Acute Kidney Injury for the ABIM
Start your One-Week Free Trial
Already subscribed? Log in »
Acute Kidney Injury (AKI) for the ABIM Exam
Definition
- Acute Kidney Injury (AKI): A rapid decline in renal function, typically over hours to days, resulting in the inability of the kidneys to maintain fluid, electrolyte, and acid-base balance. It is diagnosed by an increase in serum creatinine or a reduction in urine output.
- Diagnosis Criteria:
- Increase in serum creatinine by ≥0.3 mg/dL within 48 hours, or
- Increase in serum creatinine to ≥1.5 times baseline within the past 7 days, or
- Urine output <0.5 mL/kg/h for 6 hours.
Classification (KDIGO Staging)
- Stage 1:
- Serum creatinine increase 1.5–1.9 times baseline or ≥0.3 mg/dL increase.
- Urine output <0.5 mL/kg/h for 6–12 hours.
- Stage 2:
- Serum creatinine increase 2.0–2.9 times baseline.
- Urine output <0.5 mL/kg/h for ≥12 hours.
- Stage 3:
- Serum creatinine increase 3.0 times baseline or serum creatinine ≥4.0 mg/dL.
- Urine output <0.3 mL/kg/h for ≥24 hours or anuria for ≥12 hours.
- Initiation of renal replacement therapy (RRT) automatically classifies as Stage 3.
Etiology
- Prerenal AKI (60–70%):
- Caused by decreased renal perfusion without structural kidney damage.
- Common causes:
- Hypovolemia (e.g., dehydration, hemorrhage).
- Decreased cardiac output (e.g., heart failure, cardiogenic shock).
- Systemic vasodilation (e.g., sepsis, cirrhosis).
- Renal artery stenosis or severe hypotension.
- Intrinsic Renal AKI (25–40%):
- Involves direct damage to kidney structures.
- Common causes:
- Acute Tubular Necrosis (ATN): The most common cause of intrinsic AKI, often secondary to ischemia or nephrotoxins (e.g., contrast agents, aminoglycosides).
- Acute Interstitial Nephritis (AIN): Often drug-induced (e.g., NSAIDs, beta-lactams) and associated with fever, rash, and eosinophilia.
- Glomerulonephritis: Inflammatory damage to the glomeruli, often associated with nephritic syndrome (hematuria, proteinuria, hypertension).
- Vascular Causes: Thrombotic microangiopathy, vasculitis.
- Postrenal AKI (5–10%):
- Obstruction of urine flow anywhere along the urinary tract.
- Causes:
- Ureteral obstruction (e.g., kidney stones, tumors).
- Bladder outlet obstruction (e.g., benign prostatic hyperplasia, neurogenic bladder).
- Bilateral obstruction or obstruction in a solitary kidney.
Pathophysiology
- Prerenal AKI: Decreased blood flow to the kidneys leads to reduced glomerular filtration rate (GFR). Prolonged prerenal states may result in ischemia and progression to intrinsic renal damage (particularly ATN).
- Intrinsic Renal AKI:
- ATN: Tubular cells are sensitive to ischemia and toxins. Damage leads to tubular cell death and sloughing, which obstructs the renal tubules.
- AIN: Involves inflammation of the renal interstitium, typically with infiltration of lymphocytes, plasma cells, and eosinophils.
- Glomerulonephritis: Immune-mediated inflammation results in damage to the glomeruli and impaired filtration.
- Postrenal AKI: Urinary tract obstruction causes back pressure on the renal system, impairing GFR. If left untreated, sustained back pressure leads to hydronephrosis and permanent kidney damage.
Clinical Presentation
- General Symptoms:
- Oliguria (urine output <400 mL/day) or anuria.
- Nonspecific symptoms like fatigue, nausea, vomiting, and edema.
- Uremic symptoms in severe cases: confusion, pericarditis, bleeding diathesis.
- Physical Examination:
- Signs of volume depletion (e.g., dry mucous membranes, tachycardia) in prerenal AKI.
- Fluid overload signs (e.g., peripheral edema, jugular venous distention) in heart failure or intrinsic causes.
- Flank pain or bladder distention in postrenal AKI.
- Laboratory Findings:
- Elevated serum creatinine and blood urea nitrogen (BUN).
- Electrolyte imbalances: hyperkalemia, metabolic acidosis, hyperphosphatemia.
Diagnostic Approach
- History and Physical Exam: Identify underlying causes like dehydration, recent medication use (e.g., NSAIDs, antibiotics), or obstructive symptoms.
- Laboratory Tests:
- Serum Creatinine and BUN: Monitor for worsening renal function.
- Urine Analysis:
- Prerenal AKI: High urine specific gravity, low urine sodium (<20 mEq/L), and a BUN/creatinine ratio >20:1.
- ATN: Muddy brown granular casts, urine sodium >40 mEq/L, low specific gravity.
- AIN: Presence of WBCs, WBC casts, and eosinophils.
- Imaging:
- Renal ultrasound is useful to rule out postrenal causes, such as hydronephrosis or bladder outlet obstruction.
- Biopsy: Reserved for uncertain diagnosis, especially in suspected glomerulonephritis or vasculitis.
Management
- Prerenal AKI:
- Restore renal perfusion with intravenous fluids for volume depletion or blood products for hemorrhage.
- Treat underlying causes (e.g., discontinue offending medications, manage heart failure, or address sepsis).
- Intrinsic AKI:
- ATN: Avoid further nephrotoxic insults, maintain adequate hydration, and manage electrolyte disturbances.
- AIN: Stop the offending drug, consider corticosteroids if there is no immediate improvement.
- Glomerulonephritis: Immunosuppressive therapies (e.g., corticosteroids, cyclophosphamide) based on the underlying etiology.
- Postrenal AKI:
- Relieve the obstruction using Foley catheterization for bladder outlet obstruction or surgical intervention for ureteral obstructions.
Complications
- Electrolyte Imbalances:
- Hyperkalemia: Risk of arrhythmias.
- Metabolic Acidosis: Due to decreased acid excretion.
- Hyponatremia and volume overload: Particularly in oliguric patients.
- Uremia: Requires urgent dialysis if it leads to complications such as pericarditis, encephalopathy, or severe metabolic derangements.
- Chronic Kidney Disease (CKD): If AKI is severe or prolonged, it can lead to irreversible kidney damage and progression to CKD.
Indications for Renal Replacement Therapy (RRT)
- AEIOU Criteria:
- A: Acidosis unresponsive to medical therapy.
- E: Electrolyte imbalances (e.g., refractory hyperkalemia).
- I: Ingestion of toxins (e.g., ethylene glycol, lithium).
- O: Volume Overload unresponsive to diuretics.
- U: Uremic complications (e.g., pericarditis, encephalopathy).
Key Points
- AKI is characterized by a rapid decline in renal function, primarily diagnosed via serum creatinine and urine output changes.
- Etiologies include prerenal (e.g., hypovolemia), intrinsic (e.g., ATN, AIN), and postrenal causes (e.g., obstruction).
- Key diagnostic tools include serum creatinine, urine analysis, and renal ultrasound.
- Management focuses on correcting underlying causes and managing complications such as electrolyte imbalances and uremia.
- Indications for dialysis include severe acidosis, electrolyte disturbances, intoxications, overload, and uremia.