Normotensive primary aldosteronism

Shiroto, Hideo; Ando, Haruo; Ebitani, Isao; Hara, Masao; Numazawa, Kazuo; Kawamura, Sin’itirô; Sasaki, Hideo

doi:10.1016/0002-9343(80)90474-x

Cited by 32 publications

(21 citation statements)

References 9 publications

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“…Neither patient had a very low salt intake. In literature, the pressure response to drugs has been studied in four cases of normotensive primary hyperaldosteronism (7,8,10,13); the response to angiotensin II was unexpectedly normal in these four cases, and one patient was responsive to adrenalin (10). These results suggest that the variability of the pressure response to some agents cannot alone account for the normal blood pressure.…”

Section: Discussionmentioning

confidence: 98%

“…Only 16 cases of normotensive primary hyperaldosteronism have been reported in the literature, with only 10 in the English literature (5)(6)(7)(8)(9)(10)(11)(12)(13)(14). About 75% of cases were described in Eurasians (especially Japanese).…”

Section: Discussionmentioning

confidence: 99%

“…Arterial hypertension could be related to the early diagnosis of hyperaldosteronism (5,7,8,10,11). However, the 3-year history of hypokalemia in the first patient, and the second patient's blood pressure stability for more than one year before surgery despite hypokalemia, argue against this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

“…In particular, hypokalemia is lacking in 7 to 38% of cases (3,4). In contrast, normotensive primary hyperaldosteronism is exceedingly rare: to the best of our knowledge, only ten cases have been documented (5)(6)(7)(8)(9)(10)(11)(12)(13)(14). We report two new cases studied by means of ambulatory blood pressure monitoring (ABPM).…”

Section: Introductionmentioning

confidence: 99%

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Aldosterone-producing adenoma without hypertension: a report of two cases

et al. 1999

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Normotensive primary hyperaldosteronism is exceedingly rare. We report two new cases of this syndrome in two middle-aged women, one of Asian origin. The presenting signs were tetany in one case and an adrenal mass in the other. Neither patient had hypertension, despite repeated measurements with a manual armlet. A typical biological profile of primary hyperaldosteronism was demonstrated in both patients, including hypokalemia with inappropriate kaliuresis, elevated resting plasma aldosterone, and undetectable plasma renin activity. The circadian rhythm of blood pressure was studied by ambulatory monitoring pre-and post-operatively. It confirmed the lack of hypertension, but the circadian rhythm of blood pressure was lost before surgery in one patient. Surgical removal of the histologically typical aldosterone-producing adenomas normalized the kalemia. The main finding in these two patients was spontaneously low blood pressure in the post-operative period. This suggests that excess aldosterone induced relative hypertension in these patients whose blood pressure was spontaneously very low. Genetic screening for dexamethasone-sensitive hyperaldosteronism was negative in both patients.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aldosterone-producing adenoma without hypertension: a report of two cases

et al. 1999

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“…There have been several case reports, describing PA without hypertension, [25][26][27][28][29][30][31] although the reason for the absence of hypertension has not been clarified in any of the cases of normotensive PA reported. It is suggested that a short duration of hyperaldosteronemia could explain normotension in those patients.…”

mentioning

confidence: 99%

Should primary aldosteronism be diagnosed among normotensive subjects during general health check-up and/or at general outpatient clinics?

Nishikawa

Omura

2010

Hypertens Res

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Severe hypercalcemic hyperparathyroidism developing in a patient with hyperaldosteronism and renal resistance to parathyroid hormone

Park-Sigal

Don

Porzig

et al. 2012

Journal of Bone and Mineral Research

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We evaluated an African American woman referred in 1986 at age 33 years because of renal potassium and calcium wasting and chronic hip pain. She presented normotensive, hypokalemic, hypocalcemic, normophosphatemic, and hypercalciuric. Marked hyperparathyroidism was evident. Urinary cyclic adenosine monophosphate (cAMP) excretion did not increase in response to parathyroid hormone (PTH) infusion, indicating renal resistance to PTH. X-rays and bone biopsy revealed severe osteitis fibrosa cystica, confirming skeletal responsiveness to PTH. Renal potassium wasting, suppressed plasma renin activity, and elevated plasma and urinary aldosterone levels accompanied her hypokalemia, suggesting primary hyperaldosteronism. Hypokalemia resolved with spironolactone and, when combined with dietary sodium restriction, urinary calcium excretion fell and hypocalcemia improved, in accord with the known positive association between sodium intake and calcium excretion. Calcitriol and oral calcium supplements did not suppress the chronic hyperparathyroidism nor did they reduce aldosterone levels. Over time, hyperparathyroid bone disease progressed with pathologic fractures and persistent pain. In 2004, PTH levels increased further in association with worsening chronic kidney disease. Eventually hypercalcemia and hypertension developed. Localizing studies in 2005 suggested a left inferior parathyroid tumor. After having consistently declined, the patient finally agreed to neck exploration in January 2009. Four hyperplastic parathyroid glands were removed, followed immediately by severe hypocalcemia, attributed to ''hungry bone syndrome'' and hypoparathyroidism, which required prolonged hospitalization, calcium infusions, and oral calcitriol. Although her bone pain resolved, hyperaldosteronism persisted. ß

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Normotensive primary aldosteronism

Cited by 32 publications

References 9 publications

Aldosterone-producing adenoma without hypertension: a report of two cases

Aldosterone-producing adenoma without hypertension: a report of two cases

Should primary aldosteronism be diagnosed among normotensive subjects during general health check-up and/or at general outpatient clinics?

Severe hypercalcemic hyperparathyroidism developing in a patient with hyperaldosteronism and renal resistance to parathyroid hormone

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