La tunisie Medicale - 2018 ; Vol 96 ( n°07 ) : 454-457
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Bien que l’hyperaldostéronisme primaire soit considéré rare, il constitue l'une des causes les plus fréquentes d'hypertension artérielle (HTA)
secondaire. Basé sur des données plus anciennes, il a été estimé que l'aldostéronisme primaire représentait moins de 1% de tous les patients
souffrant d'HTA. Les données ultérieures, cependant, ont indiqué qu'il peut être retrouvé chez 5 à 15% des patients souffrant d'HTA. Nous
présentons l’observation d’un patient âgé de 66 ans suivi pour HTA chez qui le diagnostic d’hyperaldostéronisme primaire a été posé au moment
ou il a développé une insuffisance rénale sévère secondaire à une néphroangiosclérose. Ce case report, illustre les difficultés diagnostiques
rencontrées au cours de l'hyperaldostéronisme primaire, et met en evidence l’impact du délai diagnostique sur la survie des patients mais aussi
sur leur qualité de vie.

Mots Clés

Primary aldosteronism (PA) is a condition well worth detecting because it is the major cause of severe and resistant hypertension (HT) and is associated with excessive morbidity and reduced quality of life. IT can be abrogated with specific surgical or medical treatment [1,2]. Recent years have seen an explosion in knowledge of this disorder [3].In this report, we present a patient treated at our center and review the existing knowledge on primary hyperaldosteronism, the difficulties in diagnosis, treatment modalities, and prognosis.
Case report:
A66-year-old malepatient hadbeen seen at our nephrology department since 2012 for renal failure attributed to a vascular nephropathy. HT had been discovered atthe age of 55 years old and had required multiple anti-hypertensive therapies, which included furosemid, prazosine, nebivolol, moxonidine, and amlodipine. Physical examination on admission, revealed an asthenic patient, blood pressure of 220/120 mm Hg,pulse rate of 77 beats/min, and edema of the lower members. His diuresis was conserved.Dip sticks showed moderate proteinuria and no hematuria. The results of examination of the heart and lungs were unremarkable. Ambulatory blood pressure monitoring was performed, showing a severe HT profile (Figure 1). Ophthalmologic exam showed hypertensive stage3. Heart ultrasound revealed moderate left ventricular hypertrophyand a left ventricular ejection fraction 54%. Laboratory findings showed a 24 hours proteinuria at 2.1 g, protidemia at 69 g/l, and albuminimea at 39 g/l, renal failure with a serum creatinine level at 30 mg/l (creatinine MDRD clearance at 17 ml/min), serum potassium at 3,1mmol/l, serum calcium at 90 g/l, Bicarbonatemia at 18 mmol/l, and hemoglobin level at 12,2 g/dl. Renal artery doppler was performed, showing the absence of direct evidence of renal artery stenosis with a resistance index <70% (Figure 2). Abdominal ultrasound revealed small kidneys, enlarged adrenal glands with a probable left adrenal nodule (Figure 2). Determination of metanephrine was normal. Serum aldosterone level (standing) was at 1188 pmol/l, (lying down) at 802 pmol/l, serum renin level was 4.14 mUI/l with an aldosterone / renin ratio at 193.5 confirming the existence of a primary hyper aldosteronism. Abdominal MRI showed a right adrenal hyperplasia and left adrenal adenoma (Figure 3). PA diagnosis was made at this time point, and he was treated with Spironolactone,which was first introduced in November 2013, with a strict monitoring of serum potassium with a relative stabilization of blood pressure measures. Preparation for chronic hemodialysis was started in September 2013.The patient was treated with hemodialysis since November 2013 at 3 times per week.
Our patient was diagnosed mistankely with essential hypertension, at an advanced stage, when it had already affected the kidneys and other target organs.  The diagnosis of PA was made tardily, which should alert us to the necessity of early detection of PA, in order to avoid such pejorative outcome. It is recommended to detect PA by determining the aldosterone-renin ratio (ARR) under standard conditions, and that a commonlyusedconfirmatory test shouldconfirmthis condition, for high-risk groups of hypertensive patients and thosewithhypokalemia [4]. It is a diagnosis that is usually made in patients who are in the third to sixth decade of life [5]. There are no specific symptoms. Patients with marked hypokalaemia may have muscle weakness and cramping, headaches, palpitations, polydipsia, polyuria, nocturia. The degree of hypertension is usually moderate to severe and may be resistant to usual pharmacological treatments [6]. We define resistant hypertension if uncontrolled on threeconventionalantihypertensivedrugs, including a diuretic, or controlled on four or more antihypertensivedrugs [100], and thatwas the case in our patient.The findings of a high prevalence of PA in patients with severe and resistant hypertension, is consistent with long-standing observations [9-14]. Not only hypertension isharmfull, but also excessive secretion of aldosterone is associated with an increased risk of cardiovascular disease and other disorders [7,8]. Some experts recommend screening all hypertensive patients for PA. However, given the costs and false-positive assessments, it seems more reasonable to reserve diagnostic evaluation for patients who are at increased risk [15]. In fact, It is recommended that screening, should be limited to patients who present with hypokalemia, and/or patients with severe or resistant hypertension [16,100]. However, identifying this risk group is not always the case, like in our cases, in spite the presence of this resistant hypertension, he was not diagnosed on time. In addition, our patienthad hypokalemia, in spite of his severe renal failure and the treatment based on reninangiotensin system Blocker, whichnormallyinducehyperkalemia.An elevated ARR is an effective screen confirmatory testhaving a high negative predictive value [10,17,18]. In a study by Mamhudet al.and in another separate analysis [19,20], the use of spironolactone was significatively associated with a BP reduction. However, in our patient, the treatment with spironolactone was not totally effective, and was risky consideringhis chronic kidney disease with a high risk of hyperkalemia. This can be explained by the diagnosis delay and the onset of renal failure due to probable vascular nephropathy. In this population,it is recommended to initiate treatment with reduced doses of the aldosterone antagonist and assessment of serum potassium levels as soon as 1 weak of starting treatment [20].In conclusion, significantrenalimpairmentwasrevealedaftersurgery in patients with PA. In anotherstudy of Kim DH et al. oldage, long-standing hypertension, lowlevels of serum potassium, low BMI, and highlevels of serumuricacid or cholesterol are considered as  riskfactors for post operativerenalimpairment and/or chronickidneydiseasedevelopment in patients with PA [21].
PAisaconsiderable diagnostic challenge. Recognizingthis condition,isessentialbecausePA associatedhypertensioncanoftenbecured. Screening with the ARRshould include a larger group of patients with a high suspicion of PA based on clinical and biological findings. Any delay in diagnosing this disorder, may expose the patient at the riskof an accelerateddevelopementof the entirespectrum of hypertension complications including hypertensive nephropathy and retinopathy.

Figure Legends:

Figure 1: Ambulatory blood pressure monitoring showing a severe hypertension profile.

Figure 2: Renal artery doppler and renal ultrasound showing the absence renal artery stenosis and small kidneys.

Figure 3: Right adrenal hyperplasia and left adrenal adenoma at abdominal MRI.

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