Acute Kidney Injury (AKI), previously known as acute kidney disease in some clinical contexts, is characterized by a sudden decline in kidney function resulting in reduced glomerular filtration rate (GFR), accumulation of nitrogenous waste products, and disturbances in fluid, electrolyte, and acid–base balance.

AKI is commonly recognized clinically by reduced urine output of less than 0.5 mL/kg/hour for more than 6 hours or a significant rise in serum creatinine. It may be reversible if identified and treated early; however, delayed recognition can result in chronic kidney disease, multi-organ failure, prolonged hospitalization, and increased mortality.

The causes of AKI are classified into:

• Pre-renal AKI: Reduced renal blood flow without initial structural kidney damage.

• Intrinsic renal AKI: Direct injury to kidney tissue.

• Post-renal AKI: Obstruction of urine flow causing increased pressure within the urinary tract.

Early identification of the cause, correction of reversible factors, avoidance of further kidney injury, and timely referral are essential for improving outcomes.

Epidemiology

AKI is a common clinical problem affecting hospitalized patients, critically ill patients, and individuals with severe infections or underlying chronic diseases. The incidence is higher among patients admitted to intensive care units, those undergoing major surgery, and patients exposed to nephrotoxic medications.

In low- and middle-income countries, AKI remains a significant contributor to morbidity and mortality due to delayed presentation, limited access to diagnostic facilities, infectious diseases, dehydration, and inadequate availability of renal replacement therapy.

Patients who develop AKI are at increased risk of recurrent kidney injury and progression to chronic kidney disease.

Risk Factors

Common risk factors include:

• Dehydration and reduced circulating blood volume.

• Severe diarrhoea or vomiting.

• Acute blood loss.

• Burns.

• Sepsis.

• Heart failure.

• Liver failure.

• Chronic kidney disease.

• Diabetes mellitus.

• Hypertension.

• Exposure to nephrotoxic medications.

• Use of contrast media.

• Rhabdomyolysis.

• Tumour lysis syndrome.

• Urinary tract obstruction.

• Advanced age.

• Major surgery.

• Severe trauma.

Pathophysiology

AKI develops when the kidneys are unable to maintain normal filtration and homeostasis.

Pre-renal AKI

Reduced renal perfusion decreases glomerular filtration without direct damage to kidney tissue. Common causes include dehydration, blood loss, hypotension, heart failure, and liver failure.

If untreated, prolonged reduced blood flow may progress to intrinsic kidney injury, particularly acute tubular necrosis.

Intrinsic renal AKI

Direct damage to kidney structures causes impaired filtration. Causes include:

• Acute tubular injury from ischaemia or toxins.

• Glomerulonephritis.

• Interstitial nephritis.

• Rhabdomyolysis-associated kidney injury.

Post-renal AKI

Obstruction of urine flow increases pressure within the urinary tract, reducing filtration and damaging kidney tissue. Causes include:

• Benign prostatic hyperplasia.

• Urinary stones.

• Bladder stones.

• Obstructed urinary catheters.

Clinical Presentation

Clinical features depend on the severity, cause, and duration of kidney injury.

Patients may present with:

• Reduced urine output (oliguria).

• Complete absence of urine production (anuria).

• Swelling of the legs, face, or generalized oedema.

• Fatigue.

• Nausea and vomiting.

• Loss of appetite.

• Shortness of breath due to fluid overload.

• Confusion.

• Reduced level of consciousness.

Children may present with:

• Convulsions.

• Irritability.

• Reduced feeding.

• Reduced urine output.

Clinical signs may include:

• Hypertension.

• Signs of dehydration.

• Peripheral oedema.

• Raised jugular venous pressure.

• Pulmonary crackles due to fluid overload.

• Features of uraemia.

Diagnostic Criteria

AKI is diagnosed based on changes in kidney function and urine output.

Diagnostic criteria include:

• Increase in serum creatinine by ≥26 micromol/L within 48 hours, or

• Increase in serum creatinine by ≥50% within 7 days, or

• Urine output <0.5 mL/kg/hour for more than 6 hours.

Advanced AKI may be defined by:

• Urine output <0.5 mL/kg/hour for more than 12 hours.

Differential Diagnosis

Conditions that may mimic or contribute to acute kidney injury include:

1. Chronic Kidney Disease with acute deterioration

   • Progressive kidney disease presenting with worsening renal function.

2. Acute glomerulonephritis

   • May present with haematuria, proteinuria, hypertension, and reduced kidney function.

3. Nephrotic syndrome

   • May cause oedema and abnormalities in kidney function.

4. Acute urinary tract obstruction

   • Due to stones, enlarged prostate, bladder pathology, or catheter obstruction.

5. Heart failure with cardiorenal syndrome

   • Reduced kidney perfusion due to impaired cardiac function.

6. Sepsis-associated kidney injury

   • Systemic infection causing renal hypoperfusion and inflammation.

7. Acute interstitial nephritis

   • Often related to medications and presents with kidney dysfunction.

