Hypertension Journal

Show Contents

Primary Hyperaldosteronism: TypicalClinical Manifestations
  JOHTN
SECONDARY HYPERTENSION
Primary Hyperaldosteronism: Typical
Clinical Manifestations
1Amit A Bharadiya, 2GS Karthik, 3DVSNL Sharma, 4V Shanta Ram
1Registrar, 2Resident, 3Consultant, 4Professor
1Department of Cardiology, Apollo Hospital, HyderabadTelangana, India
2Department of Internal Medicine, Apollo Hospital, HyderabadTelangana, India
3Department of Urology, Apollo Hospital, Hyderabad, TelanganaIndia
4Department of Medicine, Nizams Institute of Medical SciencesHyderabad, Telangana, India
Correspondence Author: Amit A Bharadiya, Registrar, Departmentof Cardiology, Apollo Hospital, Hyderabad, Telangana, India
Phone: +919000090339
e-mail: dr.aabharadiya@gmail.com
 
ABSTRACT
A 34-year-old lady presented to the hospital with symptomsof headache and exertional dyspnea. On examination, shewas found to have blood pressure of 180/120 mm Hg, whichwas confirmed and her blood pressure was unresponsive tostandard antihypertensive therapy. She had easily inducibleand unprovoked hypokalemia even on small doses of diuretic.The possibility of primary hyperaldosteronism was considered.Her plasma aldosterone was high with low plasma renin activity,confirming the biochemical diagnosis of hyperaldosteronism. Sheunderwent workup with computed tomography of the abdomenthat showed left adrenal mass, likely an adenoma. After propermedical preparation, she underwent laparoscopic adrenalectomy.Upon successful removal of the adrenal mass, her aldosterone,renin, potassium, and blood pressure levels were normalized. Thiscase illustrates classical features of primary hyperaldosteronismwith clinical diagnostic and therapeutic considerations.
Keywords: Hypokalemia, Primary hyperaldosteronism,Secondary hypertension.
How to cite this article: Bharadiya AA, Karthik GS,Sharma DVSNL, Ram VS. Primary Hyperaldosteronism: TypicalClinical Manifestations. Hypertens J 2016;2(2):105-107.
Source of support: Nil
Conflict of interest: None
 
 

INTRODUCTION

Systemic hypertension is a common risk factor forcardiovascular disease (CVD), premature morbidity,disability, and excessive mortality. Of all the contributingfactors for CVD in India (and globally), hypertension iswidely prevalent. Despite the decades of professional andpublic education, hypertension is vastly underdiagnosedand often undertreated. Therefore, in a large proportion of patients, blood pressure level is not under control. Anoverwhelming majority of patients with hypertensionhave "primary" type, wherein a specific underlyingcause is not identified. A small percentage (about 5%)has "secondary" hypertension, wherein an underlyingcause for blood pressure elevation exists. In secondaryforms of hypertension, some are curable by correcting theunderlying cause, while in others, blood pressure levelimproves with "specific" medical treatment to counterthe causative mechanisms. Primary aldosteronism (PA),also called hyperaldosteronism, is an uncommon causeof secondary hypertension occurring in about 1% of allpatients. Primary aldosteronism is a result of spontaneousautonomous excessive production of aldosterone by theglomerular zone of the adrenal glands. Some believe thatthe incidence is much higher than the reported figures dueto improved diagnostic methods. The manifestations ofPA comprise hypertension, (inappropriate) hypokalemia,low plasma renin activity, and high aldosterone levels1-5(Table 1). The specific treatment of PA depends onthe pathological subtype responsible for the disease.We present a case of PA detected during the course ofmanaging new-onset hypertension in a young patient.
 
