Tubular secretion
Also known as: secretion, renal secretion
The transfer of substances from the peritubular capillary blood into the tubular lumen — mainly H⁺, K⁺, NH₄⁺, organic anions and cations including many drugs — allowing excretion beyond what filtration alone achieves.
Overview
Secretion adds solutes to the filtrate and is essential for (1) eliminating protein-bound substances that are poorly filtered, (2) rapid clearance of drugs and toxins, (3) K⁺ homeostasis and (4) acid–base regulation.
Proximal tubule: basolateral organic anion transporters (OAT1, OAT3) and apical MRP/OAT4 secrete PAH, urate, penicillins, cephalosporins, NSAIDs, methotrexate, furosemide and thiazides (which must reach their luminal targets by secretion); organic cation transporters (OCT2 basolateral, MATE1/2-K apical) secrete creatinine, metformin, cimetidine, trimethoprim and dopamine. H⁺ secretion via NHE3 and NH₄⁺ secretion also occur here.
Distal nephron: principal cells secrete K⁺ (ROMK, BK) under aldosterone; α-intercalated cells secrete H⁺; β-intercalated cells secrete HCO₃⁻.
- Location
Mainly the PCT (organic ions) and collecting duct (K⁺, H⁺).
Function
- Excrete drugs, toxins and metabolites
- Regulate plasma K⁺
- Excrete acid (H⁺, NH₄⁺)
Clinical significance
Drug interactions
Competition for OATs (probenecid prolongs penicillin; NSAIDs reduce methotrexate clearance → toxicity) and OCT/MATE (trimethoprim and cimetidine raise creatinine and can increase metformin levels).
Hyperkalaemia
Impaired K⁺ secretion — advanced CKD, hypoaldosteronism, ACE inhibitors/ARBs, spironolactone, amiloride, trimethoprim, NSAIDs — causes hyperkalaemia with peaked T waves and risk of arrhythmia.
Compiled from standard anatomy and physiology references — see the Urinary System sources. For education only; not medical advice.