Acute Kidney Injury for USMLE Step 2
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Acute Kidney Injury (AKI) for the USMLE Step 2 Exam
Definition
- Acute Kidney Injury (AKI): Sudden decline in kidney function over hours to days, leading to an inability to regulate fluid, electrolytes, and waste products. Diagnosis is based on serum creatinine rise or reduced urine output.
- Diagnosis Criteria:
- Increase in serum creatinine by ≥0.3 mg/dL within 48 hours or to ≥1.5 times baseline within 7 days.
- Urine output <0.5 mL/kg/h for 6 hours or more.
Etiology
- Prerenal AKI:
- Caused by reduced renal perfusion, typically without intrinsic kidney damage.
- Common causes:
- Volume depletion (e.g., dehydration, blood loss).
- Decreased cardiac output (e.g., heart failure, cardiogenic shock).
- Systemic vasodilation (e.g., sepsis, cirrhosis).
- Intrinsic AKI:
- Involves direct injury to kidney structures, primarily tubules.
- Causes:
- Acute Tubular Necrosis (ATN): Due to ischemia (e.g., prolonged hypoperfusion) or nephrotoxins (e.g., contrast agents, aminoglycosides).
- Acute Interstitial Nephritis (AIN): Often drug-induced (e.g., NSAIDs, antibiotics), associated with fever, rash, and eosinophilia.
- Glomerulonephritis: Characterized by hematuria, proteinuria, and hypertension.
- Postrenal AKI:
- Due to obstruction of urinary flow, typically involving both kidneys or a solitary kidney.
- Causes include benign prostatic hyperplasia, ureteral stones, and bladder outlet obstruction.
Pathophysiology
- Prerenal AKI: Decreased renal perfusion causes reduced glomerular filtration rate (GFR), activating compensatory mechanisms like the renin-angiotensin-aldosterone system (RAAS) to restore blood flow. Prolonged prerenal states may lead to ischemic ATN.
- Intrinsic AKI:
- ATN: Ischemia or toxins damage renal tubular cells, causing tubular cell death and obstruction.
- AIN: Involves inflammation of the renal interstitium due to drug reactions, infections, or autoimmune diseases.
- Postrenal AKI: Obstruction increases pressure in the renal tubules, impairing GFR. Prolonged obstruction can cause irreversible damage.
Clinical Presentation
- Symptoms:
- Oliguria (urine output <400 mL/day), or anuria in severe cases.
- Fatigue, nausea, confusion due to uremia or electrolyte disturbances.
- Fluid overload symptoms in intrinsic or postrenal AKI (e.g., peripheral edema, dyspnea).
- Physical Exam:
- Prerenal AKI: Signs of dehydration (e.g., tachycardia, dry mucous membranes).
- Postrenal AKI: Bladder distention or costovertebral angle tenderness.
Diagnostic Evaluation
- Laboratory Tests:
- Serum Creatinine and BUN: Elevated in all forms of AKI.
- Urine Studies:
- Prerenal AKI: Low urine sodium (<20 mEq/L), high specific gravity, and BUN/creatinine ratio >20:1.
- ATN: Urine sodium >40 mEq/L, muddy brown casts in the urine.
- AIN: Presence of WBCs, WBC casts, and eosinophils in the urine.
- Imaging:
- Renal Ultrasound: Essential to rule out postrenal causes, such as hydronephrosis.
- Biopsy: Reserved for uncertain diagnoses, especially in suspected glomerulonephritis or AIN.
Management
- Prerenal AKI:
- Restore perfusion with IV fluids or blood products.
- Address the underlying cause (e.g., heart failure management, antibiotics for sepsis).
- Intrinsic AKI:
- ATN: Supportive care, avoiding further nephrotoxic insults.
- AIN: Discontinue the offending agent; consider corticosteroids if no improvement.
- Postrenal AKI:
- Relieve obstruction with catheterization or surgical intervention (e.g., stenting for ureteral stones).
Complications
- Hyperkalemia: Can cause life-threatening arrhythmias.
- Metabolic Acidosis: Due to decreased excretion of acids.
- Uremia: Can lead to pericarditis, encephalopathy, and bleeding diathesis.
Indications for Dialysis
- AEIOU Criteria:
- A: Severe metabolic Acidosis.
- E: Refractory Electrolyte imbalances (e.g., hyperkalemia).
- I: Intoxications with dialyzable toxins.
- O: Overload of fluid unresponsive to diuretics.
- U: Symptomatic Uremia (e.g., pericarditis, encephalopathy).
Key Points
- AKI is defined by a rapid decline in kidney function, commonly detected by serum creatinine increase or decreased urine output.
- Causes include prerenal (decreased perfusion), intrinsic (ATN, AIN), and postrenal (obstruction).
- Diagnosis involves serum creatinine, urine studies, and imaging like renal ultrasound.
- Management focuses on correcting the underlying cause and addressing complications like hyperkalemia and uremia.
- Dialysis is indicated for severe metabolic derangements or uremia.