Acute Kidney Injury (AKI): A Comprehensive Guide for Nurses

Acute Kidney Injury (AKI), formerly known as acute renal failure, is a sudden decline in kidney function characterized by reduced glomerular filtration rate (GFR), accumulation of waste products, and disturbances in fluid, electrolyte, and acid-base balance. AKI is a potentially life-threatening condition requiring prompt recognition and management to prevent permanent kidney damage and improve patient outcomes. Nurses are critical in monitoring, supporting, and educating patients with AKI.

Definition

The KDIGO (Kidney Disease: Improving Global Outcomes) criteria classify AKI based on:

• Increase in Serum Creatinine:
  • ≥0.3 mg/dL within 48 hours.
  • ≥1.5 times the baseline within 7 days.
• Reduction in Urine Output:
  • <0.5 mL/kg/hour for 6 hours or longer.

Types of AKI

Prerenal AKI:

Caused by reduced blood flow to the kidneys without structural damage.

Causes:

• Hypovolemia (dehydration, blood loss).
• Decreased cardiac output (heart failure, cardiogenic shock).
• Systemic vasodilation (sepsis).

Intrinsic (Intrarenal) AKI:

Caused by direct damage to the kidney tissue.

Causes:

• Acute tubular necrosis (ATN) due to ischemia or nephrotoxins.
• Acute glomerulonephritis or vasculitis.
• Interstitial nephritis (drug-induced, infection).

Postrenal AKI:

Caused by obstruction of urine flow.

Causes:

• Kidney stones, tumors, enlarged prostate, or strictures.

Pathophysiology

Prerenal AKI:

• Reduced renal perfusion leads to decreased GFR.
• Prolonged hypoperfusion causes ischemic injury, progressing to intrinsic AKI.

Intrinsic AKI:

• Direct injury to the renal parenchyma disrupts tubular and glomerular function.
• Common mechanisms include tubular necrosis, inflammation, and oxidative stress.

Postrenal AKI:

• Obstruction increases pressure in the renal pelvis, reducing filtration and causing hydronephrosis.
• Prolonged obstruction leads to tubular damage and intrinsic injury.

Risk Factors

1. Medical Conditions:

• Chronic kidney disease (CKD).
• Diabetes mellitus.
• Hypertension.
• Heart failure.

2. Medications:

• Nephrotoxins (aminoglycosides, NSAIDs, contrast agents).
• ACE inhibitors or ARBs in patients with low renal perfusion.

3. Acute Conditions:

• Sepsis, major surgery, trauma, or severe dehydration.

4. Age:

• Elderly patients are at higher risk due to reduced renal reserve and comorbidities.

Clinical Presentation

Symptoms:

Fatigue, Weakness, or Lethargy

• Feeling unusually tired or weak.

Nausea, Vomiting, or Loss of Appetite

• Gastrointestinal disturbances due to uremia.

Decreased or Absent Urine Output:

• Oliguria (<400 mL/day); anuria (<50 mL/day).

Swelling Due to Fluid Retention

• Edema in extremities or other body parts.

Signs:

Vital Signs:

• Hypotension (prerenal causes).
• Hypertension (fluid overload in intrinsic/postrenal causes).

Edema:

• Peripheral, pulmonary, or generalized (anasarca).

Neurological Changes:

• Confusion, drowsiness, or seizures (uremia or electrolyte imbalances).

Diagnosis

1. Laboratory Tests:

• Serum Creatinine and Blood Urea Nitrogen (BUN): Elevated levels indicate impaired renal function.
• BUN:Creatinine Ratio >20:1: Suggests prerenal AKI.
• Electrolytes: Hyperkalemia, hyponatremia, hyperphosphatemia, hypocalcemia.
• Arterial Blood Gas (ABG): Metabolic acidosis in severe AKI.

2. Urine Studies:

• Urinalysis: Proteinuria, hematuria, or casts suggest intrinsic AKI.
• Fractional Excretion of Sodium (FeNa):<1% in prerenal AKI; >2% in intrinsic AKI.

