glomerular-filtrate → pt-reabsorption — via Na+/H+ + SGLT2 + carbonic anhydrase — SGLT2i + acetazolamide targets. The proximal tubule reabsorbs ~65% of filtered Na⁺/water plus glucose (SGLT2), bicarbonate (carbonic anhydrase), and amino acids. SGLT2 inhibitors and acetazolamide act here, and it is also where most drugs are actively secreted (OAT/OCT).
pt-reabsorption → tal-reabsorption — via NKCC2 (Na/K/2Cl) — LOOP DIURETIC target. The thick ascending limb’s NKCC2 cotransporter (the loop-diuretic/furosemide target) reabsorbs Na/K/2Cl and powers the countercurrent concentrating mechanism. Its loss-of-function is Bartter syndrome; loop diuretics are the most potent natriuretics.
tal-reabsorption → dct-reabsorption — via NCC (Na/Cl) — THIAZIDE target. The distal convoluted tubule’s Na/Cl cotransporter (NCC) is the thiazide target; its loss-of-function is Gitelman syndrome. Thiazides are weaker than loop diuretics but enhance distal Ca²⁺ reabsorption, reducing calcium-stone risk.
dct-reabsorption → ccd-fine-tuning — via ENaC (amiloride/triamterene) + aldosterone (spironolactone/eplerenone). The collecting duct fine-tunes Na⁺/K⁺ via aldosterone-controlled ENaC — the site of K⁺-sparing diuretics (amiloride/triamterene block ENaC; spironolactone/eplerenone block the mineralocorticoid receptor) and of ADH-driven water reabsorption (aquaporin-2).