8. Rhabdomyolysis

   • Muscle injury causing release of myoglobin and acute kidney injury.

9. Hepatorenal syndrome

   • Kidney dysfunction associated with severe liver disease.

Investigations

Investigations aim to confirm AKI, determine severity, identify the cause, and detect complications.

Early investigations

• Serum creatinine.

• Blood urea nitrogen (BUN).

• Urinalysis:

  • Dipstick testing.

  • Microscopy.

• Kidney–ureter–bladder (KUB) ultrasound.

Advanced investigations

• Serum electrolytes:

  • Potassium.

  • Sodium.

  • Chloride.

  • Bicarbonate.

  • Calcium.

  • Phosphate.

• Arterial blood gas analysis.

• Serum uric acid.

• Urine electrolytes.

• Fractional excretion of sodium.

• Chest X-ray.

• Electrocardiogram (ECG).

• Kidney biopsy when the cause is unclear clinically.

• Creatine kinase when rhabdomyolysis is suspected.

Management

Management aims to:

• Treat the underlying cause.

• Restore kidney perfusion where appropriate.

• Prevent further kidney damage.

• Correct electrolyte and acid–base disturbances.

• Manage complications.

• Determine the need for renal replacement therapy.

Non-pharmacological Treatment

General measures include:

• Maintain adequate oxygenation.

• Nurse patients with respiratory distress in semi-Fowler's position.

• Restrict salt and potassium-containing foods and fluids.

• Restrict fluid intake to approximately 10 mL/kg/day plus measurable fluid losses.

• Stop nephrotoxic medications.

• Provide adequate nutritional support with sufficient energy and appropriate protein intake.

• Consider enteral or parenteral nutrition when required.

• Monitor:

  • Urine output.

  • Body weight.

  • Fluid balance.

  • Electrolytes.

  • Kidney function.

Pharmacological Treatment

Treatment should be directed at the underlying cause.

Dehydration or volume depletion

Administer:

• 0.9% sodium chloride orally or intravenously while monitoring urine output and fluid status.

Avoid excessive fluid administration in patients with fluid overload.

Hypertension

For patients with:

• Diastolic blood pressure >100 mmHg, or

• Systolic blood pressure >150 mmHg

Consider:

• Amlodipine 5 mg orally once daily.

Fluid overload with respiratory distress

Patients with:

• Rapid respiration.

• Orthopnoea.

• Chest crackles.

• Raised jugular venous pressure.

May receive:

• Furosemide 80 mg intravenous bolus.

Higher doses may be considered depending on response.

Metabolic acidosis with respiratory distress

For patients with:

• Laboured breathing.

• Low serum bicarbonate.

Consider:

• Sodium bicarbonate 150 mEq intravenously in 1 litre of 5% dextrose.

Prevention of gastrointestinal bleeding

Consider:

• Pantoprazole 40 mg orally or intravenously once daily.

Hyperkalaemia

Manage according to CKD-associated hyperkalaemia management protocols.

Renal replacement therapy

Haemodialysis or peritoneal dialysis should be initiated when indicated.

Indications include:

• Pulmonary oedema not responding to medical therapy.

• Severe hyperkalaemia.

• Metabolic acidosis not responding to medical treatment.

• Uraemic encephalopathy.

• Uraemic pericarditis.

• Acute poisoning with dialysable substances.

Referral

Refer patients to a nephrologist or higher-level facility when:

• Glomerulonephritis is suspected, especially with haematuria and proteinuria.

• Kidney function continues worsening despite initial treatment.

• Dialysis may be required.

• Severe electrolyte abnormalities occur.

• The cause of AKI is unclear.

• There is persistent oliguria or anuria.

Patients recovering from AKI should undergo regular follow-up to monitor kidney recovery and prevent progression to CKD.

Suggested monitoring when CKD is absent:

• Weekly kidney assessment (creatinine and/or urinalysis) for one month.

• Monthly assessment for the following two months.

• Six-monthly assessment thereafter.

Complications

Potential complications include:

• Hyperkalaemia.

• Metabolic acidosis.

• Pulmonary oedema.

• Uraemic encephalopathy.

• Uraemic pericarditis.

• Fluid overload.

• Cardiac arrhythmias.

• Chronic kidney disease.

• Multi-organ failure.

• Death.

Prognosis

The outcome of AKI depends on the underlying cause, severity of kidney injury, timing of treatment, and presence of comorbid conditions.

Patients with reversible causes such as dehydration or obstruction often recover completely when treated early. However, severe AKI, delayed management, recurrent episodes, and the need for dialysis increase the risk of progression to chronic kidney disease and mortality.

Prevention

Preventive measures include:

• Early recognition and treatment of dehydration.

• Prompt management of infections and sepsis.

• Avoidance of unnecessary nephrotoxic medications.

• Monitoring kidney function in high-risk patients.

• Adequate hydration during situations causing fluid loss.

• Careful use of contrast agents.

• Early treatment of urinary obstruction.

• Regular follow-up after AKI to detect chronic kidney disease.