Acute tubular necrosis - pathophysiology (pre-renal vs ischaemic vs nephrotoxic)
Core concept
- Two segments do almost all the work and take almost all the injury: S3 proximal tubule and medullary thick ascending limb
- Highest ATP demand in the kidney (Na/K-ATPase driving solute transport)
- Sit in the outer medulla, PO2 10-20 mmHg - countercurrent exchange strips O2 from descending vasa recta
- -> permanent supply/demand mismatch; the first tissue to fail in ischaemia or toxicity
- Injury sequence: loss of polarity -> brush border shedding -> apoptosis/necrosis -> casts + back-leak
Why GFR falls
- Afferent arteriolar vasoconstriction (endothelin, dec NO)
- Tubuloglomerular feedback - macula densa senses inc distal NaCl -> constricts afferent
- Cast obstruction of the tubular lumen
- Back-leak of filtrate across denuded epithelium
3 more sections, plus exam facts
Premium unlocks every note across every specialty, and the full exam fact library behind it.
Get premium access