hyperaldosteronism/إعياء

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A disease-specific quality of life questionnaire for primary aldosteronism.

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To develop a primary aldosteronism (PA) disease-specific Health-Related Quality of Life (HRQoL) questionnaire.We included newly diagnosed patients with PA (n=26), and patients with PA after adrenalectomy (n=25) or treated with mineralocorticoid receptor

A case of primary aldosteronism revealed after renal transplantation.

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BACKGROUND A 57-year-old woman was referred to a nephrology clinic because of chronic hypokalemia. She had a history of polycystic kidney disease, resistant hypertension, atrial fibrillation, type 2 diabetes, stroke, and end-stage renal disease, and had received a kidney transplant from a deceased

Normotensive hypokalemic primary hyperaldosteronism mimicking clinical features of anorexia nervosa in a young patient: A case report

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Rationale: The typical clinical presentations of patients with primary aldosteronism (PA) include generalized weakness, fatigue, high blood pressure, and potassium deficiency. However, normotensive PA is rare. Therefore, an atypical

[Hypokalemia, a key clinical data for diagnosing primary hyperaldosteronism].

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We report a case of a 37 year-old man with a long history of hypertension under treatment, who was admitted at our institution with intense fatigue and weakness of lower limbs. The laboratory results at Emergency Department showed severe hypokalemia. A study of secondary hypertension was carried

[Diagnosis and Treatment of Primary Aldosteronism in West China Hospital of Sichuan University from 2009 to 2018]

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Objective: To summary the clinical diagnosis and treatment of primary aldosteronism (PA) in West China Hospital (WCH) of Sichuan University during 2009-2018. Methods: This

Prolonged hyperkalemia following unilateral adrenalectomy for primary hyperaldosteronism.

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Hypokalemia associated with aldosterone-producing adenomas (APA) are almost corrected following successful unilateral adrenalectomy. Prolonged hyperkalemia after unilateral adrenalectomy is rarely reported and may be overlooked. We describe a 62-year-old man who presented with fatigue and dizziness

Acid-base, calcium, potassium and aldosterone metabolism in renal tubular acidosis.

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Classic renal tubular acidosis is characterized by a primary defect in establishment of a large hydrogen ion gradient across the distal renal tubule. Thus the development of hyperchlorenic metabolic acidosis follows. In addition, hypokalemia results from renal potassium wasting secondary

Gitelman Syndrome.

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Gitelman syndrome (GS) is the most frequently inherited renal salt-wasting tubulointerstitial disease. It follows variable but usually asymptomatic benign course. We present a rare case of GS that remained clinical enigma. A 22-year male presented with severe episodic fatigue involving all limbs

Hypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman's syndrome.

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A 35-year-old male patient was admitted with fatigue and muscle weakness. He had been on methimazole due to thyrotoxicosis for 2 weeks. Laboratory tests showed overt hyperthyroidism and hypokalemia. Potassium replacement was started with an initial diagnosis of thyrotoxic hypokalemic periodic

Calcium unresponsive hypocalcemic tetany: gitelman syndrome with hypocalcemia.

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Introduction. Gitelman's syndrome (GS) is autosomal recessive renal tubular disorder characterized by hypokalemia, hypomagnesemia, hypocalciuria, metabolic alkalosis, and hyperreninemic hyperaldosteronism. It is usually associated with normal serum calcium. We report a patient presented with

Aldosteronoma in a child with localization by adrenal vein aldosterone: collective review of the literature.

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Hyperaldosteronism due to aldosteronoma is a rare but potentially curable form of pediatric hypertension. We have presented a patient who had symptoms of enuresis and fatigue, and in whom the diagnosis was suggested by low serum potassium and persistent hypertension. Diagnosis was confirmed by

Conn syndrome in a child, caused by adrenal adenoma.

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Hyperaldosteronism owing to aldosterone-producing adenoma (Conn syndrome) is a rare but potentially curable form of pediatric hypertension. The authors report on a 5-year-old girl who had symptoms of polyuria, polydipsia, and fatigue, and for whom the diagnosis of hyperaldosteronemia was suggested

Factitious Bartter's syndrome.

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A 29-year-old man had a six-month history of fatigue and hypokalemia. Gastrointestinal losses of potassium were not judged significant. The patient denied ingestion of licorice, large quantities of laxatives, or diuretics. Clinical and laboratory findings were consistent with Bartter's syndrome in

[Gitelman's Syndrome: from diagnosis to follow-up during pregnancy].

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Gitelman's Syndrome (GS) is a rare autosomal recessive salt-wasting nephropathy, classically characterized by hypokalemia, hypomagnesemia, hypocalciuria, metabolic alkalosis and low blood pressure. Fatigue, muscle weakness and muscle paralysis are common symptoms. Besides the typical electrolyte

Conn's syndrome due to adrenocortical adenoma--a rare but rewarding cause of curable hypertension.

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OBJECTIVE To determine the characteristics of an aldosterone-producing adenoma (APA) as a cause of hypertension, its mode of presentation and investigation, as well as the outcome of surgical removal. METHODS Retrospective survey with follow-up. METHODS Groote Schuur Hospital, Cape Town. METHODS 18

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