dinoprost and Hyperkalemia

1. In Gordon's syndrome (GS; a syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate), excessive proximal sodium reabsorption leads to suppression of renin and aldosterone, hyperkalaemia and hyperchloraemic acidosis. 2. Low urinary levels of vasodilator prostaglandins (PG) have been reported in GS, suggesting renal hypoprostaglandinism as a pathophysiological mechanism. 3. In four cases of GS, levels of vasodilator prostaglandins PGE2 and 6-keto-PGF1 alpha were low. 4. In one case of GS, low PGE2 levels were normalized by dietary salt restriction or diuretic therapy.

Topics: Adult; Child; Dinoprost; Dinoprostone; Family Health; Female; Glomerular Filtration Rate; Humans; Hyperkalemia; Hypertension; Male; Prostaglandins; Sodium, Dietary; Syndrome

In an infant with pseudohypoaldosteronism type I increased urinary excretion of PGE2 (1.32 ng/mg creatinine; normal mean +/- SE: 0.50 +/- 0.10) and PGF2 alpha (6.15 ng/mg creatinine; normal mean +/- SE: 2.93 +/- 0.91) was found. Prostaglandin excretion as well as the typical hyperkalemia, hyperreninemia and hyperaldosteronism normalized with adequate dietary salt supplementation. An abnormally high excretion of the renal prostaglandins was again present at age 4.4 years when the child was thriving although additional salt was withheld. These abnormalities are considered to be secondary to this condition's basic defect which remains to be elucidated.

Topics: Aldosterone; Dinoprost; Dinoprostone; Humans; Hyperkalemia; Hyponatremia; Infant; Male; Prostaglandins E; Prostaglandins F; Renin; Sodium Chloride