Diurese

Diuresis, or diurese, is the increased production of urine by the kidneys. It can occur as a normal response to a fluid load or as a pharmacologic or pathophysiologic process leading to greater urine output. The process is governed chiefly by water and electrolyte reabsorption in the renal tubules and the collecting ducts, modulated by hormones and osmotic forces.

Water reabsorption in the collecting ducts is controlled by antidiuretic hormone (vasopressin). When ADH is present, aquaporin-2 channels insert into the apical membrane, increasing water reabsorption and reducing urine volume. Conversely, reduced ADH or increased tubular flow promotes diuresis. Sodium handling also influences diuresis; aldosterone promotes sodium reabsorption, while atrial natriuretic peptide (ANP) promotes natriuresis and diuresis. Osmotic forces, gravity, and the balance of electrolytes shape the final urine volume.

Diuresis is classified by mechanism: osmotic diuresis results when osmotically active substances in the tubule (for example, glucose in uncontrolled diabetes, mannitol) draw water into the lumen; natriuretic diuresis refers to increased excretion of sodium and water, often with diuretic drugs or ANP action. Pathologic polyuria refers to abnormally high urine output, as seen in diabetes mellitus or diabetes insipidus, while polyuria can be accompanied by dehydration or electrolyte disturbances.

In clinical practice, urine output is monitored to assess kidney function, hydration status, and response to therapy. Drugs known to induce diuresis include various diuretics (loop, thiazide, potassium-sparing) as well as osmotic agents, used to treat edema, hypertension, and certain intoxications, but they may cause electrolyte imbalances and volume depletion.