Table 1: Features of primary aldosteronism
Primary Hyperaldosteronism: TypicalClinical Manifestations

CASE REPORT

A 34-year-old lady presented to our hospital with chronicbifrontal headache and exertional dyspnea of 6 monthsduration. Three months prior to the hospital visit, shewas examined by a physician and diagnosed to have highblood pressure of 180/120 mm Hg for which she was prescribedtablet olmesartan and hydrochlorothiazide oncea day (40/12.5 mg). On follow-up, she was found to havepersistently high blood pressure of > 160/100 mm Hg forwhich she was further evaluated. Her complete reports onblood, blood urea, serum creatinine, and urine examinationswere normal. However, two-dimensional (2D) echoshowed concentric left ventricular hypertrophy with normal ejection fraction. Due to the persistent high bloodpressure, the patient was referred to us for further evaluation.Based on her past history of hypokalemia, bloodsamples were sent for serum electrolytes, which showedserum sodium as 143 mEq/L and serum potassium as2.3 mEq/L. Plasma aldosterone was high (582 pmol/mL)and plasma renin activity was low (0.17 ng/mL/hour).Due to the high aldosterone to renin ratio (3423 pmol/L:ng/mL/hour), primary hyperaldosteronism was suspected.Computed tomography (CT) of the abdomen revealeda well-defined hypodense lesion of size 25 × 16 mmin the left adrenal gland, which was most likely to bean adenoma (Fig. 1). After 3 to 4 weeks of medical treatmentwith spironolactone to normalize her potassiumlevel, she underwent laparoscopic left adrenalectomy,which was successfully accomplished with an uneventfulrecovery (Fig. 2). After the 3rd postoperative day, plasmaaldosterone levels were measured again and were29.39 pmol/mL; further, plasma renin activity was0.46 ng/mL/hour, sodium levels were normal, potassiumlevels were 3.8 mEq/L, and blood pressure was 110/80mm Hg without any antihypertensive drugs. Adrenalspecimen was proved to be adenoma by histopathology.She was normotensive without any antihypertensivedrugs even at her follow-up visit after a month (Table 2).

Hypertension Journal, April-June, Vol 2, 2016 105

Amit A Bharadiya et al

Primary Hyperaldosteronism: TypicalClinical Manifestations
Fig. 1: Computed tomography scan showing left adrenal massand normal right adrenal gland

DISCUSSION

Secondary forms of hypertension constitute only a smallnumber in the vast ocean of patients with hypertension. Although unusual, secondary causes of hypertensionby no means are rare in clinical practice. It is importantto recognize secondary forms of hypertension becausespecific medical or corrective treatment may reversethe disorder. When the pathophysiology of a secondarycause is offset by "specific" therapy, blood pressure showsremarkable improvement, and in some patients, it can becurative. The suspicion of a PA depends on the presentingclinical features and laboratory findings. This casereport represents a typical patient with manifestationsof PA comprising hypertension, hypokalemia, metabolicalkalosis, low plasma renin activity, and high aldosteronelevel. Whenever a patient with hypertension demonstratesunexplained and inappropriate hypokalemia, PA shouldbe considered in the differential diagnosis. Upon confirmationof hypokalemia (by repeat testing), the possibilityof PA should be pursued. The biochemical hallmarksof PA are suppressed renin and elevated aldosteronelevels.6-8 One should remember that increased reninwith elevated aldosterone level is symbolic of "secondary"aldosteronism comprising diuretic use, volumedepletion, vasodilatory drugs, and renal ischemia.However, suppressed renin and high aldosterone levelare pathognomonic of PA in a patient with hypertensionand unexplained hypokalemia. Once the biochemicaldiagnosis of PA is made, the next diagnostic step is todetermine if the adrenal disease is unilateral (adenoma)or bilateral (hyperplasia).
 
Primary Hyperaldosteronism: TypicalClinical Manifestations
Fig. 2: Gross appearance of left adrenal gland with the massafter surgical removal

