Acute Kidney Injury (AKI): Pathophysiology, Diagnosis, and Management for the USMLE

Acute Kidney Injury (AKI) is a sudden decline in kidney function, leading to an accumulation of nitrogenous waste products (urea, creatinine) and electrolyte imbalances. It is a high-yield topic frequently tested on USMLE Step 1 and Step 2 CK, often appearing in case vignettes involving hospitalized patients. This blog will break down AKI pathophysiology, diagnosis, and management, using KOTC science visuals for better retention.

Classification of AKI

AKI is classified into three main categories:

1. Pre-Renal AKI (Most Common)

Cause: Decreased renal perfusion without intrinsic kidney damage.

• Hypovolemia: Hemorrhage, dehydration, excessive diuresis.

• Low Cardiac Output: Heart failure, cardiogenic shock.

• Renal Vasoconstriction: NSAIDs, ACE inhibitors, hepatorenal syndrome.

🔎 Urinalysis & Labs:

• BUN/Creatinine ratio > 20:1 (increased urea reabsorption due to hypoperfusion).

• FENa < 1% (low fractional excretion of sodium due to intact tubular function).

• Urine osmolality > 500 mOsm/kg (concentrated urine).

2. Intrinsic AKI

Cause: Direct injury to the kidney parenchyma.

• Acute Tubular Necrosis (ATN) – Ischemia or nephrotoxins (aminoglycosides, contrast media, myoglobin from rhabdomyolysis).

• Acute Interstitial Nephritis (AIN) – Allergic reaction to drugs (NSAIDs, penicillins, PPIs), infections.

• Glomerulonephritis – Immune-mediated inflammation (e.g., post-streptococcal GN, lupus nephritis).

🔎 Urinalysis & Labs:

• BUN/Creatinine ratio ~10-15:1 (normal urea reabsorption).

• FENa > 2% (impaired sodium reabsorption due to tubular damage).

• Urine osmolality < 350 mOsm/kg (dilute urine due to tubular dysfunction).

• Muddy brown casts in ATN, eosinophils in AIN.

3. Post-Renal AKI (Obstructive)

Cause: Urinary outflow obstruction leading to increased intratubular pressure and decreased GFR.

• Bilateral ureteral obstruction – Kidney stones, malignancy, retroperitoneal fibrosis.

• Bladder outlet obstruction – Benign prostatic hyperplasia (BPH), neurogenic bladder.

🔎 Diagnosis:

• Ultrasound: Dilated collecting system (hydronephrosis).

• Reversible with catheterization or surgical intervention.

Clinical Presentation of AKI

• Oliguria (<400 mL/day) or anuria in severe cases.

• Fluid overload, hypertension, pulmonary edema.

• Hyperkalemia, metabolic acidosis, elevated BUN/creatinine.

• Uremic symptoms (nausea, confusion, pericarditis, asterixis).

Diagnostic Workup for AKI

1. Serum Creatinine & BUN: Defines severity of renal impairment.

2. Urinalysis & Microscopy: Identifies pre-renal vs. intrinsic vs. post-renal causes.

3. Fractional Excretion of Sodium (FENa): Helps differentiate pre-renal from intrinsic AKI.

4. Renal Ultrasound: Detects hydronephrosis in post-renal AKI.

5. Electrolytes & ABGs: Check for hyperkalemia and metabolic acidosis.

Management of AKI

1. Pre-Renal AKI Treatment

• Restore Perfusion: IV fluids (isotonic saline or lactated Ringer's for hypovolemia).

• Discontinue Nephrotoxic Agents: NSAIDs, ACE inhibitors.

• Improve Cardiac Output: Manage heart failure if present.

2. Intrinsic AKI Treatment

• Acute Tubular Necrosis (ATN): Supportive care, avoid volume overload, dialysis if needed.

• Acute Interstitial Nephritis (AIN): Stop offending drugs, consider corticosteroids.

• Glomerulonephritis: Immunosuppressive therapy (steroids, cyclophosphamide) based on etiology.

3. Post-Renal AKI Treatment

• Relieve Obstruction: Catheterization for bladder outlet obstruction, stent or nephrostomy for ureteral obstruction.

• Address underlying cause: BPH, malignancy, stones.

USMLE Question Strategy

• Pre-Renal AKI: Look for hypovolemia, BUN/Cr ratio > 20:1, low FENa.

• Intrinsic AKI: Look for muddy brown casts (ATN), eosinophils (AIN), or RBC casts (glomerulonephritis).

• Post-Renal AKI: Look for urinary retention, hydronephrosis on imaging.

• Hyperkalemia in AKI? ECG changes (peaked T waves) → Immediate calcium gluconate + insulin/glucose.

💡 Pro Tip: Always check for recent contrast exposure or nephrotoxic drugs in AKI cases on the USMLE.

Conclusion

Acute Kidney Injury (AKI) is a high-yield nephrology topic for the USMLE exams. Understanding the different types of AKI, their pathophysiology, diagnostic approach, and management is essential for clinical vignettes.

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