Primary aldosteronism (PA), or Conn's syndrome, is an endocrine pathology characterized by autonomous aldosterone secretion that bypasses the physiological regulation of the renin-angiotensin-aldosterone system (RAAS). The key pathophysiological mechanisms include sodium-dependent arterial hypertension, hypokalemia, metabolic alkalosis, and, in some cases, target organ damage, including renal and cardiovascular structures. Given the frequent latency of clinical manifestations, PA was long considered a rare entity; however, contemporary screening studies indicate that the prevalence of the disease is significantly higher than previously assumed [1-3]. Epidemiological data suggest that PA is identified in 5–13% of patients with arterial hypertension and in 17–23% of patients with resistant hypertension [4, 5]. The disease is of particular relevance in young individuals, in whom arterial hypertension presents with pronounced metabolic disturbances or poor response to standard antihypertensive therapy. Given the severity of potential complications, including the development of left ventricular hypertrophy, atrial fibrillation, and chronic kidney disease, PA should be actively excluded in all patients with hypertension, particularly in the presence of hypokalemia [6-8]. The current diagnostic algorithm for suspected PA includes an initial screening step—determination of the aldosterone-to-plasma renin activity ratio (ARR)—followed by diagnostic confirmation using pharmacological suppression tests (captopril challenge test, intravenous saline infusion test, fludrocortisone suppression test) and adrenal imaging (CT, MRI). The gold standard for topical diagnosis remains selective adrenal venous sampling, which allows differentiation between lateralized aldosterone secretion (in adenoma) and bilateral adrenal hyperplasia [9-11]. The clinical significance of timely PA detection lies not only in achieving target blood pressure levels and normalizing electrolyte balance but also in the potential for complete cure through surgical removal of the aldosterone-producing tumor. An alternative to surgical treatment is medical therapy with mineralocorticoid receptor antagonists (spironolactone, eplerenone), the efficacy of which has been demonstrated in controlling blood pressure (BP) and correcting hypokalemia [12-14]. Furthermore, recent studies indicate an association between PA and progression of albuminuria, decline in glomerular filtration rate, and increased cardiovascular mortality. Thus, the disease acquires a systemic character, affecting not only blood pressure regulation but also the structure and function of target organs, primarily the kidneys and myocardium [15, 16].

The objective of this publication is to demonstrate the clinical significance of timely detection of primary aldosteronism in outpatient nephrology practice in a patient with long-standing arterial hypertension and persistent hypokalemia.

Patient N., a 34-year-old male (born 1989), has been followed for arterial hypertension since the age of 17. From the age of 25, he experienced episodes of pronounced weakness that occurred periodically and had no convincing explanation at that time. Review of outpatient records revealed that since 2019, the patient had consistently demonstrated hypokalemia ranging from 2.7 to 3.3 mmol/L. Concurrently, inadequate efficacy of antihypertensive therapy was noted, including treatment with the angiotensin-converting enzyme inhibitor fosinopril, subsequently replaced with the angiotensin II receptor blocker losartan, and the diuretic indapamide.

In January 2022, the patient was initially consulted by a nephrologist due to urinary abnormalities and arterial hypertension. At the time of consultation, blood pressure was 160/90 mm Hg. No significant complaints or clinically meaningful symptoms were reported. Complete blood count revealed no pathological changes. Urinalysis demonstrated proteinuria of 0.5 g/L, with an unremarkable urinary sediment. Biochemical blood testing revealed a decreased potassium level of 3.1 mmol/L and a creatinine level of 102 µmol/L; the estimated glomerular filtration rate (eGFR) calculated using the CKD-EPI formula was 85 mL/min/1.73 m². Ultrasound examination of the kidneys and adrenal glands revealed no structural pathology. The urine albumin-to-creatinine ratio (ACR) was 250 mg/g.

At the time of evaluation, the patient was receiving combination antihypertensive therapy: amlodipine 10 mg/day, telmisartan 80 mg/day, and indapamide 1.5 mg/day. Despite treatment, target blood pressure values could not be achieved; concurrently, persistent hypokalemia remained. The combination of long-standing arterial hypertension, treatment resistance, and persistent hypokalemia prompted targeted investigation for a secondary cause of arterial hypertension, primarily primary aldosteronism.

