This chapter discussed diuretic drugs, which are used to treat edematous conditions via selective reabsorption of water and sodium in different areas of the nephron, resulting in increased urinary output. The drugs are used individually or in combination with other diuretics to treat congestion associated with heart failure, ascites due to cirrhosis, pulmonary congestion, increased intracranial and intraocular pressure, acute and chronic renal disease, and nephrotic syndrome.
Loop diuretics increase urinary output by blocking the reabsorption of sodium in the (thick) ascending loop of Henle. These drugs work by inhibiting the action of the Na-K-2Cl (NKCC2) cotransporters in the luminal membrane, thereby inhibiting sodium and chloride reabsorption and triggering losses of potassium and magnesium.
Osmotic diuretics work by decreasing sodium and water reabsorption in the proximal tubule and the loop of Henle, which increases water loss. Mannitol, the most commonly used osmotic diuretic, is used to treat increased intracranial pressure and increased intraocular pressure. It is also approved as a diuretic for acute renal failure.
Potassium-sparing diuretics affect the reabsorption of sodium and the excretion of potassium in the connecting and collecting tubules by inhibiting the sodium transporters and blocking the mineral corticoid receptors. When the potassium-sparing drugs inhibit sodium reabsorption in this area of the nephron, potassium excretion is decreased, preserving serum potassium levels.
Thiazide and thiazide-like diuretics have three major properties: inhibition of sodium reabsorption, increased reabsorption of calcium, and creation of mild extracellular fluid losses. The thiazide drugs are considered the first line of treatment for essential hypertension.