What are the diagnostic criteria and treatment options for acute renal failure in adults?

Acute Renal Failure Diagnosis

Diagnose acute kidney injury (AKI) when serum creatinine increases by ≥0.3 mg/dL within 48 hours OR rises to ≥1.5 times baseline within 7 days OR urine output falls below 0.5 mL/kg/h for 6 consecutive hours. 1, 2

Diagnostic Criteria

Primary Definition

• Serum creatinine is more important than urine output for diagnosis because oliguria may be physiologic in certain conditions, particularly in patients with cirrhosis and ascites who retain sodium avidly despite normal kidney function 1, 2
• Either creatinine OR urine output criteria alone is sufficient for diagnosis—patients meeting one criterion qualify even without the other 2
• When baseline creatinine is unknown, estimate it using the simplified MDRD formula assuming normal GFR of 75-100 mL/min per 1.73 m², factoring in age, race, and sex 1, 2

Severity Staging (RIFLE Criteria)

The RIFLE system provides three severity levels based on the worst criterion met 1, 2:

• Risk: GFR decrease by 25% OR creatinine increase 1.5× baseline OR urine output <0.5 mL/kg/h for 6 hours 1, 3
• Injury: GFR decrease by 50% OR creatinine increase 2× baseline OR urine output <0.5 mL/kg/h for 12 hours 1, 3
• Failure: GFR decrease by 75% OR 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 1, 2

Critical Distinction: Acute vs. Chronic

Never assume a single abnormal creatinine represents chronic disease—repeat testing within days is mandatory. 2

Indicators of AKI (not CKD): 2

• Recent volume depletion, nephrotoxic medication, or contrast exposure
• No prior documentation of reduced GFR
• Clinical context suggesting acute process

Indicators of CKD (not AKI): 2

• Prior eGFR <60 mL/min/1.73 m² documented for >3 months
• Small kidneys on imaging, persistent albuminuria
• History of diabetes, hypertension, or glomerulonephritis

Etiologic Classification

Prerenal AKI (60-70% of cases)

Reduced renal perfusion without structural damage 3, 4:

• Hypovolemia (bleeding, dehydration, excessive diuresis)
• Decreased cardiac output (heart failure, cardiogenic shock)
• Systemic vasodilation (sepsis, anaphylaxis)
• Renal artery occlusion
• BUN-to-creatinine ratio >20:1 suggests prerenal etiology 3

Intrinsic Renal AKI

Direct parenchymal damage 1, 3:

• Acute tubular necrosis (most common): ischemic or nephrotoxic injury with muddy brown casts on urinalysis 3
• Glomerulonephritis, interstitial nephritis, vasculitis
• Drugs and toxins (aminoglycosides, NSAIDs, contrast agents)
• BUN-to-creatinine ratio <15:1 suggests intrinsic disease 3

Postrenal AKI (<3% of cases)

Urinary tract obstruction 1, 3:

• Bilateral ureteral obstruction or unilateral in solitary kidney
• Bladder outlet obstruction (prostatic hypertrophy, neurogenic bladder)
• Urethral obstruction

Diagnostic Workup Algorithm

Step 1: Laboratory Evaluation

• Serum creatinine and BUN: Calculate BUN/creatinine ratio for prerenal vs. intrinsic differentiation 3, 5
• Complete blood count: Assess for anemia, thrombocytopenia suggesting systemic disease 5
• Urinalysis with microscopy: Look for casts (muddy brown = ATN, RBC casts = glomerulonephritis, WBC casts = interstitial nephritis) 1, 5
• Fractional excretion of sodium (FENa): <1% suggests prerenal, >2% suggests intrinsic AKI 5
• Basic metabolic panel: Identify hyperkalemia, metabolic acidosis requiring urgent intervention 5

Step 2: Imaging

• Renal ultrasound is mandatory in most patients to assess kidney size and rule out hydronephrosis indicating obstruction 6, 3, 5
• Small echogenic kidneys suggest underlying CKD rather than pure AKI 1

Step 3: Medication Review

• Identify nephrotoxins: NSAIDs, aminoglycosides, ACE inhibitors/ARBs, contrast agents 1, 7
• Recent procedures involving radiocontrast media 7

Step 4: Volume Status Assessment

• Physical examination for signs of hypovolemia (orthostatic hypotension, dry mucous membranes) or volume overload (edema, pulmonary congestion) 5
• Recent fluid losses (vomiting, diarrhea, bleeding) or third-spacing (cirrhosis, pancreatitis) 3

Common Pitfalls to Avoid

• Do not rely on a fixed creatinine threshold of 1.5 mg/dL as this often indicates GFR is already markedly decreased to ~30 mL/min 1
• Serum creatinine lags behind actual kidney injury due to decreased muscle mass in cirrhosis, dilution from fluid overload, and interference from elevated bilirubin 1, 6
• Urine output criteria are unreliable in cirrhotic patients who may be oliguric despite normal GFR due to avid sodium retention 1, 2
• Always review past creatinine measurements to determine if findings represent new injury or progression of known disease 2
• Do not delay nephrology consultation for severe AKI (RIFLE-Failure stage) or AKI persisting >48 hours 6

Risk Factors Requiring Heightened Surveillance

High-risk populations for AKI development 7, 5:

• Older age, diabetes mellitus, baseline chronic kidney disease
• Sepsis, hypovolemia/shock, heart failure, liver failure
• Cardiac surgery (especially valve replacement)
• Rhabdomyolysis, intra-abdominal hypertension
• Exposure to nephrotoxic agents or radiocontrast media

Acute Kidney Disease (AKD)

If AKI persists beyond 7 days but less than 90 days, reclassify as Acute Kidney Disease (AKD) representing a critical transition period requiring distinct management considerations and close monitoring for progression to CKD 6, 3