Acute Kidney Injury for USMLE Step 3
Acute Kidney Injury (AKI) for the USMLE Step 3 Exam
Definition
- Acute Kidney Injury (AKI): A sudden decline in kidney function occurring over hours to days, resulting in an inability to excrete waste products and regulate electrolytes and fluid balance. AKI is identified by a rise in serum creatinine or a decrease in urine output.
- Diagnosis Criteria:
- Increase in serum creatinine by ≥0.3 mg/dL within 48 hours or to ≥1.5 times baseline in the previous 7 days.
- Urine output <0.5 mL/kg/h for 6 hours or more.
Etiology
- Prerenal AKI:
- Results from reduced renal perfusion without structural kidney damage.
- Causes:
- Hypovolemia (e.g., dehydration, hemorrhage).
- Decreased cardiac output (e.g., heart failure, cardiogenic shock).
- Systemic vasodilation (e.g., sepsis, cirrhosis).
- Intrinsic AKI:
- Direct damage to the kidneys, typically involving the tubules.
- Causes:
- Acute Tubular Necrosis (ATN): Often due to ischemia (e.g., prolonged hypotension) or nephrotoxins (e.g., contrast agents, aminoglycosides).
- Acute Interstitial Nephritis (AIN): Commonly drug-induced (e.g., NSAIDs, beta-lactams) and associated with fever, rash, and eosinophilia.
- Glomerulonephritis: Often presents with nephritic syndrome (hematuria, proteinuria, and hypertension).
- Postrenal AKI:
- Caused by obstruction of urine flow, usually affecting both kidneys or a solitary kidney.
- Causes:
- Bladder outlet obstruction (e.g., benign prostatic hyperplasia, neurogenic bladder).
- Ureteral obstruction (e.g., stones, malignancy).
Pathophysiology
- Prerenal AKI:
- Reduced renal perfusion leads to a decrease in glomerular filtration rate (GFR). Prolonged hypoperfusion can progress to ischemic ATN if left untreated.
- Intrinsic AKI:
- ATN: Ischemia or nephrotoxins damage tubular cells, leading to cell death, sloughing, and obstruction of the tubules.
- AIN: Involves an immune-mediated inflammation of the renal interstitium.
- Postrenal AKI:
- Urinary tract obstruction increases pressure in the renal system, decreasing GFR and causing hydronephrosis if prolonged.
Clinical Presentation
- Symptoms:
- Oliguria or anuria, fatigue, nausea, and signs of fluid overload (e.g., edema, dyspnea).
- Uremic symptoms: confusion, pericarditis, or encephalopathy in severe AKI.
- Physical Exam:
- Prerenal AKI: Dry mucous membranes, hypotension, and tachycardia.
- Postrenal AKI: Bladder distention, costovertebral angle tenderness.
Diagnostic Evaluation
- Serum Creatinine: Elevated in all types of AKI.
- Urine Studies:
- Prerenal AKI: Urine sodium <20 mEq/L, BUN/creatinine ratio >20:1, high specific gravity.
- ATN: Urine sodium >40 mEq/L, muddy brown casts, and low urine osmolality.
- AIN: Eosinophils and WBC casts.
- Renal Ultrasound: Used to rule out obstructive causes such as hydronephrosis or stones.
Management
- Prerenal AKI:
- Fluid resuscitation with isotonic saline for volume depletion.
- Treat underlying conditions (e.g., sepsis, heart failure).
- Intrinsic AKI:
- ATN: Supportive care, managing electrolyte disturbances, and avoiding further nephrotoxic agents.
- AIN: Stop the offending agent, consider corticosteroids if no improvement is seen.
- Postrenal AKI:
- Relieve obstruction with Foley catheterization or surgical intervention (e.g., removal of stones or stenting).
Complications
- Hyperkalemia: Can lead to life-threatening arrhythmias.
- Metabolic Acidosis: Due to impaired acid excretion.
- Uremia: Can result in encephalopathy, pericarditis, and bleeding diathesis.
- Volume overload: Can cause heart failure and pulmonary edema.
Indications for Dialysis
- AEIOU Criteria:
- A: Acidosis unresponsive to medical therapy.
- E: Electrolyte imbalances (e.g., hyperkalemia).
- I: Intoxication with dialyzable toxins.
- O: Volume Overload unresponsive to diuretics.
- U: Uremic complications (e.g., pericarditis, encephalopathy).
Key Points
- AKI is defined by a rapid decline in renal function, typically diagnosed by rising serum creatinine and reduced urine output.
- Common causes include prerenal (hypoperfusion), intrinsic (ATN, AIN), and postrenal (obstruction).
- Diagnosis involves serum creatinine, urine studies, and imaging such as renal ultrasound.
- Treatment is directed at addressing the underlying cause, correcting electrolyte imbalances, and managing complications.
- Dialysis is indicated for severe acidosis, electrolyte imbalances, uremia, and refractory volume overload.