diuresi

Diuresi, or diuresis, is the increased production of urine by the kidneys. It can occur as a normal response to higher fluid intake or reduced water reabsorption, and may also be produced intentionally with medications known as diuretics. Diuresis results from changes in tubular water reabsorption and solute handling, often mediated by hormones and pharmacologic agents.

In the nephron, water and solute reabsorption is tightly controlled. Antidiuretic hormone promotes water reabsorption in the collecting ducts via aquaporin-2 channels, concentrating urine. Aldosterone increases sodium reabsorption in the distal nephron, with accompanying potassium loss. Diuretics reduce reabsorption of sodium and/or water at specific segments, leading to increased urine volume.

Osmotic diuresis occurs when non-reabsorbed solutes such as glucose or mannitol raise tubular osmolarity, pulling water into the filtrate. Pharmacologic diuretics include loop diuretics (block Na-K-2Cl in the loop of Henle), thiazides (block Na-Cl in the distal tubule), and potassium-sparing diuretics (collecting ducts). Indications include treatment of hypertension, edema, congestive heart failure, and certain renal or endocrine conditions; conversely, diabetes mellitus and diabetes insipidus can cause polyuria.

Clinically, diuresis is assessed by urine output, osmolality, and electrolyte status. Diuretic therapy requires monitoring of volume status and electrolytes to prevent dehydration, hyponatremia, or hypokalemia. Adverse effects depend on the agent and underlying condition, and therapy is individualized to balance fluid removal with maintaining fluid and electrolyte balance.