What are the 5 Principles of AKI Management?

What are the 5 Principles of AKI Management?

Medically Reviewed by Dr. Andrew Stein MD, Consultant Nephrologist (Hospital Kidney Specialist). Last updated: June 2026

Acute Kidney Injury (AKI) is a very common clinical condition (affecting 20% of hospital admissions) associated with significant morbidity and mortality if not recognised and managed promptly.

Early identification of the underlying cause, appropriate supportive care, and timely specialist involvement are essential to prevent further kidney damage and improve patient outcomes.

Here are MyHSN’s 5 principles of AKI management.

1. Initial Assessment and Monitoring

Effective AKI management begins with identifying the cause and severity while monitoring for complications.

• Determine the underlying cause and stage of AKI (there are 3 stages).
• Use staging to guide monitoring frequency and risk assessment.
• Regularly monitor electrolytes and acid-base status.
• Adjust investigation frequency according to AKI stage and patient risk factors.

Note 1. Remember 90% of AKI cases are pre-renal, most due to dehydration and sepsis.

Note 2. AKI is not a single diagnosis. It is a syndrome (common disease presentation) with many causes.

Note 3. There is no universally accepted validated risk score for AKI for either primary or secondary care.

2. Fluid Managment, Diagnosis and Investigation

Optimising volume status and correcting reversible factors are key to preventing further kidney injury.

• Correct hypovolemia promptly with appropriate intravenous fluids.
• Avoid fluid overload, particularly in patients with oliguria or heart failure.
• Identify and treat reversible causes:
  • Sepsis: Perform urgent septic screening and follow local protocols.
  • Nephrotoxins: Stop and avoid kidney-damaging medications, especially ‘DAMN’ drugs:
    • Diuretics
    • ACE/ARBs
    • Metformin
    • NSAIDs
  • Obstruction: Relieve urinary tract obstruction through urgent specialist referral.

Diagnosis

• AKI can be recognised clinically in some cases by a low urine output (oliguria, <400 ml/24h), or no urine output (anuria, <100 ml/24h; v rare); but AKI can occur without symptoms, and normal urine output
• Polyuria can also occur – i.e. the urinary volume is not a reliable way of diagnosing/excluding AKI
• But in most cases, diagnosis is made by comparison of blood creatinine levels with baseline; this will identify the presence and/or severity of AKI
• This is why a baseline serum creatinine should be measured in all acutely ill patients on admission

Investigation (3 big test groups)

• Bloods
  • U+E
  • ABGs – especially K, pH and lactate
  • Renal immunological screen is required if intrinsic renal disease is suspected, or renal referral is made
• Urine
  • uACR – heavy proteinuria points to a glomerular cause
  • MSU
• Imaging
  • Chest x-ray – ASAP
  • Renal US – within 24h

3. STOP AKI Protocol

The STOP AKI framework provides a practical approach to immediate management.

• S – Sepsis: Initiate local sepsis bundles within one hour when indicated.
• T – Toxins: Stop nephrotoxic (‘DAMN’) drugs (see above) and aminoglycosides.
• O – Optimise volume status/BP: Assess fluid status, administer IV fluids, and review antihypertensives and diuretics.
• P – Prevent harm: Manage complications, adjust drug doses, and avoid excessive fluid administration.

4. Sepsis and Acute Complications

Sepsis and severe AKI complications require rapid recognition and treatment.

“In all patients with AKI, ask yourself ‘is this sepsis’?”

• Consider sepsis in any acutely deteriorating patient with evidence of infection.
• Seek urgent senior clinical review and follow local sepsis guidance.
• Promptly manage its 4 life-threatening complications (and indications for dialysis, see below):
  • Severe hyperkalaemia
  • Metabolic acidosis
  • Pulmonary oedema
  • Uraemia

5. Specialist Referral and Indications for Dialysis

Specialist involvement is required when AKI is severe, complicated, or diagnostically uncertain.

• Consider dialysis (Renal Replacement Therapy, RRT) if these complications persist despite medical management:
  • Severe hyperkalaemia (K . 6.5 mmol/L)
  • Metabolic acidosis (pH < 7.2)
  • Pulmonary oedema
  • Uraemia
    • If the urea is over 50 mmol/L, you need a good reason not to dialyse
• Speclialist referral
  • Refer urgently to nephrology or critical care for:
    • RRT requirement
    • Uncontrolled complications
    • Haemodynamic instability or multi-organ failure
  • Discuss with nephrology within 24 hours if:
    • Diagnosis is unclear
    • Intrinsic renal disease is suspected (especially if vasculitis/glomerulonephritis (GN) possible)
    • Stage 3 AKI is present
    • Pre-existing Stage 4/5 CKD exists (especially if known to renal team)
    • The patient is a kidney transplant recipient
  • Refer urgently to urology/radiology for upper urinary tract obstruction, especially with pyonephrosis, bilateral obstruction, or a solitary obstructed kidney.
• Arrange nephrology follow-up after recovery if eGFR remains ≤30 mL/min/1.73 m² or persistent hypertension or proteinuria is present.

Note. Overall mortality is high, 20% overall in a ward setting; 50% if patient is dialysed; 70% if dialysed on ICU.

Other resources

What is AKI?

AKI: 5Rs Approach