Nursing Guide to Acute Kidney Injury: Nursing Diagnosis, Interventions, & Care Plans

Why AKI Replaced ARF as the Diagnostic Term

AKI was introduced to replace ARF because it reflects a continuum of kidney damage, ranging from mild, temporary injury to severe, potentially permanent kidney failure. In contrast, ARF implies a binary state of "failure," which doesn't capture the spectrum of kidney injuries or the potential for reversibility with timely intervention.

Acute Kidney Injury etiology and epidemiology 

Acute kidney injury (AKI), previously known as acute renal failure (ARF), is characterized by the sudden loss of the kidneys' ability to filter waste products effectively, leading to toxin accumulation and fluid and electrolyte imbalances. It can develop rapidly, within hours or days, and poses significant morbidity and increased mortality risk. AKI affects approximately 7.5% of all hospitalized patients, with a prevalence of 20% to 40% among intensive care unit (ICU) admissions in Europe and the United States. 

Risk factors for AKI

Certain factors increase the risk of developing AKI: 

• Advanced age, due to decreased renal reserve and comorbidities.
• Chronic illnesses, such as diabetes, hypertension, and heart failure.
• Sepsis, leading to hypotension and decreased renal perfusion.
• Recent surgery, especially cardiac or major abdominal surgery, which may cause hemodynamic instability.
• Nephrotoxic drugs, including NSAIDs, aminoglycosides, radiocontrast agents, and chemotherapeutics.
• Volume depletion from causes like diarrhea, vomiting, diuretics, or blood loss.
• Prolonged hypotension or MAP <65 mm Hg, leading to prerenal AKI. 

Diagnosis criteria for AKI (KDIGO Guidelines) 

According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, acute kidney injury (AKI) is diagnosed based on any of the following criteria: 

1. Increase in serum creatinine by ≥0.3 mg/dL within 48 hours
2. Increase in serum creatinine to ≥1.5 times the baseline, known or presumed to have occurred within the prior seven days
3. Urine volume <0.5 mL/kg/hour for six hours 

Note: These diagnostic criteria should only be applied after optimizing the patient's volume status to ensure that volume depletion is not falsely influencing results. Urinary tract obstruction needs to be excluded if urine volume is used as the sole criterion. 

Causes of AKI

AKI is classified into three major categories: prerenal, intrarenal (intrinsic), and postrenal. 

1. Prerenal causes 

   a. Prerenal AKI is the most common form, caused by decreased renal perfusion without intrinsic kidney damage. 

   b. Causes include: 

   Hypotension (e.g., sepsis, dehydration, hemorrhage). 

   Hypovolemia from excessive diuresis, GI losses, or burns. 

   Reduced cardiac output from heart failure or myocardial infarction. 

   c. Early detection and fluid resuscitation can reverse prerenal AKI. 

    

2. Intrarenal (intrinsic) causes 

   a. Direct damage to kidney tissues results from: 

   Nephrotoxins (e.g., NSAIDs, aminoglycosides, radiocontrast). 

   Acute tubular necrosis (ATN), often a progression from prolonged prerenal AKI. 

   Glomerular disorders like glomerulonephritis or interstitial nephritis. 

    

3. Postrenal causes 

   a. Obstructions in the urinary tract prevent normal urine flow, increasing intratubular pressure. 

   b. Causes include benign prostatic hypertrophy (BPH), stones, strictures, and improperly placed catheters. 

   c. Early identification and resolution of obstruction are essential to prevent permanent damage. 

Clinical workup to diagnose AKI

A thorough clinical workup is crucial to identify the cause and severity of AKI: 

Laboratory tests 

• Serum creatinine: Rising levels indicate worsening renal function.
• Blood urea nitrogen (BUN): Elevated BUN/creatinine ratio (>20:1) suggests prerenal AKI.
• Serum electrolytes: Monitor potassium, sodium, and bicarbonate levels.
• Urine analysis: Assess for sediment, protein, and specific gravity to distinguish between prerenal, intrarenal, and postrenal causes.
• Urine sodium & osmolality: Low urine sodium (<20 mEq/L) suggests prerenal AKI, while high urine sodium (>40 mEq/L) indicates intrarenal damage. 

Imaging studies 

• Renal ultrasound: Identifies structural abnormalities or obstructions.
• Doppler ultrasound: Assesses renal blood flow.
• CT Abdomen/Pelvis: Useful for detecting stones, masses, or obstructions.

Additional tests 

• ABG analysis: Detects metabolic acidosis.
• Renal biopsy: Reserved for unclear diagnoses, like glomerulonephritis or interstitial nephritis. 

Technology in AKI monitoring 

• Advanced AKI monitoring devices can detect early changes in urine output, creatinine, and other biomarkers, enabling timely intervention.
• Devices like this provide real-time data on urine output, intra-abdominal pressure, and fluid balance, helping to prevent prerenal AKI and guide volume resuscitation.
• These tools are particularly useful in critically ill patients, where AKI can develop insidiously and alter management strategies. 

