Renal: RAAS & water/electrolyte handling

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• Aldosterone causes sodium and water RETENTION and potassium and hydrogen EXCRETION at the distal nephron; hyperaldosteronism therefore causes hypertension with hypokalaemic metabolic alkalosis, and aldosterone antagonists (spironolactone) cause hyperkalaemia.
• ADH is driven by osmoreceptors (a 1 to 2 percent rise in osmolality) and by a large fall in blood volume; it inserts aquaporin-2 channels in the collecting duct — loss of ADH (central) or renal response (nephrogenic) causes diabetes insipidus.
• The countercurrent multiplier builds the medullary osmotic gradient (up to about 1200 mOsm per kg); loop diuretics abolish it, and a loss of medullary tonicity (interstitial disease) prevents urine concentration.
• ANP and BNP, released by atrial and ventricular stretch, promote sodium excretion and oppose the RAAS — they are the natural counterweight to volume overload.
• Angiotensin II constricts the efferent arteriole and supports GFR; blocking it (ACE inhibitors, ARBs) can cause a functional GFR fall, and it is also the basis for hyperkalaemia when RAAS blockers are combined with potassium-sparing agents.