Types of Acute Renal Failure (ARF) / Acute Kidney Injury (AKI)
Acute kidney injury is classified into three anatomic categories based on the site of dysfunction: prerenal (reduced renal perfusion), intrarenal/intrinsic (direct kidney parenchymal damage), and postrenal (urinary tract obstruction), with prerenal and intrarenal causes accounting for over 97% of cases. 1, 2
Primary Classification System
Prerenal AKI
Prerenal AKI results from reduced renal perfusion without structural kidney damage. 1 This represents a functional impairment where the kidney itself is intact but receives inadequate blood flow.
Specific causes include: 1
- Hypovolemia (hemorrhage, gastrointestinal losses, burns, diuretic overuse)
- Decreased cardiac output (heart failure, myocardial infarction, arrhythmias)
- Systemic vasodilation (sepsis, anaphylaxis, medications)
- Renal vasoconstriction (NSAIDs, ACE inhibitors, hepatorenal syndrome)
- Renal artery occlusion (thrombosis, embolism, dissection)
A BUN-to-creatinine ratio >20:1 suggests prerenal azotemia, while a ratio <15:1 suggests intrarenal disease. 1, 2 This distinction is clinically useful for rapid bedside differentiation.
Intrarenal (Intrinsic) AKI
Intrarenal AKI involves direct damage to kidney parenchyma, most commonly acute tubular necrosis (ATN) caused by either ischemia or nephrotoxicity. 3 This category represents structural kidney injury requiring different management than prerenal causes.
The presence of cellular casts, particularly renal tubular epithelial cell casts on urinalysis, suggests acute tubular necrosis. 4 This finding distinguishes intrinsic from prerenal causes even when the BUN-to-creatinine ratio is equivocal.
Additional intrarenal causes include: 3, 5
- Glomerular diseases (glomerulonephritis, vasculitis)
- Interstitial diseases (acute interstitial nephritis from medications, infections)
- Vascular diseases (thrombotic microangiopathy, renal vein thrombosis)
Postrenal AKI
Postrenal AKI results from obstruction of urine flow at any level of the urinary tract. 1, 2
Anatomic sites of obstruction include: 1, 2
- Ureteral obstruction (bilateral stones, retroperitoneal fibrosis, malignancy)
- Bladder outlet obstruction (benign prostatic hyperplasia, bladder cancer, neurogenic bladder)
- Urethral obstruction (strictures, blood clots)
Renal ultrasound is recommended to evaluate kidney size and rule out obstruction, with hydronephrosis indicating postrenal causes. 4 This imaging should be obtained early when postrenal AKI is suspected.
Modern Classification Framework
RIFLE Classification System
The RIFLE criteria provide a standardized classification with five categories: Risk, Injury, Failure, Loss, and End-stage kidney disease. 6 This system was the first consensus definition developed by the Acute Dialysis Quality Initiative (ADQI) group. 6
The classification uses both GFR/creatinine criteria and urine output criteria, with patients classified by whichever criterion leads to the worst classification: 6
- Risk: Increased serum creatinine ×1.5 or GFR decrease >25%, OR urine output <0.5 ml/kg/h for 6 hours
- Injury: Increased serum creatinine ×2 or GFR decrease >50%, OR urine output <0.5 ml/kg/h for 12 hours
- Failure: Increased serum creatinine ×3 or GFR decrease >75% or serum creatinine >4 mg/dl with acute rise ≥0.5 mg/dl, OR urine output <0.3 ml/kg/h for 24 hours or anuria for 12 hours
- Loss: Persistent ARF requiring renal replacement therapy for >4 weeks
- End-stage kidney disease: Need for dialysis >3 months
Special designations include RIFLE-FC for "acute-on-chronic" disease when criteria are met in patients with baseline chronic kidney disease, and RIFLE-FO when failure classification is achieved by urine output criteria alone. 6
KDIGO Staging System
The KDIGO criteria define AKI as an increase in serum creatinine ≥0.3 mg/dL within 48 hours, or an increase to ≥1.5 times baseline within 7 days, or urine output <0.5 mL/kg/hr for 6 consecutive hours. 4, 2, 7
KDIGO staging provides three severity levels: 4, 2
- Stage 1: Serum creatinine 1.5-1.9× baseline OR ≥0.3 mg/dL increase, OR urine output <0.5 mL/kg/hr for 6-12 hours
- Stage 2: Serum creatinine 2.0-2.9× baseline, OR urine output <0.5 mL/kg/hr for ≥12 hours
- Stage 3: Serum creatinine ≥3.0× baseline OR ≥4.0 mg/dL (with acute rise >0.3 mg/dL) OR initiation of renal replacement therapy, OR urine output <0.3 mL/kg/hr for ≥24 hours OR anuria for ≥12 hours
Even small increases in creatinine (≥0.3 mg/dL) independently associate with approximately four-fold increased hospital mortality, and progression through AKI stages strongly correlates with increased mortality. 4, 2 This underscores the clinical importance of early stage 1 detection.
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 between acute injury and chronic kidney disease. 6, 1 This newer classification recognizes that kidney dysfunction extending beyond the acute phase requires distinct management considerations.
AKD can occur with or without preceding AKI and represents evolving kidney dysfunction. 1 The ADQI 16 workgroup established this category to capture patients in the recovery or progression phase who no longer meet AKI criteria but have not yet developed CKD. 6
Clinical Approach to Classification
The KDIGO guidelines suggest distinguishing between conditions that reduce glomerular function versus those causing tubular/glomerular injury rather than relying solely on traditional prerenal/intrarenal/postrenal categories. 1 This functional approach better reflects modern understanding of AKI pathophysiology.
Initial evaluation should include review of medication history for nephrotoxins, assessment of volume status, urine microscopy, and renal ultrasound to identify hydronephrosis in suspected postrenal obstruction. 1 Novel biomarkers like NGAL can help distinguish ATN from other causes, though they don't necessarily separate prerenal from intrinsic components. 1
A common pitfall is that urine output criteria may be problematic in certain populations, such as patients with cirrhosis and ascites who may be oliguric despite relatively normal kidney function. 4 In these cases, serum creatinine criteria should be prioritized for classification.
When baseline creatinine is unknown, the simplified MDRD formula can estimate baseline creatinine assuming a GFR of 75-100 ml/min per 1.73 m², allowing classification based on change from estimated baseline. 6