hypoaldosteronism/bjúgur

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[A case of lupus nephritis with hyporeninemic hypoaldosteronism].

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We report a case of 67-year-old woman with systemic lupus erythematosus presenting hyporeninemic hypoaldosteronism. She admitted because of anasarca in March, 1990. She manifested nephrotic syndrome, and hyperkalemia and hyperchloremic metabolic acidosis. The hyperkalemia was disproportionate to the

Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism.

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Transient hyperkalemia has been reported to occur in patients with acute glomerulonephritis, but the pathogenetic mechanism has not been investigated systematically. We studied the mechanism of hyperkalemia (5.7 to 6.7 mmol/liter) in four men with post-infectious glomerulonephritis. All four

Licorice induced hypokalemia, edema, and thrombocytopenia.

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Licorice originates from the root of Glycyrrhiza glabra, which has a herbal ingredient, glycyrrhizic acid, and has a mineralocorticoid-like effect. Chronic intake of licorice induces a syndrome similar to that found in primary hyperaldosteronism. Excessive intake of licorice may cause a

Renal tubular acidosis type IV as a complication of lupus nephritis.

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Renal tubular acidosis (RTA) is a rare complication of renal involvement of systemic lupus erythematosus (SLE). We describe a 24-year-old male with type IV lupus nephropathy as a presenting manifestation of SLE. He presented with improvement of renal function following induction therapy with three

Addison disease presenting with acute neurologic deterioration: a rare presentation yields new lessons from old observations in primary adrenal failure.

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OBJECTIVE To report a rare case of Addison disease presenting with acute neurologic deterioration, and to discuss previous reports and illustrative clinical lessons drawn from the case. METHODS We detail the clinical presentation and sequence of events leading to diagnosis of Addison disease in a

Liddle's-like syndrome associated with nephrotic syndrome secondary to membranous nephropathy: the first case report.

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BACKGROUND Liddle's syndrome is a rare monogenic form of hypertension caused by truncating or missense mutations in the C termini of the epithelial sodium channel (ENaC) β or γ subunits. Patients with this syndrome present with early onset of hypertension, hypokalemia, metabolic alkalosis,

Combined therapy of captopril and spironolactone for refractory congestive heart failure.

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It is traditionally considered that angiotensin--converting enzyme inhibitor (ACEI) and spironolactone could not be used simultaneously because of the assumed risk of hyperkalemia. However, despite ACEI therapy edema and congestive status remain in some of the patients with severe congestive heart

Renal side effects of nonsteroidal antiinflammatory drugs: clinical relevance.

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Nonsteroidal antiinflammatory drugs (NSAIDs) induce a variety of renal side effects. We review their prevalence and clinical relevance, and identify the patients who are most at risk for these complications. NSAIDs induce hemodynamic renal failure in states of compromised renal perfusion and in the

[Transtubular potassium gradient in the diagnosis of potassium metabolism disorders].

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The transtubular potassium gradient (TTKG) is a simple physiologically based clinical test to study the renal excretion of potassium. This article reviews the most important physiological changes influencing TTKG, the hypokalaemia and hyperkalaemia, the effect of mineralocorticoids, alkalosis,

Occurrence of renal tubular dysfunction in lupus nephritis.

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We prospectively evaluated 30 patients who presented with active systemic lupus erythematosus (SLE) for the presence of tubular abnormalities. All patients fulfilled the American Rheumatology Association criteria for SLE. When appropriate, a renal biopsy was performed. Of the 30 patients studied, 12

Membranous nephropathy with renal salt wasting: role of neurohumoral factors in sodium retention.

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The role of neurohumoral factors in the sodium retention of nephrotic syndrome is controversial. We report a case with abrupt onset of severe nephrotic-range proteinuria and hypoalbuminemia due to membranous glomerulonephritis that was associated with renal salt wasting and hypovolemia without

Renal toxicity of the nonsteroidal anti-inflammatory drugs.

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NSAIDs pose little threat of renal insult in normal, healthy persons at therapeutic dosages. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. Such acute noxious renal effects are mediated by products of

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