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Primary Aldosteronism—Not Just About Potassium and Blood Pressure

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Primary Aldosteronism—Not Just About Potassium and Blood Pressure QJM: An International Journal of Medicine, 2017, 175–177 doi: 10.1093/qjmed/hcw224 Advance Access Publication Date: 9 January 2017 Case report CASE REPORT Primary aldosteronism—not just about potassium and Downloaded from https://academic.oup.com/qjmed/article-abstract/110/3/175/2875723 by guest on 27 November 2019 blood pressure T.H. Toh, C.V. Tong and H.C. Chong From the Department of Internal Medicine, Malacca General Hospital, Malacca, Malaysia Address correspondence to T.H. Toh, Department of Internal Medicine, Malacca General Hospital, Malacca, Malaysia. email: [email protected] She presented again in the subsequent years with body Learning point for clinicians weakness, recurrent low electrolyte levels and was hyperten- sive. Gitelman or Bartter syndrome was considered initially due Primary aldosteronism is one of the few potentially cur- to certain overlapping features. The development of hyperten- able causes of hypertension and it requires a high index of suspicion in making an accurate diagnosis. This case sion later prompted the investigation for hyperaldosteronism. illustrates the importance of looking at electrolytes other Phaechromocytoma and Cushing’s syndrome were also ruled than just the potassium in a patient with severe primary out. We performed an aldosterone renin ratio, followed by a sa- aldosteronism. line suppression test. Patient was on prazosin and verapamil when these tests were carried out and had serum potassium >4 mmol/l with potassium supplements. Her laboratory results are in Table 1. Computed tomography of the adrenal showed a well defined Introduction hypodense lesion in the medial limb of the left adrenal gland Primary aldosteronism is a well established cause of secondary measuring 2.5 Â 1.6 Â 1.6 cm. She underwent a peritoneoscopic hypertension, typically manifesting with hypertension, hypo- left adrenalectomy in 2016, resulting in normalization of the kalemia and metabolic alkalosis. On the other hand, its effects blood pressure and all of the electrolyte levels (Figure 1). The on calcium, magnesium and phosphate metabolism are less histopathological examination was consistent with an adrenal well reported. In this report, we present a case of severe primary adenoma. aldosteronism due to adrenal adenoma who presented with a prolonged period of hypocalcemia, hypomagnesemia and hypo- Discussion phosphatemia along with uncontrolled hypertension and hypokalemia. A combination of hypokalemia, hypocalcemia, hypomagnes- emia and metabolic alkalosis, should raise the suspicion for Bartter or Gitelman syndrome. Gitelman’s syndrome is usually Case report diagnosed by late childhood or even adulthood, presenting with 1 A 29-year-old woman first presented in 2010 with peripheral cramps, fatigue, polyuria and nocturia. Bartter syndrome is numbness and a urinary tract infection. There were no gastro- characterized by hypokalemia, hypochloremia, metabolic alkal- intestinal losses. Her family history was unremarkable. She also osis and hyperreninemia with normal blood pressure.2 The denied taking any medications. Clinical examination revealed presence of hypertension and low plasma renin in our patient no significant findings. Her blood pressure was normal. She was made these differential diagnoses unlikely. found to have hypokalemia, hypocalcemia, hypomagnesemia The diagnosis in this case was not easy as the hypertension and hypophosphataemia. She was treated with antibiotics, po- only unveiled itself in later years. The prevalence of masked tassium and calcium correction and was given a clinic review. hypertension in general was found to be higher in patients who Due to logistics and social issues, she was unable to attend her went through 24-h ambulatory BP monitoring compared to follow-up visits. home BP monitoring.3 Submitted: 15 November 2016; Revised (in revised form): 24 November 2016 VC The Author 2017. