Examinando por Autor "Solari, Sandra"

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    Low-renin hypertension in incidental adrenal adenomas and response to aldosterone-targeted therapy: a prospective study
    (Elsevier, 2026-06-27) Uslar, Thomas; Sanfuentes, Benjamín; Olmos, Roberto; Burnier, Alberth; Böhm, Pauline; Guarda, Francisco J.; Huete, Álvaro; Mertens, Nicolás; Besa, Cecilia; Andía, Marcelo; Majerson, Alejandro; Cartes, Jaime; Tapia-Castillo, Alejandra; Carvajal, Cristian A.; Fardella, Carlos E.; Allende, Fidel; Solari, Sandra; Vaidya, Anand; Baudrand, Rene
    Background: Incidental adrenal adenomas are common, yet renin status is infrequently assessed in hypertensive patients. Emerging evidence supports a spectrum of renin-independent aldosterone excess associated with adverse cardiovascular risk. Objective and methods: To determine the frequency of a low-renin phenotype in a prospective cohort of hypertensive patients with adrenal adenomas and to evaluate the clinical response to aldosterone-targeted therapy across baseline aldosterone categories. Low-renin phenotype was defined as suppressed renin (PRA <1.0 ng/mL/ h or DRC <10 μIU/mL). Among these patients, plasma aldosterone concentration (PAC) was categorized as 5–10 ng/dL (Group 1), 10–15 ng/dL (Group 2), and >15 ng/dL (Group 3). Patients with suppressed renin were treated with MR antagonists or adrenalectomy and followed longitudinally using PAMO/PASO criteria. Results: Low renin was present in 47% (138/290) of hypertensive patients. Increasing aldosterone levels were associated with higher systolic blood pressure (SBP), resistant hypertension, higher antihypertensive treatment burden, lower potassium, and reduced eGFR (p-trend <0.001). After a mean follow-up of 24±18 months (n = 121), aldosterone-targeted therapy (75% medical, 25% surgical) led to significant reductions in SBP (-18, -26, and -30 mmHg across Groups 1–3; all p < 0.001), decreased medication and significant increases in renin (all p < 0.001), irrespective of aldosterone category. Conclusions: Nearly half of hypertensive patients with adrenal incidentalomas exhibit suppressed renin levels associated with greater blood pressure burden and favorable response to aldosterone-targeted therapy, even in lower aldosterone levels categories. These findings support systematic renin assessment in hypertensive patients with incidental adrenal adenomas and provide a rationale for testing aldosterone-targeted therapy in broader hypertensive populations beyond adrenal adenomas
  • Miniatura
    Ítem
    Progressive 11β-Hydroxysteroid Dehydrogenase Type 2 Insufficiency as Kidney Function Declines
    (Endocrine Society, 2024-09) Uslar, Thomas; Newman, Andrew J.; Tapia-Castillo, Alejandra; Carvajal, Cristian A.; Fardella, Carlos E.; Allende, Fidel; Solari, Sandra; Tsai, Laura C.; Milks, Julia; Cherney, Michael; Stouffer, David G.; Auchus, Richard; Brown, Jenifer M.; Baudrand, René; Vaidya, Anand
    Background: It has been postulated that chronic kidney disease (CKD) is a state of relative 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) insufficiency, resulting in increased cortisol-mediated mineralocorticoid receptor (MR) activation. We hypothesized that relative 11βHSD2 insufficiency manifests across a wide spectrum of progressively declining kidney function, including within the normal range. Methods: Adult participants were recruited at 2 academic centers. A discovery cohort (n = 500) enrolled individuals with estimated glomerular filtration rate (eGFR) ranging from normal to CKD stage 5, in whom serum cortisol-to-cortisone (F/E) was measured as a biomarker of 11βHSD2 activity. A validation cohort (n = 101) enrolled only individuals with normal kidney function (eGFR ≥ 60 mL/min/1.73 m2) in whom 11βHSD2 activity was assessed via serum F/E and 11-hydroxy-to-11-keto androgen (11OH/K) ratios following multiple maneuvers: oral sodium suppression test, dexamethasone suppression test (DST), and ACTH-stimulation test (ACTHstim). Results: In the discovery cohort, lower eGFR was associated with higher F/E (P-trend < .001). Similarly, in the validation cohort, with normal eGFR, an inverse association between eGFR and both F/E and 11OH/K ratios was observed (P-trend < .01), which persisted following DST (P-trend < .001) and ACTHstim (P-trend < .05). The fractional excretion of potassium, a marker of renal MR activity, was higher with higher F/E (P-trend < .01) and with lower eGFR (P-trend < .0001). Conclusion: A continuum of declining 11βHSD2 activity was observed with progressively lower eGFR in individuals spanning a wide spectrum of kidney function, including those with apparently normal kidney function. These findings implicate cortisol-mediated MR activation in the pathophysiology of hypertension and cardiovascular disease in CKD.