Menoufia Medical Journal

: 2021  |  Volume : 34  |  Issue : 1  |  Page : 398--400

Role of adrenal venous sampling and radiological imaging in primary hyperaldosteronism: a case report

Mostafa N Mohrag 
 Department of Internal Medicine, Faculty of Medicine, Jazan University, Jazan, Saudi Arabia

Correspondence Address:
Mostafa N Mohrag
Department of Internal Medicine, Faculty of Medicine, Jazan University, Jazan
Saudi Arabia


The authors present a case of a 63-year-old male patient who was evaluated for consistent hypokalemia and longstanding uncontrolled hypertension. Iatrogenic hypokalemia was excluded. The patient underwent a series of laboratory investigations which showed high levels of aldosterone and an increased aldosterone/renin ratio. A renal/adrenal ultrasound showed a mass in the right adrenal gland, which was presumed to be an adenoma. Adrenal venous sampling was conducted to establish the diagnosis and secretory ability of the mass, but the results showed a paradoxical low aldosterone secretion. The patient was further examined through MRI, which confirmed the adrenal mass, based on which he underwent laparoscopic adrenalectomy that resulted in the normalization of aldosterone, serum potassium, and blood pressure.

How to cite this article:
Mohrag MN. Role of adrenal venous sampling and radiological imaging in primary hyperaldosteronism: a case report.Menoufia Med J 2021;34:398-400

How to cite this URL:
Mohrag MN. Role of adrenal venous sampling and radiological imaging in primary hyperaldosteronism: a case report. Menoufia Med J [serial online] 2021 [cited 2021 Dec 6 ];34:398-400
Available from:

Full Text


Primary hyperaldosteronism (PHA) is one of the most common causes of secondary hypertension [1]. When left undiagnosed, it can cause considerable cardiovascular and cerebrovascular morbidity and mortality [2],[3],[4]. Patients with PHA usually have a vague presentation, which presents a diagnostic challenge. The most common subtypes of PHA are bilateral adrenal hyperplasia and aldosterone-producing adenomas. Other rarer forms include unilateral adrenal hyperplasia and glucocorticoid-responsive aldosteronism. The diagnosis of all these subtypes can be clinically challenging [5]. Adrenal venous sampling (AVS) is considered the gold standard for the diagnosis and secretory function assessment of adrenal lesion [6]. This case report is of particular interest because (a) AVS unexpectedly exhibits paradoxical levels of aldosterone secretion and (b) supplementing the role of AVS with noninvasive radiological modalities seems to aid the diagnosis and treatment of such lesions.


A 63-year-old male patient was referred to our clinic for evaluation of unexplained hypokalemia. He had a history of uncontrolled hypertension for 20 years with two episodes of hypertensive emergency in the previous 2 years. He had no symptoms or other complaints at presentation, neither did he report any underlying medical disorder or licorice consumption. Further, there was no significant family history of hypertension and endocrine or renal disease. He did not report any allergies and was taking nifedipine 30 mg, losartan 100 mg, atenolol 100 mg, and potassium chloride extended-release 750 mg two tablets every 12 h.

A physical examination did not yield any abnormal findings. However, his blood pressure (BP) was slightly elevated (145/90 mmHg).

During laboratory investigations, serum electrolytes showed a low level of potassium 3.2 mmol/l (normal: 3.5–5.3 mmol/l), and normal levels of sodium 140 mmol/l (normal: 133–146 mmol/l), chloride 103 mEq/l (95–108 mEq/l), and bicarbonate 28 mEq/l (22–29 mEq/l).

Renal function tests showed a high-normal level of serum urea 7.3 (2.5–7.8 mmol/l) and a high level of serum creatinine 135 μmol/l (normal: 64–104 μmol/l). There was a moderate decrease in estimated glomerular filtration rate 48 ml/min/1.73 m2 (normal: 90+). Urinalysis, serum protein electrophoresis, and 24-h urine creatinine level were normal.

Differential diagnoses under consideration were PHA, Cushing's disease/syndrome, and renal artery stenosis. Lack of clinical features, a normal cortisol level, and a dexamethasone suppression test ruled out Cushing disease/syndrome. However, we found an elevated serum aldosterone level 3818 pm (normal: 100–400 pm) and a high aldosterone/renin ratio of 1317 (normal: <680).

We then proceeded with renal/adrenal ultrasound to look for an adrenal adenoma and/or hyperplasia. The ultrasound demonstrated a mass of ~2.7 × 2.4 × 2.9 cm over the right adrenal gland [Figure 1]. At this point, the patient was started on spironolactone 100 mg. His home BP readings improved, as did his potassium level (~3.7 mmol/l).{Figure 1}

We continued investigating with AVS to confirm the right adrenal adenoma as a cause of aldosterone excess and rule out a remote possibility of bilateral adrenal hyperplasia. Surprisingly, the right AVS had the lowest concentration of aldosterone among all sampled locations. The readings were as follows (pmol/l):

Right adrenal sample: 455, left adrenal sample: 1189.

Right renal vein sample: 1217, left renal vein sample: 1260.