Initial hormonal evaluation, performed without discontinuation of antihypertensive therapy, revealed a low renin level (0.8 µIU/mL) and an aldosterone level of 16.8 ng/dL. The aldosterone-to-renin ratio (ARR) was 21, which was considered highly suggestive of primary aldosteronism. Based on the constellation of clinical and laboratory findings, primary aldosteronism was suspected, accompanied by hyporeninemic arterial hypertension and renal manifestations in the setting of long-standing hypokalemia.

Subsequently, the patient was evaluated by an endocrinologist. Following adjustment of therapy, including discontinuation of the diuretic and angiotensin II receptor blocker, repeat hormonal evaluation was performed: renin level was 0.5 µIU/mL, aldosterone level was 26 ng/dL, and the aldosterone-to-renin ratio (ARR) was 52. A captopril suppression test was additionally performed, which demonstrated inadequate suppression of aldosterone secretion: aldosterone level was 29 ng/dL before the test and 35 ng/dL after test administration. These findings confirmed autonomous aldosterone secretion. For topical diagnostic purposes, computed tomography of the adrenal glands was performed, revealing a 20 × 14 mm lesion in the lateral limb of the left adrenal gland, with a density of 15 HU, consistent with an adrenal adenoma. In preparation for surgical treatment, the patient was initiated on spironolactone at a dose of 200 mg/day in combination with potassium chloride supplements. During this therapy, normalization of serum potassium levels and improved blood pressure control were observed.

In November 2022, the patient underwent adrenalectomy. In the postoperative period, normalization of blood pressure was achieved without the need for continued antihypertensive therapy. Potassium levels remained within reference ranges, the albumin-to-creatinine ratio normalized, and glomerular filtration rate remained stable.

This clinical case illustrates the importance of timely identification of PA in young patients with long-standing arterial hypertension. According to the literature, hypokalemia is not present in all patients with PA; however, its presence significantly increases clinical suspicion [1, 4, 7]. In our case, hypokalemia (down to 2.7 mmol/L) persisted for many years, was not corrected, and was not considered as a clinical marker of secondary arterial hypertension.

It should be noted that renin and aldosterone measurements were performed during ongoing antihypertensive therapy (ARB and diuretic), which, as is well known, stimulates renin secretion. Despite this, renin levels were markedly suppressed and ARR was substantially elevated (52), suggesting high specificity of the observed hormonal alterations even without complete drug withdrawal. Such diagnostic approaches are considered acceptable in the literature when medication discontinuation is not feasible, particularly in cases with high risk of clinical deterioration [2, 5, 10].

It must be emphasized that ultrasound examination of the adrenal glands in routine practice has low sensitivity for detecting aldosterone-producing tumors, particularly small ones. In our case, contrast-enhanced CT imaging allowed verification of a lateralized adenoma measuring 20 × 14 mm, which confirmed the diagnosis of PA and determined the treatment strategy. According to meta-analyses, CT has high sensitivity (up to 95%) for tumors larger than 1 cm [3, 6, 9].

Following surgical treatment, sustained normalization of blood pressure was achieved without medications, further confirming the autonomous nature of aldosterone secretion. Potassium levels returned to normal, and the albumin-to-creatinine ratio decreased, indicating reduction of the nephropathogenic effects of aldosterone. Several studies have demonstrated regression of both albuminuria and left ventricular hypertrophy following resolution of hyperaldosteronism [8, 14, 16].

Thus, this clinical situation underscores the importance of recognizing PA in patients with hypertension, particularly at a young age and in the presence of hypokalemia. Emphasis should be placed on timely determination of renin and aldosterone levels, even during ongoing therapy if it cannot be withdrawn. Given the high potential for complete cure, PA should be actively excluded in any case of hypokalemia associated with arterial hypertension, especially when resistant to standard therapy.