La tunisie Medicale - 2018 ; Vol 96 ( n°07 ) : 454-457
[ 1491 times seen ]

Although initially considered a rarity, primary aldosteronism now is one of the more common causes of secondary hypertension. Based on older
data, it was originally estimated that primary aldosteronism accounted for less than 1% of all patients with hypertension. Subsequent data,
however, indicated that it may actually occur in as many as 5-15% of patients with hypertension. Here we present a 66-year-old patient with a
history of hypertension who was diagnosed with primary hyperaldosteronism at the time he had developed a severe renal failure secondary to
a vascular nephropathy. This case report illustrates the difficulties in diagnosis of primary hyperaldosteronism, and highlights the effects of the
delay of diagnosis on renal survival and on patient quality of life.

Key - Words

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.

  1. Rossi GP, Bernini G, Caliumi C, et al. A prospective study of the prevalence of primary aldosteronism in 1125 hypertensive patients. J Am CollCardiol. 2006;48:2293-300.
  2. Douma S, Petidis K, Doumas M, et al. Prevalence of primary hyperaldosteronism in resistant hypertension: a retrospective observational study. Lancet. 2008;371:1921-6.
  3. Stowasser M1. Update in primary aldosteronism.J ClinEndocrinolMetab. 2015;100(1):1-10..2014-3663.
  4. John W. Funder, Robert M. Carey, Franco Mantero, et al. The Management of PrimaryAldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline. J Clin EndocrinolMetab. 2016 DOI:
  5. Young, W.F. Jr& Klee, G.G. Primary aldosteronism. Diagnostic evaluation. Endocrinology and Metabolism Clinics of North America. 1988;17:367-95.
  6. Funder JW, Carey RM, Fardella C, et al. Endocrine Society. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical practice guideline. J ClinEndocrinolMetab. 2008;93:3266-81.
  7. Kudva YC, SawkaAM, Young WF Jr. The laboratory diagnosis of adrenal pheochromocytoma: the Mayo Clinic experience. J ClinEndocrinolMetab 2003;88:4533-9.
  8. Young WF Jr. Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol. 2007 May;66(5):607-18.
  9. Bravo EL, Fouad-Tarazi FM, Tarazi RC, Pohl M, Gifford RW, Vidt DG: Clinical implications of primary aldosteronism with resistant hypertension. Hypertension. 1988;11:I207-11.
  10. Kaplan NM. The current epidemic of primary aldosteronism: causes and consequences. J Hypertens. 2004;22:863-9.
  11. Weinberger MH, Grim CE, Hollifield JW, Kem DC, Gangualy A, Kramer NJ, Yune HY, Wellman H, Donohue JP: Primary aldosteronism: Diagnosis, localization, and treatment. Ann Intern Med90 :386– 395,1979
  12. Bravo EL, Tarzi RC, Dustan HP, Fouad FM, Textor SC, Gifford RW, Vidt DG: The changing clinical spectrum of primary aldosteronism. Am J Med74 :641– 651,1983
  13. Weinberger MH, Fineberg NS: The diagnosis of primary aldosteronism and separation of two major subtypes. Arch Intern Med. 1993;153:2125-9.
  14. Young, W.F.Secondary Hypertension: Clinical Presentation, Diagnosis and Treatment.Humana Press, Totowa, NJ. 2004;119-37.
  15. Kearney PM, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data. Lancet. 2005;365:217–223.
  16. 11 Faselis C, Doumas M, Papademetriou V. Common secondary causes of resistant hypertension and rational for treatment. Int J Hypertens. 2011;2011:236239.
  17. Rye P, So B, Harvey A, et al. Unadjusted plasma renin activity as a ‘first look’ test to decide upon further investigations for primary aldosteronism. J Clin Hypertens. 2015;17:541–6.
  18. Kline GA, Pasieka JL, Harvey A, et al. High-probability features of primary aldosteronism may obviate the need for confirmatory testing without increasing false-positive diagnoses. J ClinHypertens. 2014;16:488–96.
  19. Mahmud A, Mahgoub M, Hall M, Feely J: Does aldosterone-to-renin ratio predict the antihypertensive effect of the aldosterone antagonist spironolactone? Am J Hypertens. 2005;18:1631-5.
  20. Karagiannis A. Treatment of primary aldosteronism: where are we now? Rev EndocrMetabDisord. 2011;12:15–20.
  21. Do HeeKim ,Hee Jin Kwon , Sang A. Jib , HyeRyoun Jang , Sin-Ho Jung , Jung-Han Kim, Jae Hyeon Kim, Jung Eun Lee. Riskfactors for renalimpairmentrevealedafterunilateraladrenalectomy in patients withprimaryaldosteronism.Medicine (2016) 95:27
E-mail :
Password :
Remember Me Forgot password? Sign UP
Keywords most used
Child treatment diagnosis surgery prognosis Tunisia Children Crohn’s disease Breast cancer screening Cancer epidemiology Ulcerative colitis Risk factors mammography
Sign up to receive our newsletter
E-mail :
Stay in Touch
Join Us! !