Definition and Staging
KDIGO Definition of AKI
An abrupt decrease in kidney function, defined as any of the following criteria within 48 hours:
- Serum creatinine increase ≥0.3 mg/dL
- Serum creatinine increase ≥1.5× baseline (known or presumed to have occurred within the prior 7 days)
- Urine volume <0.5 mL/kg/h for 6 hours
KDIGO Staging System for AKI
| Stage |
Serum Creatinine Criteria |
Urine Output Criteria |
| Stage 1 |
1.5-1.9× baseline OR ≥0.3 mg/dL increase |
<0.5 mL/kg/h for 6-12 hours |
| Stage 2 |
2.0-2.9× baseline |
<0.5 mL/kg/h for ≥12 hours |
| Stage 3 |
≥3.0× baseline OR Increase to ≥4.0 mg/dL OR Initiation of RRT |
<0.3 mL/kg/h for ≥24 hours OR Anuria for ≥12 hours |
The Temporal Disconnect in AKI
A fundamental challenge in AKI management is the lag between the actual kidney injury and its clinical recognition. Serum creatinine may not rise for 24-48 hours after the insult. This means by the time AKI is diagnosed, the critical window for early, potentially protective interventions may have already passed. This highlights the importance of risk stratification and prevention.
Classification and Diagnostic Approach
Prerenal AKI (60-70% of cases)
Pathophysiology & Causes
Caused by reduced renal perfusion with structurally intact nephrons. Common causes include true volume depletion (hemorrhage, GI losses), decreased effective circulating volume (heart failure, cirrhosis), and medications that alter renal hemodynamics (NSAIDs, ACEi/ARBs).
Diagnostic Clues
- History: Vomiting, diarrhea, hemorrhage, heart failure exacerbation.
- Exam: Hypotension, tachycardia, dry mucous membranes, low JVP.
- Labs: BUN/Cr ratio >20:1, FENa <1%, FEUrea <35%.
- Urine: Concentrated (SG > 1.020), bland sediment with hyaline casts.
Intrinsic Renal AKI (25-40% of cases)
Acute Tubular Necrosis (ATN)
The most common cause of intrinsic AKI, resulting from ischemic or nephrotoxic injury to the tubules.
- Ischemic ATN: Follows prolonged prerenal state (e.g., shock).
- Nephrotoxic ATN: Caused by drugs (aminoglycosides, contrast), endogenous toxins (myoglobin, hemoglobin).
Diagnostic Clues
- History: Sepsis, prolonged hypotension, contrast exposure, rhabdomyolysis.
- Labs: BUN/Cr ratio ~10-15:1, FENa >2%.
- Urine: Muddy brown granular casts, renal tubular epithelial cells.
Acute Interstitial Nephritis (AIN)
An inflammatory infiltrate in the interstitium, most often a hypersensitivity reaction to drugs.
- Common Drugs: Antibiotics (beta-lactams, sulfonamides), NSAIDs, PPIs.
- Other Causes: Infections, autoimmune diseases (sarcoidosis, lupus).
Diagnostic Clues
- History: New medication started 7-14 days prior.
- Classic Triad (rare, <10%): Fever, rash, eosinophilia.
- Urine: White blood cell casts, eosinophiluria (low sensitivity).
Postrenal AKI (5-10% of cases)
Pathophysiology & Causes
Caused by obstruction of urine flow. Obstruction must be bilateral (or unilateral in a patient with a single functioning kidney) to cause significant AKI.
- Upper Tract: Stones, tumors, retroperitoneal fibrosis.
- Lower Tract: Benign prostatic hyperplasia (BPH), bladder neck obstruction, urethral stricture.
Diagnostic Clues
- History: Urinary hesitancy, frequency, nocturia, history of stones or pelvic malignancy.
- Exam: Palpable bladder, enlarged prostate.
- Imaging: Renal ultrasound showing hydronephrosis is the key diagnostic test.
Treatment and Complications
Management depends on the etiology. Prerenal AKI is treated by restoring perfusion (e.g., fluids). Postrenal AKI requires relief of the obstruction (e.g., Foley catheter). Intrinsic AKI is managed supportively by treating the underlying cause, avoiding further insults, and managing complications.
Indications for Urgent Dialysis (AEIOU)
- Acidosis (severe, pH <7.1, refractory to medical therapy)
- Electrolytes (severe, refractory hyperkalemia)
- Ingestions (certain dialyzable toxins like salicylates, ethylene glycol, methanol, lithium)
- Overload (refractory pulmonary edema)
- Uremia (symptomatic, e.g., pericarditis, encephalopathy, bleeding)