What are the types of acute kidney injury (AKI)?

Types of Acute Kidney Injury

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

Prerenal AKI

Prerenal AKI results from reduced renal perfusion without structural kidney damage—the kidney itself remains intact but receives inadequate blood flow. 1

Specific causes include:

• Hypovolemia (hemorrhage, gastrointestinal losses, excessive diuresis) 1
• Decreased cardiac output (heart failure, cardiogenic shock) 1
• Systemic vasodilation (sepsis, anaphylaxis) 1
• Renal vasoconstriction (NSAIDs, calcineurin inhibitors, hepatorenal syndrome) 1
• Renal artery occlusion (thrombosis, embolism) 1

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 specifically, prerenal AKI accounts for approximately 68% of hospitalized cases with decompensated cirrhosis. 3

Intrarenal (Intrinsic) AKI

Intrarenal AKI involves direct damage to kidney parenchyma, most commonly acute tubular necrosis (ATN) caused by either ischemia or nephrotoxicity. 1

The four subcategories of intrinsic AKI are:

• Tubular diseases: ATN from ischemia or nephrotoxins (aminoglycosides, contrast agents, rhabdomyolysis); presence of muddy brown granular casts or renal tubular epithelial cells on urinalysis suggests ATN 1, 4
• Glomerular diseases: acute glomerulonephritis, vasculitis 1
• Interstitial diseases: acute interstitial nephritis (often drug-induced), pyelonephritis 1
• Vascular diseases: renal artery or vein thrombosis, atheroembolic disease 1

Novel biomarkers like NGAL can help distinguish ATN from other causes such as hepatorenal syndrome (HRS) in cirrhotic patients, though they don't necessarily separate prerenal from intrinsic components. 3, 2, 5

Postrenal AKI

Postrenal AKI results from obstruction of urine flow at any level of the urinary tract, though it is uncommon in decompensated cirrhosis. 3, 1

Anatomic sites of obstruction include:

• Ureteral obstruction: bilateral ureteral stones, retroperitoneal fibrosis, malignancy 1, 2
• Bladder outlet obstruction: benign prostatic hyperplasia, bladder cancer, neurogenic bladder 1, 2
• Urethral obstruction: strictures, blood clots 1, 2

Renal ultrasound is recommended to evaluate kidney size and rule out obstruction, with hydronephrosis indicating postrenal causes. 1, 5

Special Considerations in Cirrhosis

All types of AKI can occur in patients with cirrhosis: prerenal AKI, hepatorenal syndrome-AKI (HRS-AKI), intrarenal AKI (particularly ATN), and postrenal AKI. 3

The key clinical challenge is differentiating HRS-AKI from ATN, as most prerenal cases resolve with volume expansion and postrenal AKI is uncommon. 3

Common precipitating factors in cirrhotic patients include:

• Infections (spontaneous bacterial peritonitis) 3
• Diuretic-induced excessive diuresis 3
• Gastrointestinal bleeding 3
• Therapeutic paracentesis without adequate volume expansion 3
• Nephrotoxic drugs and NSAIDs 3
• Increased intra-abdominal pressure from tense ascites 3

Acute Kidney Disease (AKD): The Transition 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

AKD can occur with or without preceding AKI and represents evolving kidney dysfunction requiring distinct management considerations. 3, 2

The KDIGO consensus conference established that:

• AKD without AKI represents patients with subacute kidney disease who never met strict AKI criteria 3
• AKD with AKI includes patients either during or after an AKI episode 3
• Both can occur in association with underlying CKD 3

Common Pitfalls

A critical 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. 1

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. 1

Even small increases in creatinine (≥0.3 mg/dL) independently associate with approximately four-fold increased hospital mortality, emphasizing that all AKI stages matter clinically. 1