Renal

AKI Categories

Prerenal vs Intrinsic (ATN) vs Postrenal

AKI Categories
Feature	Prerenal	Intrinsic	Postrenal
Mechanism
Mechanism	Reduced renal perfusion; parenchyma intact	Direct tubular/glomerular/interstitial injury	Obstruction to urine outflow
Assessment
Urine findings	Bland sediment; concentrated urine (high osmolality, low Na)	Muddy-brown granular casts; isothenuric; Na higher	Variable; may be anuric
POCUS	Collapsible IVC; small/hyperkinetic LV if hypovolemia	Often nonspecific	Bilateral hydronephrosis (absence does not exclude obstruction — sensitivity limited)
History	Diuretics, GI losses, bleeding, poor intake, heart failure	Sepsis, nephrotoxins (aminoglycosides, contrast, pigments), prolonged ischemia	BPH, malignancy, stones, new anuria, catheter malfunction
Management
Response to fluids	Improves with perfusion restored	No brisk improvement; supportive until recovery	No improvement until obstruction relieved (flush/check catheter first!)
Traps & pitfalls
Common causes	Hemorrhage, diarrhea, over-diuresis, third-spacing	ATN from sepsis/ischemia/toxins; AIN from drugs	Clot retention, neurogenic bladder, bilateral ureteric obstruction
FeNa / FeUrea	Traditionally low — BUT unreliable on diuretics, with CKD, in sepsis, or after contrast	Traditionally higher — same caveats; never diagnose on indices alone	Not applicable — examine/image and relieve obstruction

Comparing: Prerenal

Reduced renal perfusion; parenchyma intact

Bland sediment; concentrated urine (high osmolality, low Na)

Collapsible IVC; small/hyperkinetic LV if hypovolemia

Diuretics, GI losses, bleeding, poor intake, heart failure

Improves with perfusion restored

Hemorrhage, diarrhea, over-diuresis, third-spacing

Traditionally low — BUT unreliable on diuretics, with CKD, in sepsis, or after contrast

For healthcare-professional education. Clinical decisions require patient-specific assessment and local protocols.