Common nursing interventions to protect kidney function 

• IV hydration: Ensure adequate hydration, especially before procedures involving IV contrast, to maintain renal perfusion and prevent prerenal AKI.
• Medication adjustments: Hold nephrotoxic drugs like NSAIDs and metformin in patients with rising creatinine.
• Maintaining MAP >65 mm Hg: Implement vasopressor support if needed to sustain renal perfusion.
• Electrolyte monitoring and management: Regularly check for hyperkalemia, hyperphosphatemia, and other imbalances; implement dietary restrictions and medication adjustments.
• Diuretic use: Administer diuretics like furosemide for fluid overload, but cautiously in patients with prerenal AKI to prevent worsening hypovolemia.
• Patient education: Use clear, narrative explanations about the importance of dietary and fluid restrictions, medication adherence, and recognizing early signs of worsening kidney function. 

Dietary considerations for AKI

Dietary modifications

• High caloric intake: Recommended to prevent catabolism.
• Low protein diet: To reduce urea production and prevent further stress on the kidneys.
• Low potassium diet: To prevent hyperkalemia; avoid foods like bananas, oranges, and potatoes.
• Low sodium diet: To prevent fluid overload and hypertension; limit processed foods, canned soups, and fast food. 

Fluids 

Restrict to the volume of urine output plus 500 mL/day to prevent fluid overload. 

Monitoring 

Collaborate with a dietitian to tailor dietary recommendations based on lab values and clinical status. 

AKI nursing care plan 

A comprehensive nursing assessment is vital to detect early signs and manage AKI effectively: 

• Vital signs: Monitor for hypotension, tachycardia, fever, and respiratory rate changes.
• Fluid status: Assess for volume depletion (e.g., dry mucous membranes, decreased skin turgor) or fluid overload (e.g., edema, pulmonary crackles).
• Urine output: Track volume, color, and sediment.
• Neurological status: Monitor for confusion, lethargy, or altered mental status, which may indicate uremia.
• Cardiovascular assessment: Check for arrhythmias, jugular venous distention (JVD), and peripheral pulses.
• Skin integrity: Inspect for edema, skin breakdown, or pressure injuries. 

North American Nursing Diagnosis Association's (NANDA) nursing diagnoses for AKI

1. Ineffective renal tissue perfusion: elated to decreased renal blood flow secondary to hypovolemia, hypotension, or cardiac dysfunction, as evidenced by decreased urine output, increased serum creatinine, and elevated BUN.
2. Risk for electrolyte imbalance: related to impaired renal function, as evidenced by hyperkalemia, hyponatremia, or metabolic acidosis.
3. Excess fluid volume: related to decreased urine output and impaired kidney function, as evidenced by edema, weight gain, and crackles in lung fields.
4. Altered thought processes: related to increased uremic toxins, as evidenced by confusion, lethargy, or altered mental status.
5. Impaired skin integrity: related to edema and immobility, as evidenced by redness, pressure injuries, or breakdown in bony areas.
6. Risk for infection: related to invasive procedures (e.g., dialysis catheter placement), as evidenced by elevated WBC count, fever, or signs of localized infection.
7. Deficient knowledge: related to lack of information about AKI management, as evidenced by patient’s questions or misconceptions about the disease process and treatment. 

Indications for renal replacement therapy (dialysis or CRRT) 

Initiate renal replacement therapy (RRT) in the following situations: 

• Refractory hyperkalemia is unresponsive to medical management.
• Severe metabolic acidosis (pH < 7.1) is unresponsive to medical therapy.
• Refractory fluid overload is causing pulmonary edema or hemodynamic instability.
• Uremic complications, such as pericarditis, encephalopathy, or significant bleeding.
• CRRT is preferred in critically ill or hemodynamically unstable patients for gradual fluid and toxin removal, minimizing the risk of hypotension. 

Patient education for AKI 

• Condition explanation: Explain AKI, its causes, and potential outcomes in simple terms.
• Fluid and dietary management: Educate about restrictions and the rationale behind a low-protein, low-potassium, and low-sodium diet.
• Signs of worsening AKI: Teach patients to recognize symptoms like decreased urine output, weight gain, or mental confusion.
• Medication adherence: Emphasize the importance of taking prescribed medications and avoiding over-the-counter NSAIDs. 

Expected outcomes 

• Improved renal function with decreasing creatinine and adequate urine output.
• Stable fluid balance, avoiding hypovolemia or fluid overload.
• Normalization of electrolytes with maintained potassium, sodium, and bicarbonate levels.
• Patient and family understanding of AKI, its management, and the importance of follow-up care. 

Additional Information

Content Release Date 

11/6/2024

Content Expiration

12/31/2027