Hypokalaemic alkalosis.
نویسندگان
چکیده
منابع مشابه
Enamel-renal syndrome associated with hypokalaemic metabolic alkalosis and impaired renal concentration: a novel syndrome?
Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Department of Endocrinology and Metabolism, Hyogo Children’s Hospital, Kobe, Department of Pediatrics, Saiseikai Hyougoken Hospital, Kobe, Department of Environmental Health and Safety, Kobe University Graduate School of Medicine, Kobe and Department of Nephrology, National Center for Child Health and Development, Toky...
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Hypokalaemia is the most important result of the adrenal hyperfunction seen in the recently described Conn's syndrome (Conn and Louis, 1956). In this syndrome aldosterone is produced excessively, but evidence of the same excess of other hormones is lacking and the excretion of 17-ketosteroids and 17-ketogenic steroids in the urine is normal. Hypokalaemia may also occur in cases with a high urin...
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Renal tubular magnesium loss in association with a defect in tubular chloride reabsorption has been reported in Bartter’s and Gitelman’s syndromes. Clinically, both syndromes are characterized by hypokalaemic metabolic alkalosis, renal salt wasting, hyperreninaemic hyperaldosteronism and altered renal prostaglandin metabolism [1]. In Bartter’s syndrome, hypomagnesaemia occurs in 20% of patients...
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This investigation represents a continuation and extension of the work initiated by Mr. D. Burkitt. We are grateful to Mr. Burkitt and Mr. S. Kyalwazi, who between them treated nearly all the cases reported in this series, for permission to follow up their patients. Special acknowledgement is due to both the past and the present pathologists at Makerere Medical School, and in particular to Dr. ...
متن کاملCLCN5 mutation (R347X) associated with hypokalaemic metabolic alkalosis in a Turkish child: an unusual presentation of Dent's disease.
Dent’s disease, an X-linked recessive tubular disorder, is characterized by low molecular weight proteinuria (LMWP) and nephrolithiasis associated with nephrocalcinosis and hypercalciuria. It is due to mutations that inactivate the renal voltage-gated chloride channel ClC-5 [1,2], which is encoded by a gene (CLCN5) located on chromosome Xp11.22. It is possible, however, that causative mutations...
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ژورنال
عنوان ژورنال: Postgraduate Medical Journal
سال: 1998
ISSN: 0032-5473
DOI: 10.1136/pgmj.74.871.305