hypoaldosteronism/asthenia

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Diagnosis and management of hypoaldosteronism without hypoadrenocorticism in an alpaca.

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METHODS Primary hypoaldosteronism without concurrent hypoadrenocorticism was diagnosed in an 8-year-old female alpaca with acute onset of weakness progressing to recumbency within 6 hours after onset. RESULTS Hematologic testing at admission revealed profound hyponatremia, hypochloremia, and

Pseudohypoparathyroidism (PHP) type II and selective hypoaldosteronism in a patient with retinitis pigmentosa.

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A 53-year-old man with retinitis pigmentosa, who had two years' complaints of general malaise and muscle weakness, noticed occasional attacks of the cramps of the lower legs about three months prior to admission. At that time, hypocalcemia (7.6 mg/dl) and hyperphosphatemia (5.2 mg/dl) were pointed

Liddle's syndrome, an uncommon form of hyporeninemic hypoaldosteronism: functional and histopathological studies.

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Liddle's syndrome was diagnosed in a 72-year-old man who presented clinically with hypertension and muscle weakness. This disorder has been characterized by hyporeninemic hypoaldosteronism, hypertension, hypokalemia and enhanced erythrocyte sodium influx. Administration of spironolactone failed to

Primary hypoaldosteronism in a dog with pituitary and adrenal T-cell lymphoma.

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A 7-year-old mixed breed dog was presented with a 2-week history of vomiting, diarrhoea, weakness and loss of appetite. Initial laboratory tests revealed hyponatraemia and hyperkalaemia consistent with hypoadrenocorticism. Basal plasma cortisol and adrenocorticotropic hormone concentrations were not

[An elderly fludrocortison-responsive woman with hyponatoremia].

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An 89-years-old woman had anorexia for at least 1 month, and had been given symptomatic treatment at a nearby hospital. She was admitted to our hospital on August 22, 2003, for thorough examination and appropriate treatment for lack of spontaneity and appetite loss. On admission, laboratory data

Liddle's Syndrome: A Case Report.

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A thirty-eight years old female presented with frequent proximal weakness, severe hypertension, and persistent kaliuresis despite hypokalemia. After normalized serum potassium level, hyporeninemic hypoaldosteronism was detected Pedigree study supported an autosomal dominant inherited disease. A

A physiology-based approach to a patient with hyperkalemic renal tubular acidosis.

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Hyperkalemic renal tubular acidosis is a non-anion gap metabolic acidosis that invariably indicates an abnormality in potassium, ammonium, and hydrogen ion secretion. In clinical practice, it is usually attributed to real or apparent hypoaldosteronism caused by diseases or drug toxicity. We describe

Recurrent hyperkalaemia due to selective aldosterone deficiency: correction by angiotensin infusion.

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A patient with recurrent weakness and blurring of consciousness associated with hyperkalaemia due to aldosterone deficiency is reported. The plasma concentrations of renin, angiotensin II, and aldosterone were low and did not increase during sodium deprivation. Blood angiotensin I was also low while

Beating the odds--surviving extreme hyperkalemia.

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Severe hyperkalemia (>7 mmol/L) is a medical emergency because of possible fatal arrhythmias. We here report the case of a 58-year-old woman surviving extreme hyperkalemia (>10 mmol/L). The patient with a history of congestive heart failure, a DDD pacemaker and mild chronic renal insufficiency was

An autopsy case of licorice-induced hypokalemic rhabdomyolysis associated with acute renal failure: special reference to profound calcium deposition in skeletal and cardiac muscle.

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A 78-year-old man was hospitalized because of muscular weakness and acute renal failure. He had been taking glycyrrhizin (280 mg/day) for the last 7 years. Hypertension was noted in his history. Serum potassium was 1.9 mEq/l with metabolic alkalosis. There was hyporeninemic hypoaldosteronism. Serum

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