3. Imaging:

• Ultrasound: Evaluate for hydronephrosis in postrenal AKI.
• CT Scan: Identify stones, tumors, or obstructions.
• Avoid contrast: Unless essential, as it may worsen AKI.

4. Biopsy:

• Reserved for suspected intrinsic AKI with unclear etiology.

Management of AKI

Goals of Treatment:

• Identify and treat the underlying cause.
• Restore and maintain fluid, electrolyte, and acid-base balance.
• Prevent and manage complications.

1. General Measures:

Fluid Management:

• Isotonic crystalloids (e.g., normal saline) for hypovolemia in prerenal AKI.
• Avoid overhydration, especially in intrinsic or postrenal AKI.

Diuretics:

• Loop diuretics (e.g., furosemide) for fluid overload.
• Not routinely used to improve GFR.

2. Electrolyte and Acid-Base Correction:

Hyperkalemia:

• Calcium gluconate to stabilize the myocardium.
• Insulin with glucose, sodium bicarbonate, or beta-agonists to shift potassium intracellularly.
• Kayexalate or dialysis to remove potassium.

Metabolic Acidosis:

• Sodium bicarbonate if pH <7.2 or severe acidosis.

Hypocalcemia:

• Treat symptomatic cases with calcium supplementation.

3. Treat the Underlying Cause:

Prerenal AKI:

• Address dehydration, hypotension, or sepsis.

Intrinsic AKI:

• Remove nephrotoxic agents.
• Treat glomerulonephritis or interstitial nephritis with appropriate therapies (e.g., steroids).

Postrenal AKI:

• Relieve obstruction with catheters, stents, or surgery.

4. Dialysis:

• Indicated for severe AKI with:
• Refractory hyperkalemia.
• Severe metabolic acidosis.
• Volume overload unresponsive to diuretics.
• Uremic symptoms (e.g., pericarditis, encephalopathy).

Nursing Interventions

1. Assessment and Monitoring:

• Monitor urine output closely (hourly if necessary).
• Assess for signs of fluid overload (e.g., edema, crackles, or weight gain).
• Regularly check vital signs, especially blood pressure.

2. Lab Monitoring:

• Track trends in serum creatinine, BUN, electrolytes, and ABG results.
• Report critical electrolyte abnormalities promptly.

3. Medication Administration:

• Administer prescribed diuretics or electrolyte supplements.
• Adjust dosages of medications excreted by the kidneys (e.g., antibiotics, analgesics).

4. Nutrition Management:

• Collaborate with dietitians to implement a low-protein, low-potassium, low-sodium diet.
• Monitor for signs of malnutrition or fluid imbalances.

5. Patient Education:

• Teach patients about AKI prevention, including staying hydrated and avoiding nephrotoxic medications.
• Educate on signs of worsening kidney function, such as reduced urine output or swelling.

Complications of AKI

• Electrolyte Imbalances: Hyperkalemia, hyponatremia, hyperphosphatemia.
• Volume Overload: Pulmonary edema, hypertension.
• Uremia: Encephalopathy, pericarditis, or bleeding.
• Chronic Kidney Disease (CKD): Persistent damage can lead to CKD or end-stage renal disease (ESRD).
• Infections: Increased risk of sepsis in critically ill patients.

Prevention of AKI

1. Hydration:

• Ensure adequate hydration during illnesses or procedures.

2. Avoid Nephrotoxins:

• Use alternatives to nephrotoxic drugs or adjust doses for at-risk patients.

3. Prompt Management of Infections:

• Early treatment of sepsis or urinary tract infections.

4. Monitoring:

• Regular renal function testing in high-risk patients.

Conclusion

Acute kidney injury is a potentially reversible condition if identified and managed promptly. Nurses play a pivotal role in monitoring, supporting interventions, and educating patients to prevent recurrence. Through evidence-based practices and collaborative care, nurses can significantly improve outcomes for patients with AKI.