Acute Kidney Injury (AKI)

Definition | Stages | Aetiology | Pathophysiology | Risk Factors | Signs and Symptoms | Investigations | Management | Patient Advice

Definition

Acute Kidney Injury (AKI) is a sudden reduction in kidney function over hours to days, leading to an inability to excrete waste products, maintain electrolyte balance, and regulate fluid volume. It is a clinical syndrome identified through serum creatinine rise or reduced urine output.

Stages

AKI is classified into three stages based on serum creatinine rise or urine output:

• Stage 1:
  • Serum creatinine rise by ≥ 26 µmol/L within 48 hours, or
  • Serum creatinine rise 1.5–1.9× baseline.
• Stage 2:
  • Serum creatinine rise 2–2.9× baseline.
• Stage 3:
  • Serum creatinine rise ≥ 3× baseline, or
  • Serum creatinine ≥ 354 µmol/L, or
  • Initiation of renal replacement therapy (RRT).

Aetiology

1. Pre-renal Causes:

• Hypovolaemia (e.g., dehydration, blood loss).
• Low cardiac output (e.g., heart failure).
• Systemic vasodilation (e.g., sepsis).

2. Intrinsic Renal Causes:

• Acute tubular necrosis (e.g., ischaemia, nephrotoxins).
• Glomerulonephritis.
• Acute interstitial nephritis.

3. Post-renal Causes:

• Obstruction (e.g., kidney stones, enlarged prostate).

Pathophysiology

AKI results from a combination of factors that lead to impaired glomerular filtration, tubular injury, or obstruction. Pre-renal AKI is due to reduced renal perfusion, while intrinsic AKI involves direct injury to renal parenchyma, and post-renal AKI is caused by obstruction to urine outflow.

Risk Factors

• Pre-existing kidney disease.
• Diabetes mellitus.
• Use of nephrotoxic drugs (e.g., NSAIDs, ACE inhibitors).
• Hypovolaemia or sepsis.
• Older age.

Signs and Symptoms

• Oliguria or anuria (reduced or absent urine output).
• Fluid overload (e.g., peripheral oedema, pulmonary oedema).
• Fatigue, confusion, or lethargy.
• Signs of underlying cause (e.g., fever in infection, haematuria in glomerulonephritis).

Investigations

Key investigations include:

• Serum Creatinine: To monitor kidney function and stage AKI.
• Blood Urea Nitrogen (BUN): Elevated in AKI.
• Urinalysis: To detect proteinuria, haematuria, or signs of infection.
• Ultrasound Kidney: To assess for obstruction or anatomical abnormalities.
• Full Blood Count and CRP: To identify infection or inflammation.
• Electrolytes: To monitor for hyperkalaemia and hyponatraemia.

Management

1. Recognise AKI:

• Identify the stage of AKI based on serum creatinine rise or urine output.

2. Review:

• Review and stop nephrotoxic medications (e.g., ACE inhibitors, NSAIDs).
• Check and correct fluid status; advise on rehydration if appropriate.
• Perform a urine dipstick:
  • If infection is present, avoid nephrotoxic antibiotics like trimethoprim.
  • If blood or protein is present, consider intrinsic renal pathology.
• Exclude palpable bladder (post-renal obstruction).
• Investigate and treat the underlying cause of AKI.

3. Respond:

• Stage 1: Repeat U+Es in 5–7 days.
• Stage 2: Repeat U+Es in 48–72 hours; organise outpatient renal ultrasound scan.
• Stage 3: Immediate referral to renal team for specialist advice and ongoing management.

Note: Refer to urology if obstruction is suspected.

Patient Advice

• Maintain hydration and avoid dehydration.
• Avoid nephrotoxic medications unless advised by the clinician.
• Monitor for signs of worsening, such as reduced urine output, swelling, or confusion, and seek urgent medical advice.
• Attend follow-up appointments to monitor kidney function.