Expansion
Ischaemic or toxic injury to tubular cells, with an oliguric then polyuric phase
Expansion
Causes
- Ischaemic: prolonged hypotension, sepsis, major surgery, haemorrhage. The commonest
- Nephrotoxic: aminoglycosides, contrast, cisplatin, amphotericin, myoglobin in rhabdomyolysis, haemoglobin, urate in tumour lysis, ethylene glycol
Vulnerable segments: the proximal tubule S3 segment and the thick ascending limb in the outer medulla, both because of high metabolic demand and a marginal oxygen supply.
Clinical course
- Initiation: the insult
- Oliguric (maintenance) phase: 1 to 3 weeks. Risk of hyperkalaemia, acidosis and fluid overload
- Polyuric (recovery) phase: tubules regenerate but concentrating ability lags, so a large diuresis with potassium and magnesium loss occurs
- Recovery: often complete, since tubular cells regenerate, provided the basement membrane is intact
Distinguishing from prerenal failure: acute tubular necrosis gives FENa above 2 per cent, urine osmolality below 350 mOsm/kg, urine sodium above 40 and muddy brown casts, and it does not respond to fluid. Prerenal failure gives the opposite and does respond.
Prolonged prerenal failure progresses to acute tubular necrosis, so the two form a continuum.