At this stage, we considered a diagnosis of bilateral adrenal hyperplasia with an incidental adenoma. We consulted the endocrinology team as the findings were confounding given the low aldosterone level on the right side. They considered the possibility of an anomaly during sample procurement and processing. Further noninvasive imaging was recommended, and MRI was deemed reasonable. The MRI report showed a 2.9 × 2.5 cm right adrenal nodule with imaging features in keeping with an adenoma. The left adrenal gland was normal.

Then, the surgical team was consulted, and they deemed that the patient's history, biochemical testing, and MRI findings pointed toward an aldosterone-secreting adenoma. They recommended surgical removal of the right adrenal mass. Therefore, the patient underwent laparoscopic right adrenalectomy. After the surgery, BP stabilized, with average readings of 90/60 mmHg and the last reading of 115/81 mmHg. Antihypertensive drugs were discontinued. Serum potassium was 5.2 mmol/l.


Primary aldosteronism is one of the most common causes of secondary hypertension, accounting for up to 10% of patients referred to hypertension units [1]. Diagnosis and treatment are particularly important because primary aldosteronism is associated with an increased risk of cardiovascular and cerebrovascular events [2],[3],[4]. Licorice-induced pseudoaldosteronism, a condition that could result in medical emergencies, should be excluded in such patient with hypokalemia and hypertension [7].

The diagnosis of primary aldosteronism comprises three steps, namely screening, confirmatory or exclusion testing, and subtype diagnosis [8],[9]. The last step is of fundamental importance to allocate patients to the correct management: unilateral adrenalectomy for aldosterone-producing adenoma and unilateral adrenal hyperplasia, or pharmacotherapy with mineralocorticoid receptor antagonists if the surgery cannot be performed or for individuals with bilateral adrenal hyperplasia [8]. The subtype diagnosis comprises computed tomography (CT) scans and AVS [6].

AVS is a challenging technique that requires a skilled radiologist. However, despite its diagnostic significance, there is poor reproducibility and interpretation of the results obtained between centers owing to scarce standardization of protocols (i.e. different criteria and protocols are used to define cannulation of the adrenal veins and lateralization of aldosterone production) [10],[11]. The absence of a standardized and widely accepted AVS protocol has made practitioners reluctant to employ it [6].

A review of the literature concluded that the diagnosis of PHA when it was only based on CT scans or MRI data, led to inappropriate treatment in 37.8% of patients [10]. However, AVS, combined with CT or MRI may greatly enhance the ability to diagnose and treat PHA, as observed in the present case.


AVS is considered the gold standard for diagnosing PHA. However, owing to a lack of standardization and uniformity across diagnostic centers, results may be difficult to interpret. Nonetheless, AVS can greatly enhance the ability to diagnose and treat PHA when combined with advanced radiological imaging techniques such as CT scans or MRI, along with a multidisciplinary approach of consulting relevant subspecialists when necessary.


The authors acknowledge Dr Majed Darraj, Dr Nael Shaat, and Dr Mohammed Abdulrasak for their support.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Hannemann A, Wallaschofski H. Prevalence of primary aldosteronism in patient's cohorts and in population-based studies--a review of the current literature. Horm Metab Res 2012; 44:157–162.
2Mulatero P, Monticone S, Bertello C, Viola A, Tizzani D, Iannaccone A, et al. Long term cardio- and cerebrovascular events in patients with primary aldosteronism. J Clin Endocrinol Metab 2013; 98:4826–4833.
3Catena C, Colussi G, Nadalini E, Chiuch A, Baroselli S, Lapenna R, et al. Cardiovascular outcomes in patients with primary aldosteronism after treatment. Arch Intern Med 2008; 168:80–85.
4Savard S, Amar L, Plouin PF, Steichen O. Cardiovascular complications associated with primary aldosteronism: a controlled cross-sectional study. Hypertension 2013; 62:331–336.
5Stewart PM. Mineralocorticoid hypertension. Lancet 1999; 353:1341–1347.
6Monticone S, Viola A, Rossato D, Veglio F, Reincke M, Gomez-Sanchez C, et al. Adrenal vein sampling in primary aldosteronism: towards a standardised protocol. Lancet Diabetes Endocrinol 2015; 3:296–303.
7Breidthardt T, Namdar M, Hess B. A hypertensive urgency induced by the continuous intake of a herbal remedy containing liquorice. J Hum Hypertens 2006; 20:465–466.
8Funder JW, Carey RM, Fardella C, Gomez-Sanchez CE, Mantero F, Stowasser M, et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an endocrine society clinical practice guideline. J Clin Endocrinol Metab 2008; 93:3266–3281.
9Mulatero P, Monticone S, Veglio F. Diagnosis and treatment of primary aldosteronism. Rev Endocr Metab Disord 2011; 12:3–9.
10Stewart PM, Allolio B. Adrenal vein sampling for primary aldosteronism: time for a reality check. Clin Endocrinol (Oxf) 2010; 72:146–148.
11Kempers MJ, Lenders JW, van Outheusden L, van der Wilt GJ, Schultze Kool LJ, Hermus AR, et al. Systematic review: diagnostic procedures to differentiate unilateral from bilateral adrenal abnormality in primary aldosteronism. Ann Intern Med 2009; 151:329–337.