Hyporeninemic Hypoaldosteronism Medication
- Author: James H Sondheimer, MD, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Medications employed in the management of renal tubular acidosis (RTA) type IV include loop and thiazide diuretics, mineralocorticoids, ion-exchange resins, and alkalinizing agents.
Diuretics increase sodium and potassium loss in the urine. The latter usually is considered an adverse effect but is the desired effect in treating patients with RTA type IV.
Furosemide inhibits reabsorption of chloride, predominantly in the thick ascending limb of the loop of Henle. The high efficacy of this drug is largely due to the large amount of sodium usually reabsorbed in this site.
These agents provide pharmacologic amounts of mineralocorticoid activity, so that the patient can overcome tubular resistance to physiologic amounts of aldosterone.
Fludrocortisone is used as a third-line agent in patients for whom treatment with diuretics, sodium bicarbonate, and dietary measures has failed. It promotes increased reabsorption of sodium and loss of potassium from renal distal tubules.
By increasing gut excretion of potassium, these agents bypass renal impairment of potassium excretion. Difficult to take on a regular basis, limiting its use in long-term therapy.
Sodium polystyrene sulfonate exchanges sodium for potassium and binds in the gut, primarily in the large intestine; it also decreases total body potassium. The time to onset of action ranges from 2-12 hours after oral administration and is longer after rectal administration.
Alkalinizing agents provide bicarbonate anion for repletion of patients with metabolic acidosis. They alkalinize the urine, enhancing kaliuresis.
Sodium bicarbonate is administered intravenously (IV) for emergency treatment of hyperkalemia. It is given orally to patients with metabolic acidosis and hyperkalemia.
Thiazide diuretics are useful in the treatment of RTA type IV by virtue of their kaliuretic effects. They are less likely to produce marked volume depletion than loop diuretics are, and they may be better antihypertensive agents.
Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium, water, potassium, and hydrogen ions.
Chlorothiazide inhibits the reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as of potassium and hydrogen ions.
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