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A patient with hypokalemic alkalosis, normotensive hyperreninism, hyperaldosteronism, increased levels of urinary and plasma prostaglandin E, and vascular hyporesponsivity to angiotensin II was thought to have Bartter's syndrome. Results of a kidney biopsy showed hyperplasia of the juxtaglomerular
Rationale: The typical clinical presentations of patients with primary aldosteronism (PA) include generalized weakness, fatigue, high blood pressure, and potassium deficiency. However, normotensive PA is rare. Therefore, an atypical
Bartter's syndrome characteristically exhibits the constellation of hypokalemic alkalosis with moderate kaliuresis, normotensive hyperreninemia, hyperaldosteronism, urinary hyperexcretion of prostaglandin E (PGE) and vascular hyporesponsivity to pressor agents. We describe precise biochemical
Gitelman's syndrome is an autosomal recessive salt-losing tubulopathy showing hypokalemic hypomagnesemic hypocalciuria with metabolic alkalosis and hyperreninemic hyperaldosteronism. This syndrome is caused by mutations in the SLC12A3 gene that encodes sodium-chloride cotransporter expressed at the
A 54-year-old woman presented with a history of nausea, vomiting, diarrhea, and recurrent episodes of severe hypokalemia requiring hospitalization. Imaging revealed a pancreatic mass with liver metastases, histologically confirmed to be a neuroendocrine tumor. Elevated active renin and aldosterone
We report a hypertrophic pyloric stenosis case with an unusual initial presentation of seizures and Bartter's syndrome like symptoms. This case suffered from vomiting, diarrhea and poor appetite for several days, and seizures developed after these symptoms. From laboratory tests, hypochloremic and
Pseudohypoaldosteronism type 1 is a rare syndrome of resistance to aldosterone manifested by salt wasting, hyponatremia, hyperkalemia, hyperchloremic metabolic acidosis, and hiperreninemic hyperaldosteronism. The syndrome may be genetic, secondary to uropathies and urinary tract infection among
Laxative abuse syndrome (LAS) is a type of Münchausen syndrome characterized by surreptitious abuse of purgatives. Clinical findings are often perplexing and may mimic inflammatory bowel disease or malabsorption syndromes. Patients frequently complain of diarrhea alternating with constipation and
Objective
Type III Bartter syndrome (BS) is caused by loss-of-function mutations in the gene encoding basolateral chloride channel ClC-Kb (
CLCNKB), and is characterized by hypokalemic metabolic alkalosis and hyperreninemic
hyperaldosteronism. Here, we investigated the
Metabolic alkalosis is defined as a primary increase in plasma bicarbonate concentration. As a consequence of this increase, systemic alkalemia and secondary hypercapnia develop. In most instances metabolic alkalosis arises from loss of acid through the kidney or gastrointestinal tract. The causes
Gastric diverticula are rare and usually asymptomatic. This report, however, describes two examples of symptomatic gastric diverticula successfully treated by laparoscopic resection. Both patients were male and in their sixth decade of life. One patient was relatively healthy with no past medical
Bartter syndrome (BS) is a rare autosomal recessive disorder of salt reabsorption at the thick ascending limb of the Henle loop, characterized by hypokalemia, salt loss, metabolic alkalosis, hyperreninemic hyperaldosteronism with normal blood pressure. BS type III, often known as Bartter's syndrome (BS) is a disease with severe hypokalaemia due to renal potassium wasting. The potassium loss is due to lesions at different sites within the renale tubule. Additional features include metabolic alkalosis, excess renal production of prostaglandins, hyperreninaemia,
This paper is intended to give a review of the etiology and symptoms of potassium deficiency in man, as an introduction to the section on potassium and cardiac arrhythmias of this symposium. A review is given of different conditions where hypokalemia and/or total potassium deficiency is or might be