Acute Kidney Injury for the PA Exam
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Acute Kidney Injury (AKI) for the Physician Assistant Licensing Exam
Definition
- Acute Kidney Injury (AKI): Sudden decrease in kidney function over hours to days, causing the kidneys to fail in maintaining homeostasis. It is identified by an increase in serum creatinine or a decrease in urine output.
- Diagnosis:
- Increase in serum creatinine by ≥0.3 mg/dL in 48 hours or to ≥1.5 times baseline.
- Urine output <0.5 mL/kg/h for more than 6 hours.
Pathophysiology
- Prerenal AKI:
- Due to reduced renal perfusion without direct kidney damage.
- Common causes:
- Hypovolemia (e.g., dehydration, blood loss).
- Decreased cardiac output (e.g., heart failure).
- Systemic vasodilation (e.g., sepsis).
- Decreased GFR triggers compensatory mechanisms, including activation of the renin-angiotensin-aldosterone system (RAAS), to maintain perfusion.
- Intrinsic AKI:
- Direct damage to the kidneys, most commonly due to Acute Tubular Necrosis (ATN).
- ATN causes:
- Ischemic: Prolonged hypoperfusion.
- Nephrotoxic: Medications (e.g., aminoglycosides, radiocontrast), rhabdomyolysis.
- Other causes include Acute Interstitial Nephritis (AIN) and glomerulonephritis.
- ATN involves tubular cell death and obstruction from cellular debris.
- Postrenal AKI:
- Due to obstruction of urinary outflow, often affecting both kidneys or a solitary kidney.
- Common causes include benign prostatic hyperplasia, kidney stones, and bladder outlet obstruction.
Clinical Presentation
- Symptoms:
- Fatigue, nausea, and confusion (from electrolyte imbalances or uremia).
- Oliguria (urine output <400 mL/day) or anuria in severe cases.
- Volume overload in cases of heart failure or intrinsic kidney disease (e.g., peripheral edema, pulmonary congestion).
- Physical Exam:
- Hypovolemia signs in prerenal AKI: Dry mucous membranes, low blood pressure.
- Fluid overload signs in heart failure or intrinsic AKI: Peripheral edema, elevated jugular venous pressure.
- Bladder distension or flank pain in postrenal AKI.
Diagnosis
- Serum Creatinine: 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.
- Intrinsic AKI: In ATN, muddy brown casts, urine sodium >40 mEq/L, and low urine osmolality.
- Postrenal AKI: Initially concentrated urine; late findings include dilute urine with increasing creatinine.
- Renal Ultrasound: Useful to detect postrenal causes like hydronephrosis or stones.
Management
- Prerenal AKI:
- Fluid resuscitation to restore volume and renal perfusion.
- Treat underlying conditions (e.g., manage sepsis, heart failure).
- Intrinsic AKI:
- ATN: Supportive care, avoiding nephrotoxic drugs, and managing electrolytes.
- AIN: Stop offending drugs, consider corticosteroids for severe cases.
- Postrenal AKI:
- Relieve obstruction (e.g., bladder catheterization, removal of kidney stones).
Complications
- Hyperkalemia: Risk of cardiac arrhythmias.
- Metabolic acidosis: Decreased acid excretion.
- Volume overload: Leading to heart failure or pulmonary edema.
Indications for Dialysis
- AEIOU Criteria:
- A: Acidosis unresponsive to medical therapy.
- E: Electrolyte imbalances (e.g., hyperkalemia).
- I: Ingestion of toxins.
- O: Volume Overload unresponsive to diuretics.
- U: Uremic symptoms (e.g., pericarditis, encephalopathy).
Key Points
- AKI is defined by a rapid reduction in kidney function with an increase in serum creatinine or decreased urine output.
- Causes include prerenal (hypoperfusion), intrinsic (e.g., ATN, AIN), and postrenal (obstruction).
- Diagnosis involves serum creatinine, urine studies, and imaging such as renal ultrasound.
- Management focuses on correcting the underlying cause and preventing complications such as hyperkalemia and metabolic acidosis.
- Dialysis is indicated for severe electrolyte imbalances, acidemia, uremia, and volume overload.