Bartter's syndrome.
The syndrome of juxtaglomerular hyperplasia with hypokalemic, hypochloremic alkalosis, aldosteronism, hyperreninemia, and normal blood pressure may be familial, and is probably inherited as a recessive trait. It can usually be distinguished from salt-losing chronic glomerulo-nephritis by the histologic appearance of the kidneys, and by the absence of sodium "leak" with a low-sodium intake. Urinary, and thus renal, prostaglandin E is increased in the untreated patient: when this is lowered with prostaglandin synthetase inhibitors, the plasma renin and aldosterone decrease, and the plasma potassium concentration rises. These and other results suggest a partial control of renin secretion by prostaglandin E, and also suggest that prostaglandin E is an essential feature of the syndrome; it may, indeed, be a "proximal" cause of all the essential features.
D000315:Adrenalectomy; D001477:Bartter Syndrome / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications / Q000209:etiology; D011448:Prostaglandin Antagonists / Q000627:therapeutic use; D011458:Prostaglandins E / Q000097:blood / Q000652:urine; D012083:Renin / Q000097:blood; D012964:Sodium / Q000652:urine; D013148:Spironolactone / Q000627:therapeutic use
D011448:Prostaglandin Antagonists; D011458:Prostaglandins E; D013148:Spironolactone; D012964:Sodium; D012083:Renin