Cases reported "Hyperaldosteronism"

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1/131. Primary aldosteronism with aldosterone-producing adrenal adenoma in a pregnant woman.

    A 30-year-old pregnant woman complained of muscle weakness at 29 weeks' gestation. She was hypertensive with severe hypokalemia. Lower plasma renin activity and higher aldosterone level than the normal values in pregnancy suggested primary aldosteronism. A cesarean delivery was performed at 31 weeks' gestation because of pulmonary congestion. The neonatal course was uncomplicated. The laparoscopic adrenalectomy for a 2.0-cm right adrenal adenoma resulted in normalizing of her blood pressure and serum potassium level. Although primary aldosteronism is rare, especially during pregnancy, it should be always considered as one of etiologies of hypertension in pregnancy.
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2/131. aldosterone-producing adenoma without hypertension: a report of two cases.

    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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3/131. Primary aldosteronism caused by aldosterone-producing adenoma in pregnancy--complicated by EPH gestosis.

    pregnancy in conjunction with primary aldosteronism is an unusual occurrence. We report a 28-year-old woman who presented with mild hypertension and hypokalemia as manifestations of primary aldosteronism caused by an aldosterone-producing adenoma in the left adrenal gland during pregnancy. Although the diagnosis was straightforward, the patient refused to undergo the proposed operation during the second trimester of her pregnancy. She was not admitted to hospital until she developed EPH gestosis in the 27th week of gestation, which had an unfavourable outcome for the infant who died nine days after delivery. The patient underwent a laparoscopic adrenalectomy which resulted in normalization of blood pressure and blood potassium levels. In cases of aldosterone-producing adenoma, surgery in the second trimester is the most appropriate option to avoid a poor obstetric outcome.
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4/131. Abolished nocturnal blood pressure fall in a boy with glucocorticoid-remediable aldosteronism.

    Glucocorticoid-remediable aldosteronism (GRA) is a rarely recognised cause of arterial hypertension. We report the features of a 13-year-old boy with hypertension (casual blood pressure (BP) 140-180/95-110 mm Hg) discovered during a routine paediatric check. Ambulatory BP monitoring (ABPM) revealed significant hypertension with an abolished nocturnal BP fall (mean daytime BP 155/108 mm Hg, mean night-time BP 156/104 mm Hg, nocturnal BP fall 0/4%) which was indicative of secondary hypertension. Despite triple antihypertensive drug therapy the hypertensive control was unsatisfactory. Laboratory tests revealed hypokalaemia (3.0 mmol/l), suppressed plasma renin activity (0.012 nmol/l/h) and high plasma aldosterone (1.190 nmol/l). The diagnosis of primary hyperaldosteronism was established and GRA was further confirmed by the presence of the chimaeric GRA-gene and dexamethasone therapy was initiated. During the next 2 months of dexamethasone therapy all three antihypertensive drugs were discontinued and BP remained under control with restoration to a normal nocturnal BP fall (mean daytime BP 129/77 mm Hg, mean night-time BP 113/64, nocturnal BP fall 12/17%). A change of therapy from dexamethasone to spironolactone was necessary due to the side effects of corticosteroids after 3 months. spironolactone alone (0.8-2 mg/kg/day) was able to control the BP sufficiently. In conclusion, to our knowledge, this is the first reported case of abolished nocturnal BP fall in a patient with genetically proven GRA. This study indicates that GRA can cause severe hypertension even in children, associated with an abolished nocturnal BP fall. GRA thus should be excluded in all hypertensive patients with circadian BP rhythm disturbances.
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5/131. Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism.

    The discovery of two forms of secondary hypertension in the same patient is unusual and suggests similar pathophysiological mechanisms, a predisposition to one type in the presence of the other or a chance occurrence. We describe two patients with renal artery stenosis who after successful correction of the stenotic lesions were discovered to have primary hyperaldosteronism associated with bilateral adrenal hyperplasia. Initially prior to revascularisation of the renal artery stenosis, the diagnosis of primary hyperaldosteronism was not evident. Both patients were subjected to further diagnostic evaluation after the appearance of hypokalaemia in one patient and continued resistant hypertension in both patients. The addition of spironolactone therapy reduced blood pressure impressively in both patients. Clinicians should be aware of the possibility that these two forms of secondary hypertension may be present in the same patient and that optimal blood pressure control requires diagnostic assessment and intervention for both disorders.
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6/131. hypokalemia and metabolic alkalosis: algorithms for combined clinical problem solving.

    This article reviews an approach to patients with hypokalemia and metabolic alkalosis using the information obtained from spot urine chloride values, blood pressure determinations, and renin and aldosterone measurements in order to simplify clinical problem solving.
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7/131. Primary aldosteronism in pregnancy.

    Aldosteronism is a rare complication of pregnancy. We report a case of a 26-year-old woman who became pregnant soon after a diagnosis of primary aldosteronism due to left adrenal adenoma was made. Only oral potassium supplementation was required in addition to routine prenatal care until 36 weeks' gestation. Subsequently, antihypertensive medication was needed to control elevated blood pressure. A healthy male infant was delivered by cesarean section because of abruptio placentae. The postoperative course was uneventful. Left adrenalectomy was conducted eight months after delivery under laparoscopic visualization. In this case report, we discuss management of aldosteronism in pregnancy and review the literature.
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8/131. Primary hyperaldosteronism without suppressed renin due to secondary hypertensive kidney damage.

    Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory hypertension, and normal to high normal PRA levels whose aldosterone/renin ratios were still elevated because of disproportionately high aldosterone levels. All available medical data on the patients as well as publications on the aldosterone/renin relationship in primary hyperaldosteronism were reviewed to explain the unusual findings. In one patient, histologically proven renal arteriolosclerosis was the probable cause of the escape of PRA from suppression by an aldosterone-producing adenoma. In the other two patients, hypertensive kidney damage due to primary hyperaldosteronism was the most likely explanation for the inappropriately high PRA, as in patient 1. All patients had high normal or slightly elevated serum creatinine levels and responded to 200 mg spironolactone/day with increased serum creatinine and hyperkalemia. hyperkalemia was probably due to a decreased filtered load of sodium and a spironolactone-induced decrease in mineralocorticoid function. Two patients were cured of hyperaldosteronism by unilateral adrenalectomy but still need some antihypertensive therapy, whereas one patient has probable bilateral adrenal disease, with normal blood pressure on a low dose of spironolactone. In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. An increased aldosterone/PRA ratio is still useful in screening for primary hyperaldosteronism. These patients may respond to spironolactone therapy with a strong increase in serum creatinine and potassium. Early specific treatment of primary hyperaldosteronism is therefore indicated, and even a patient with advanced hypertension will profit from adrenalectomy or cautious spironolactone treatment.
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9/131. Conn's syndrome and bilateral renal artery stenosis in the presence of multiple renal arteries.

    We report the case of a 42-year-old male who was admitted to our hospital after an acute hypertensive crisis despite four-way anti-hypertensive therapy. The renal scintigraphy, the excretory urogram and the biochemical profile performed two years before were unremarkable, except for slightly elevated serum creatinine and plasma aldosterone, in presence of normal aldosterone/renin ratio. The renal arterial angiography that was performed despite a second unremarkable scintigraphy revealed high-grade bilateral arterial stenosis in the presence of multiple renal arteries. Following dilatation of the left stenosis, the aldosterone/renin ratio was pathologic. Recumbent and orthostatic aldosterone values were 830 pg/ml and 1824 pg/ml, respectively, and recumbent and orthostatic renin values were 0.82 and 1.21 ng angiotensin i/ml/h, respectively. The abdominal computed tomography performed to investigate a possible concomitant Conn's syndrome resulted in the detection of a left adrenal tumor. After resection of the lesion, plasma-aldosterone levels normalized and a pronounced rise in serum potassium levels was observed. Following angioplasty of the right renal artery stenosis, blood pressure could easily be managed with combined beta and calcium channel blocker therapy. Particularly in cases of bilateral (but also in the presence of unilateral) renal artery stenosis in association with Conn's syndrome, all the available screening methods for these disorders can fail. In cases of poor response to combination hypertensive therapies, renal arteriography and a fludrocortisone-suppression test should be performed in order to rule out both renal arterial stenosis and Conn's syndrome, even in the absence of clinical and biochemical findings suspicious for either disorder.
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10/131. A case of unilateral adrenal hyperplasia: the diagnostic dilemma of hyperaldosteronism.

    OBJECTIVE: To report the successful laparoscopic surgical management of a case of right unilateral adrenal hyperplasia. methods: We present a case of unilateral adrenal hyperplasia and review the pertinent literature. The effectiveness of surgical treatment of unilateral adrenal hyperplasia is evaluated. RESULTS: A 50-year-old man had a 7-year history of hypertension, which had been treated with antihypertensive medications. On initial assessment, he was taking long-acting diltiazem, 240 mg twice a day, and his blood pressure was 150/84 mm Hg. He was noted to have recurrent hypokalemia, low plasma renin activity, increased plasma aldosterone concentration, and high urinary aldosterone levels. magnetic resonance imaging of the adrenal glands revealed a normal left adrenal gland and fullness of the right adrenal gland. Selective adrenal vein catheterization showed findings consistent with a right-sided adrenal gradient. Surgical removal of the right adrenal gland laparoscopically alleviated his symptoms and cured his hypertension and hypokalemia. Pathologic examination of the right adrenal gland revealed diffuse hyperplasia of the zona fasciculata and zona reticularis. plasma aldosterone, renin, and potassium levels returned to normal postoperatively, and his blood pressure declined to 120/70 mm Hg. At 1-year follow-up, the patient remained normotensive without the need for antihypertensive agents. CONCLUSIONS: This rare type of hyperaldosteronism, known as unilateral adrenal hyperplasia, is difficult to categorize not only because it fails to typify a conventional subtype but also because it is difficult to confirm the pathologic diagnosis. Recognition of the variety of provocative, biochemical, and imaging results that may be seen in this disorder is important in making the correct diagnosis. Determining unilaterality of disease by selective adrenal vein sampling can result in a cure of hypertension and hypokalemia by surgical resection.
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