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: [email protected] 175 176 | QJM: An International Journal of Medicine, 2017, Vol. 110, No. 3 Table 1. Blood parameters of the patient since presentation. Parameter Value Normal range Potassium 2.7 mmol/l 3.5–5.1 Sodium 137 mmol/l 136–145 Chloride 91 mmol/l 98–106 Corrected calcium 1.97 mmol/l 2.2–2.5 Magnesium 0.62 mmol/l 0.65–1.05 Phosphate 0.66 mmol/l 0.87–1.45 Venous blood gas pH 7.47, HCO338, BE 15, Urine pH 8 iPTH 16 pg/m 5–39 Downloaded from https://academic.oup.com/qjmed/article-abstract/110/3/175/2875723 by guest on 27 November 2019 25hydroxyvitamin D 64.4 nmol/l 50–80 TSH 2.5 mU/l 0.4–4.0 Free T4 16 pmol/l 12–22 24-h urinary calcium 8.2 mmol/d 2.5–7.5 24-h urinary potassium 135 mmol/d 25–125 24-h urinary phosphate 3 mmol/d 12.9–42 Overnight dexamethasone suppression test (cortisol) 30 nmol/l 24-h urine catecholamine Norepinephrine 4.7 lg/d 12.1–85.5 Epinephrine 3.8 lg/d 1.7–22.4 Dopamine 5.5 lg/d <498 Aldosterone 2911 pmol/l 102.5–858.7 supine, 102.5–1196.6 upright Direct renin 3.9mU/l 4.2–59.7 supine, 5.3– 99.1 upright Aldosterone to renin ratio 746 <91 unlikely, >122 primary aldosteronism Aldosterone post saline suppression test >2770 pmol/l Aldosterone >400–primaryaldosteronism Figure 1. Pre- and postoperative levels of serum phosphate, magnesium and calcium. The persistently low levels magnesium and calcium in this mineralocorticoid promoting distal tubular Naþ reabsorption case were likely related to the direct effect of hyperaldosteron- without retarding magnesium or calcium excretion.4 This was ism. Studies on rats given aldosterone salt treatment produced actually consistent in our patient where urinary calcium excre- hypermagnesuria and hypercalciuria. The probable mechanism tion was high. Patients with primary aldosteronism were also is thought to be related to expansion of the extravascular space, detected to have significantly higher concentration of parathy- resulting in decreased proximal tubular reabsorption and roid hormone compared to both normotensive and essential thereby increased distal delivery of Naþ,Mg2þ,Ca2þ, with the hypertensive subjects.5 This also echoes in rats with T.H. Toh et al. | 177 aldosteronism. Ca2þ and Mg2þ losses lead to a fall in concentra- 2. Stein JH. The pathogenetic spectrum of Bartter’s syndrome. tion of Ca2þ and Mg2þ with secondary hyperparathyroidism Kidney Int 1985; 28:85. and bone resorption.4 Chronic hypomagnesemia on the other 3. Kang YY, Li Y, Huang QF, Song J, Shan XL, Dou Y, et al. hand can lead to intracellular magnesium deficiency causing Accuracy of home versus ambulatory blood pressure monitor- impairment of PTH secretion and response to PTH.1 The normal ing in the diagnosis of white-coat and masked hypertension. PTH level in our patient could be due to conflicting effects of J Hypertens 2015; 33:1580–7. both hypocalcemia and hypomagnesemia. 4. Chhokar VS, Sun Y, Bhattacharya SK, Ahokas RA, Myers LK, Xing Z, et al. Hyperparathyroidism and the calcium paradox of Conflict of interest: None declared. aldosteronism. Circulation 2005; 111:871–8. 5. Rossi E, Sani C, Perazzoli F, Casoli MC, Negro A, Dotti C. References Alternations of calcium metabolism and of parathyroid func- 1. Kasifoglu T, Akalin A, Cansu DU, Korkmaz C. Hypokalemic par- tion in primary aldosteronism, and their reversal by spirono- Downloaded from https://academic.oup.com/qjmed/article-abstract/110/3/175/2875723 by guest on 27 November 2019 alysis due to primary hyperaldosteronism simulating gitel- lactone or by surgical removal of aldosterone-producing man’s syndrome. Saudi J Kidney Dis Transpl 2009; 20:285–7. adenomas. Am J Hypertens 1995; 8:884–93..
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