morbidity and mortality risk dropped substantially from previous surgical reconstruction rates. Several trials designed to compare the efficacy of these procedures with medical therapy suggested no benefit over aggressive medical therapy alone among adults with atherosclerotic renal artery stenosis.1–3 Nonetheless, there may be benefit in certain subgroups of individuals with atherosclerotic renal artery stenosis who were not rep resented in the trials, including those with progressively worsening kidney function or sudden onset of pulmonary edema.3 The absence of severe albuminuria is associated with better outcomes after endovascular renal artery ste nosis interventions.7,8 In contrast, renal artery angioplasty Downloaded from http://ahajournals.org by on October 7, 2026