natriuresis
Summary
Increased renal sodium excretion. Driven physiologically by atrial natriuretic peptide (ANP/BNP), pressure natriuresis, and inhibition of sodium reabsorption (e.g., loop, thiazide, K-sparing diuretics, SGLT2 inhibitors).
Detail
Natriuresis is the cornerstone of volume regulation. ANP is released by atrial stretch in volume overload; it dilates afferent arterioles (increasing GFR), inhibits Na reabsorption in the inner medullary collecting duct, suppresses renin/aldosterone/ADH, and antagonizes the RAAS — producing diuresis and natriuresis. Pressure natriuresis is the kidney's intrinsic response to elevated renal perfusion pressure (downregulates Na/H exchanger, decreases proximal Na reabsorption) and underlies aldosterone escape and the chronic blood-pressure setpoint. Pathologic causes: SIADH (euvolemic hyponatremia with high urine Na), cerebral salt wasting (hypovolemic hyponatremia), Addison's, and diuretic use. ANP elevation also explains polyuria after relief of paroxysmal SVT or atrial distension.
Sources
- First Aid for USMLE Step 1 2024
- Costanzo Physiology
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