Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 14-year-old boy with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome) is described. The patient's clinical symptoms consisted of periodic paralysis, slight metabolic acidosis of the proximal type and hypercalciuria. Prostaglandin excretion was normal. Infusion of atrial natriuretic peptide had no effect on electrolyte excretion or glomerular function although a normal increase in cyclic guanosine monophosphate was demonstrated in plasma and urine. This lack of sensitivity to atrial natriuretic peptide offers a new pathophysiological concept in this syndrome. Treatment with hydrochlorothiazide was successful in this case.
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PMID:The syndrome of hypertension and hyperkalaemia with normal glomerular function (Gordon's syndrome). A pathophysiological study. 297 68

Thyrotoxic periodic paralysis (TPP), a hyperthyroidism-related hypokalemia and muscle-weakening condition resulting from a sudden shift of potassium into cells, has been seen increasingly in Western countries. Failure to recognize TPP may lead to improper management. Many patients with TPP have no obvious symptoms related to hyperthyroidism. Therefore, several important clues may help in diagnosing and managing TPP: presentation in an adult male with no family history of periodic paralysis; presence of systolic hypertension, tachycardia, high QRS voltage, first-degree atrioventricular block on electrocardiography; presence of low-amplitude electrical compound muscle action potential on electromyography and no notable changes in amplitudes after low doses of epinephrinine; and typical acid-base and electrolyte findings such as normal blood acid-base state, hypokalemia with low urinary potassium excretion, hypophosphatemia associated with hypophosphaturia, and hypercalciuria. Immediate therapy with potassium chloride supplementation may foster a rapid recovery of muscle strength, but with a risk of rebound hyperkalemia. Nonselective beta-blockers may provide an alternative choice. Long-term therapy with definite control of hyperthyroidism completely abolishes attacks. Early diagnosis and prompt treatment of TPP prevent life-threatening complications of this treatable and curable disorder.
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PMID:Thyrotoxic periodic paralysis. 1600 4

Hypokalemic periodic paralysis can occur secondarily to excessive potassium loss. Thyrotoxicosis, diuretic ingestions, hyperaldosteronism, barium poisoning, Gitelman syndrome, and Bartter syndrome are among the disorders causing secondary hypokalemic periodic paralysis. Clinical presentation of Bartter syndrome with hypokalemic periodic paralysis is rare. A 12-year-old boy was admitted to our hospital because of transient paralysis. He had been suffering from transient weakness attacks for 2 years and had had a total of 10 attacks, lasting 1 to 3 days. He had growth retardation, polyuria, and polydipsia. Laboratory examinations revealed hypokalemic alkalosis, normomagnesemia, hypercalciuria, and hyperaldosteronism. The clinical and laboratory findings were in accordance with Bartter syndrome. He has been followed up for 6 months and has suffered no further paralytic attacks under indomethacin therapy. This case highlights the importance of blood pH measurement in patients with hypokalemic periodic paralysis; it might prevent misdiagnosis and mismanagement in such diseases.
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PMID:Case of Bartter syndrome presenting with hypokalemic periodic paralysis. 1690 32