It shouldbe kept in mind that an aldosterone producing adenomacan be treated medically if surgery is not possible but abilateral adrenal hyperplasia should always be managedwith medical therapy only; surgery is not recommended.A properly done CT scan of the adrenal glands (with small thin cuts) and/or magnetic resonance imaging(MRI) should suffice in the radiological localization ofPA. Due to technical difficulties and challenges in locatingthe right adrenal vein, we do not recommend adrenalvein catheterization for diagnostic purpose. It is best tomake therapeutic plans and follow-up on the basis of wellperformedCT or MRI of adrenal glands. Similarly, adrenalgland scintigraphy is not generally required to localizePA.12 In summary, PA is an unusual cause of hypertension.However, it is amenable to specific surgical or medicaltherapy that ameliorates hypokalemia and improves theblood pressure control as was demonstrated in our patient.Hypertension can be severe in patients with PA and cancause target organ damage.13,14 The clinical diagnosis issuspected on the basis of unexplained hypokalemia in apatient with hypertension and high aldosterone; further,it can be confirmed by aldosterone - renin ratio (ARR) andradiological findings on a CT scan (thin slice) or MRI of theadrenal glands. Depending on the unilaterality or bilateralityof the adrenal gland abnormality, specific medicalor surgical therapy is planned, which cures hypokalemiaand often improves or cures hypertension as well. The former is best managed bysurgical removal of affected gland, whereas the latter isbest managed by chronic medical therapy inclusive ofan aldosterone antagonist (spironolactone).9-11
 
106

Primary Hyperaldosteronism: Typical Clinical Manifestations

REFERENCES

  1. Ram CVS. Primary aldosteronism - recognition andmanagement. Rhode Island Med J 1977 Jun;60(6):301-305.
  2. Ram CVS. Primary aldosteronism - its role in hypertension.Consultant 1981;21:2-11.
  3. Ram CVS. Hypertension: when to suspect underlyingpheochromocytoma or aldosteronism. Consultant 1996;33:147-153.
  4. Lim PO, Rodgers P, Cardale K, Watson AD, MacDonald TM.Potentially high prevalence of primary aldosteronism in aprimary-care population. Lancet 1999 Jan 2;353(9146):40.
  5. Loh KC, Koay ES, Khaw MC, Emmanuel SC, Young WF Jr.Prevalence of primary aldosteronism among Asian hypertensivepatients in Singapore. J Clin Endocrinol Metab 2000Aug;85(8):2854-2859.
  6. Stowasser M, Gordon RD. The aldosterone-renin ratio forscreening for primary aldosteronism. Endocrinologist2004;14:267-276.
  7. Stowasser M, Gordon RD. Primary aldosteronism: carefulinvestigation is essential and rewarding. Mol Cell Endocrinol2004 Mar 31;217(1-2):33-39.
  8. Oliveri O, Ciacciarelli A, Signorelli D, Pizzolo F, Guarini P,Pavan C, Corgnati A, Falcone S, Corrocher R, Micchi A,et al. Aldosterone to renin ratio in a primary care setting.The Bussolengo study. J Clin Endocrinol Metab 2004Sep;89(9):4221-4226.

 
  1. Rutherford JC, Taylor WL, Stowasser M, Gordon RD. Successof surgery in primary aldosteronism judged by residualautonomous aldosterone production. World J Surg 1998Dec;22(12):1243-1245.
  2. Rutherford JC, Stowasser M, Tunny TJ, Klemm SA, Gordon RD.Laparoscopic adrenalectomy. World J Surg 1996;20(7):758-760.
  3. Parthasarathy HK, Menard J, White WB, Young WF Jr,Williams GH, Williams B, Ruilope LM, McInnes GT,Connell JM, MacDonald TM. A double-blind, randomizedstudy comparing the antihypertensive effect of eplerenone andspironolactone in patients with hypertension and evidence ofprimary aldosteronism. J Hypertens 2011 May;29(5):980-990.
  4. Stowasser M, Gordon RD, Rutherford JC, Nikwan NZ,Daunt N, Slater GJ. Diagnosis and management of primaryaldosteronism. J Renin Angiotensin Aldosterone Syst 2001Sep;2(3):156-169.
  5. Rossi GP, Sacchetto A, Visentin P, Canali C, Graniero GR,Palatini P, Pessina AC. Changes in left ventricular anatomyand function in hypertension and primary aldosteronism.Hypertension 1996 May;27(5):1039-1045.
  6. Rossi GP, Bernini G, Desideri G, Fabris B, Ferri C, Giacchetti G,Letizia C, Maccario M, Mannelli M, Matterello MJ. Renaldamage in primary aldosteronism: results of the PAPY study.Hypertension 2006 Aug;48(2):232-238.

Hypertension Journal, April-June, Vol 2, 2016 107