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By admin / June 4, 2015

The diagnosis is suggested by the finding of hypokalemia; the serum potassium

Level is usually less than 2.5 meq/L. Supportive findings include normal blood

Pressure; defective platelet aggregation; hypochloremia; metabolic alkalosis;

Elevated plasma levels of renin, aldosterone, and prostaglandin E2 ; and high

Urinary levels of potassium and chloride. Some patients may also have

Hypercalciuria, hyperuricemia, hypomagnesemia, and urinary sodium wasting. The

Diagnosis may be confirmed by the histologic demonstration of hyperplasia of the

Juxtaglomerular apparatus, but this abnormality is not found in all patients and

Is frequently absent in young children.

Bartter syndrome must be differentiated from licorice abuse, laxative or

Diuretic use, persistent vomiting or diarrhea, pyelonephritis, and diabetes

Insipidus. Several of these (laxative use, vomiting, diarrhea, diabetes

Insipidus) are associated with hypovolemia, which results in a low urinary

Chloride level, whereas Bartter syndrome is associated with an elevated level.

Bartter syndrome may be confused with Gitelman syndrome. Both disorders are

Associated with hypokalemia, renal potassium wasting, activation of the

Renin-angiotensin-aldosterone axis, and normal blood pressure. Gitelman syndrome

Commonly presents in older children and young adults with muscle weakness,

Carpopedal spasms, or tetany. Patients with Bartter syndrome have normal to

Decreased serum magnesium levels, normal urinary magnesium excretion, and normal

To increased calcium excretion; patients with Gitelman syndrome have

Hypomagnesemia, increased urinary magnesium, and decreased calcium excretion.

Gitelman syndrome results from a mutation of the gene for the thiazide-sensitive

Sodium-chloride co-transporter of the distal tubule located on chromosome 16.