Types of Acute Kidney Injury
Primary Classification System
Acute kidney injury is classified into three anatomic categories based on the site of dysfunction: prerenal, intrarenal (intrinsic), and postrenal, with prerenal and intrarenal causes accounting for over 97% of cases. 1, 2
Prerenal AKI
Prerenal AKI results from reduced renal perfusion without structural kidney damage, representing a functional impairment where the kidney itself remains intact but receives inadequate blood flow. 1, 2
Specific Causes:
- Hypovolemia (volume depletion from bleeding, dehydration, excessive diuresis) 1, 2
- Decreased cardiac output (heart failure, cardiogenic shock) 1, 2
- Systemic vasodilation (sepsis, anaphylaxis) 1, 2
- Renal vasoconstriction (NSAIDs, hepatorenal syndrome) 1, 2
- Renal artery occlusion (thrombosis, embolism) 1, 2
Clinical Pearl:
- A BUN-to-creatinine ratio >20:1 suggests prerenal azotemia, while a ratio <15:1 suggests intrarenal disease, providing rapid bedside differentiation. 1, 2
- In cirrhotic patients, prerenal AKI accounts for approximately 68% of hospitalized cases with decompensated cirrhosis. 3, 2
Intrarenal (Intrinsic) AKI
Intrarenal AKI involves direct damage to kidney parenchyma, most commonly from acute tubular necrosis (ATN) caused by either ischemia or nephrotoxicity. 2
Subtypes:
- Acute tubular necrosis (ATN) - the most common intrarenal cause, identified by cellular casts on urinalysis 2, 4
- Glomerular diseases (glomerulonephritis, vasculitis) 2
- Interstitial diseases (acute interstitial nephritis from medications, infections) 2
- Vascular diseases (renal vein thrombosis, atheroembolic disease) 2
Key Diagnostic Feature:
- The presence of cellular casts on urinalysis suggests ATN and helps distinguish intrarenal from prerenal causes. 2
Postrenal AKI
Postrenal AKI results from obstruction of urine flow at any level of the urinary tract, though it accounts for less than 3% of AKI cases overall. 1, 2
Anatomic Sites of Obstruction:
- Ureteral obstruction (bilateral stones, retroperitoneal fibrosis, malignancy) 1, 2
- Bladder outlet obstruction (prostatic hypertrophy, bladder cancer, neurogenic bladder) 1, 2
- Urethral obstruction (strictures, blood clots) 1, 2
Diagnostic Approach:
- Renal ultrasound is recommended to evaluate for hydronephrosis, particularly in patients with history of stones, obstruction, frequent UTIs, or family history of polycystic kidney disease. 2, 5
- Postrenal AKI is uncommon in decompensated cirrhosis. 3, 2
Special Considerations in Cirrhosis
All types of AKI can occur in cirrhotic patients: prerenal AKI, hepatorenal syndrome-AKI (HRS-AKI), intrarenal AKI (particularly ATN), and postrenal AKI. 3, 2
Critical Distinction:
- The key clinical challenge is differentiating HRS-AKI from ATN, as most prerenal cases resolve with volume expansion and postrenal AKI is uncommon. 3, 2
- Novel biomarkers like NGAL can help distinguish ATN from HRS in cirrhotic patients. 2, 5
Common Precipitating Factors in Cirrhosis:
- Infections 3, 2
- Diuretic-induced excessive diuresis 3, 2
- Gastrointestinal bleeding 3, 2
- Therapeutic paracentesis without adequate volume expansion 3, 2
- Nephrotoxic drugs and NSAIDs 3, 2
- Increased intra-abdominal pressure from tense ascites 3, 2
Acute Kidney Disease (AKD): A Fourth Category
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. 3, 1, 2
Key Features:
- AKD can occur with or without preceding AKI and represents evolving kidney dysfunction requiring distinct management considerations. 3, 1, 2
- AKD that persists beyond 90 days is considered chronic kidney disease. 3
- Recovery from AKD is defined as a reduction in peak AKI stage based on KDIGO criteria, with further refinement by changes in serum creatinine, GFR, biomarkers, or return of renal reserve. 3
Clinical Importance:
- The ADQI 16 workgroup established this category to capture patients in the recovery or progression phase who require ongoing monitoring and intervention. 2
- Limited evidence exists to guide routine follow-up for patients with AKD, highlighting the need for standards in evaluation of kidney function, risk identification, and surveillance for complications. 3
Common Pitfalls
- Do not assume AKI is a homogeneous entity - congestive heart failure and dehydration can produce identical creatinine changes but require opposite treatments (diuresis vs. volume expansion). 6
- Urine output criteria may be problematic in cirrhotic patients with ascites, who may be oliguric despite relatively normal kidney function. 2
- When baseline creatinine is unknown, the simplified MDRD formula can estimate baseline assuming a GFR of 75-100 ml/min per 1.73 m², but this overestimates GFR in cirrhotic patients. 3, 2