Natriureesi

Natriuresis, also known as natriureesi in Finnish, is the increased excretion of sodium in the urine. It is a key mechanism for regulating extracellular fluid volume, osmolar balance, and blood pressure. Natriuresis occurs when filtered sodium load exceeds tubular reabsorptive capacity or when reabsorption is actively reduced by hormonal or hemodynamic factors.

Physiology and regulation include the coordinated actions of the nephron and circulating hormones. The kidneys filter sodium, and most of it is ordinarily reabsorbed along the tubules. Natriuresis increases when sodium reabsorption is inhibited or when glomerular filtration and renal perfusion favor sodium loss. Atrial and B-type natriuretic peptides promote natriuresis by increasing sodium delivery to the distal nephron and by inhibiting the renin-angiotensin-aldosterone system. In contrast, activation of RAAS and sympathetic activity tends to reduce natriuresis to conserve volume.

Mechanisms and pharmacology involve several pathways. Diuretics are commonly used to induce natriuresis: loop diuretics block NKCC2 in the thick ascending limb, thiazide diuretics block NCC in the distal convoluted tubule, and potassium-sparing diuretics reduce sodium reabsorption via ENaC. Osmotic diuresis, such as in hyperglycemia, can also cause natriuresis. Natriuretic peptides themselves directly promote sodium excretion.

Clinical significance includes assessment of volume status and diuretic response. Natriuresis plays a central role in heart failure management, kidney diseases, and certain salt-wasting conditions. Measurement of urinary sodium or the fractional excretion of sodium (FENa) helps evaluate renal handling of sodium.