Types of Acute Kidney Injury
Acute kidney injury is classified into three anatomic categories: prerenal, intrarenal (intrinsic), and postrenal, with prerenal and intrarenal causes accounting for over 97% of cases. 1
The Three Main Categories
Prerenal AKI
Prerenal AKI results from reduced renal perfusion without structural kidney damage. The specific causes include: 1
- Hypovolemia (hemorrhage, gastrointestinal losses, burns, diuretic overuse) 1
- Decreased cardiac output (heart failure, myocardial infarction, cardiogenic shock) 1
- Systemic vasodilation (sepsis, anaphylaxis, medications) 1
- Renal vasoconstriction (NSAIDs, ACE inhibitors, hepatorenal syndrome) 1
- Renal artery occlusion (thrombosis, embolism, dissection) 1
A BUN-to-creatinine ratio >20:1 suggests prerenal azotemia, while a ratio <15:1 suggests intrarenal disease. 1
Intrarenal (Intrinsic) AKI
Intrarenal AKI involves direct structural damage to kidney parenchyma. The major subcategories include: 2, 3
- Acute tubular necrosis (ATN) - the most common form, caused by ischemia or nephrotoxins 3
- Acute interstitial nephritis - typically drug-induced (antibiotics, NSAIDs, PPIs) 2
- Glomerulonephritis - immune-mediated glomerular injury 2
- Vascular injury - vasculitis, thrombotic microangiopathy, atheroembolic disease 2
Postrenal AKI
Postrenal AKI results from obstruction of urine flow. The anatomic sites include: 1
- Ureteral obstruction (bilateral stones, retroperitoneal fibrosis, malignancy) 1
- Bladder outlet obstruction (benign prostatic hyperplasia, bladder cancer, neurogenic bladder) 1
- Urethral obstruction (strictures, blood clots) 1
Renal ultrasonography should be performed in most patients, particularly older men, to rule out obstruction. 2
Important Clinical Caveats
The traditional classification into discrete prerenal, intrinsic, and postrenal categories is problematic because these mechanisms frequently coexist and evolve dynamically, particularly in septic patients. 4 For example, a patient may initially have prerenal azotemia from volume depletion that progresses to ATN if not promptly corrected. 3
Why This Classification Has Limitations
- Multifactorial etiology is the rule, not the exception - most hospitalized patients with AKI have overlapping mechanisms 3
- Fractional excretion of sodium (FENa) has questionable value in distinguishing prerenal from intrinsic AKI, especially in sepsis, because the pathophysiology doesn't fit neatly into these categories 4
- The KDIGO guidelines suggest it may be more useful to distinguish between conditions that reduce glomerular function versus those causing tubular/glomerular injury rather than using traditional categories 4
Diagnostic Approach Based on Type
Initial evaluation should include: 5
- Review medication history for nephrotoxins (NSAIDs, aminoglycosides, contrast agents, ACE inhibitors) 5
- Assess volume status through physical examination (orthostatic vital signs, jugular venous pressure, skin turgor, mucous membranes) 5
- Urine microscopy - muddy brown casts suggest ATN, white blood cell casts suggest interstitial nephritis, red blood cell casts suggest glomerulonephritis 5, 2
- Renal ultrasound to identify hydronephrosis in suspected postrenal obstruction 5
Novel biomarkers like NGAL can help distinguish ATN from other causes, though they don't necessarily separate prerenal from intrinsic components. 5, 4
Beyond the Initial Classification: Acute Kidney Disease (AKD)
AKI that persists beyond 7 days but less than 90 days is classified as Acute Kidney Disease (AKD), representing a critical transition period. 6, 4 This concept recognizes that kidney injury extends beyond simple functional impairment to include ongoing structural damage and loss of renal reserve. 4
AKD can occur with or without preceding AKI and represents evolving kidney dysfunction that requires distinct management considerations from both acute AKI and chronic kidney disease. 6