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The occurrence of chondrocalcinosis in patients with Bartter's syndrome has been reported as a typical example of hypomagnesemia-associated calcium pyrophosphate dihydrate crystal (CPPD) deposition disease. However, hypomagnesemia is a feature of Gitelman's variant of Bartter's syndrome, whereas
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OBJECTIVE
Familial occurrence of Bartter's syndrome is well known, but the simultaneous occurrence of hypokalemia/hypomagnesemia and chondrocalcinosis in one family has not been described. We present the clinical, laboratory and radiological findings of a family, in which 7 members were affected by
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A female patient aged 45 years is described with a rare form of chondrocalcinosis caused by hypomagnesaemia due to excessive renal loss of magnesium. The patient also had impaired renal conservation of potassium leading to a hypokalemia. She most probably had an idiopathic renal tubular dysfunction.
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Gitelman syndrome (GS) is an inherited salt-wasting tubulopathy characterized by hypocalciuria, hypokalemia, hypomagnesemia and metabolic alkalosis, due to inactivating mutations in the SLC12A3 gene. Symptoms may be systemic, neurological, cardiovascular, ophthalmological or musculoskeletal. We
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Gitelman's syndrome (GS) is a rare disease with autosomal recessive trait, characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria and hyperkinemic hyperaldosteronism. While muscle weakness, tetany, stomachache, nausea and fever are very common, it could sometimes be
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Primary and secondary meniscal chondrocalcinoses lead to typical changes in X-ray pictures of isolated menisci. Combined X-ray, light and electron microscopic examination of the four menisci in 70 autopsy cases showed calcifications in 13 cases (18.6%). Three types of calcification could be
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Bartter-Gitelman syndromes are rare inherited autosomal recessive salt-losing tubulopathies characterized by severe and chronic hypokalemia associated with metabolic alkalosis and secondary hyperaldosteronism. Bartter syndrome results from a furosemide-like defect in sodium reabsorption in the
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BACKGROUND
We describe a 79-year-old man with biochemical and radiological features of Gitelman syndrome: hypokalemia, hypomagnesemia, hyperreninemic hyperaldosteronism in absence of secondary hyperaldosteronism causes, and chondrocalcinosis.
RESULTS
The diagnosis was confirmed by sequence analysis
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An 80-year-old man was referred to our department for evaluation of repetitive loss of consciousness and faintness with hypokalemia. He had relatively low blood pressure, hypomagnesemia, hypocalciuria and chondrocalcinosis in the knee, clinically suggesting Gitelman's syndrome. A renal clearance
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A patient with primary hyperparathyroidism who presented with hypokalaemia and hypertension is described. Renal potassium wasting was documented and cured by removal of a parathyroid adenoma. Possible mechanisms for this unusual manifestation of hyperparathyroidism are mentioned. Other features of
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OBJECTIVE
Acute gout is traditionally treated with NSAIDs, corticosteroids, and colchicine. However, the presence of comorbid conditions and advancing age, often seen in hospitalised patients, may prevent their use. We reviewed the published data on the use of ACTH in the treatment of acute gouty
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Gitelman syndrome (GS), also referred to as familial hypokalemia-hypomagnesemia, is characterized by hypokalemic metabolic alkalosis in combination with significant hypomagnesemia and low urinary calcium excretion. The prevalence is estimated at approximately 1:40,000 and accordingly, the prevalence
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Bartter's and Gitelman's syndromes are two different genetic renal diseases, but are both characterised by hypokalaemia and metabolic alkalosis. Bartter's syndrome is characterised by multiple gene mutations (Na-K-2Cl cotransporter; K(+) channels renal outer medullary potassium channel (ROMK); Cl
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