Acute Kidney Injury (AKI)

Overview & Definition

Acute Kidney Injury (AKI) is a rapid decrease in renal function leading to a failure of the kidneys to excrete nitrogenous waste products and maintain fluid–electrolyte balance. According to KDIGO criteria, AKI is defined by any of the following:

• Rise in serum creatinine by ≥26.5 µmol/L within 48 hours, or

• Increase in serum creatinine to ≥1.5 times baseline within the previous 7 days, or

• Urine output <0.5 mL/kg/h for 6 hours.

Common Causes

• Prerenal (↓ Renal Perfusion)

  • Dehydration (e.g. vomiting, diarrhoea, poor oral intake)

  • Haemorrhage

  • Cardiac failure (low cardiac output)

  • Hypoalbuminaemia (e.g. cirrhosis, nephrotic syndrome)

• Intrarenal (Direct Kidney Damage)

  • Sepsis (systemic inflammatory response → acute tubular necrosis)

  • Nephrotoxins:

    • Drugs (e.g. NSAIDs, aminoglycosides, IV contrast, some chemotherapy agents)

    • Rhabdomyolysis (myoglobin)

    • Multiple myeloma (light chains)

• Postrenal (Obstruction)

  • Ureteric stones

  • Malignancy (bladder, prostate, pelvic)

  • Benign prostatic hyperplasia (BPH; bladder outlet obstruction)

Classification of AKI Causes

1. Prerenal AKI (Decreased Renal Perfusion)

• Causes

  • Volume depletion: Vomiting, diarrhoea, dehydration, haemorrhage

  • Cardiac failure (reduced renal blood flow)

  • Hypoalbuminaemia (e.g. cirrhosis, nephrotic syndrome)

• Typical Laboratory Findings

  • High BUN/Cr ratio (often > 20:1)

  • Low fractional excretion of sodium (FENa) <1% (if the patient is not on diuretics)

• Initial Management Plan

  • IV fluids if volume depletion is suspected (e.g. normal saline or balanced crystalloids)

  • Diuretics if signs of volume overload (e.g. in heart failure)

  • Optimise cardiac output if relevant (e.g. treat arrhythmias, consider inotropes if severe)

2. Postrenal AKI (Obstruction)

• Causes

  • Ureteric stones

  • Pelvic or retroperitoneal malignancy

  • BPH (common in older men)

• Investigations

  • Renal ultrasound (US) or CT KUB (kidneys, ureters, bladder) to assess for hydronephrosis, stones, or masses

  • Bladder scan or urethral catheter to check for urinary retention

• Management Plan

  • Relieve obstruction:

    • Catheterisation if bladder outlet obstruction

    • Urological intervention if stones are large or obstructing

    • Specialist referral if malignancy or complex obstruction suspected

3. Intrarenal AKI (Direct Kidney Parenchyma Damage)

• Causes

  • Glomerular: Nephritic syndromes (e.g. IgA nephropathy, lupus nephritis)

  • Interstitial: Drug-induced interstitial nephritis (e.g. beta-lactams, NSAIDs, PPIs), autoimmune conditions

  • Acute Tubular Necrosis (ATN): Hypoperfusion, contrast nephropathy, myoglobin (rhabdomyolysis), toxins

  • Sepsis-related: Prolonged hypotension, inflammatory damage to renal tubules

• Urine Microscopy Clues

  • RBC casts → Glomerulonephritis

  • WBC casts → Pyelonephritis or interstitial nephritis

  • Muddy brown casts → ATN (common in prolonged hypotension or nephrotoxic injury)

• Management Plan

  • Identify and remove offending agent (e.g. nephrotoxic drugs)

  • Manage sepsis aggressively (appropriate antibiotics, fluid resuscitation, haemodynamic support)

  • Correct electrolyte disturbances (hyperkalaemia, acidosis)

Medications That Can Cause or Worsen AKI

SADMANS (Hold in Dehydration/AKI Risk Situations)

1. Sulfonylureas (risk of hypoglycaemia if renal function drops)

2. ACE Inhibitors (ACEi)

3. Diuretics

4. Metformin (risk of lactic acidosis; adjust if eGFR <60 mL/min/1.73m^2, stop if eGFR <30)

5. ARBs (Angiotensin II Receptor Blockers)

6. NSAIDs (except low-dose aspirin)

7. SGLT2 inhibitors

Triple Whammy (Avoid in Dehydration/CKD)

• NSAIDs (except low-dose aspirin)

• Diuretics

• ACEi/ARB

Combining these three increases the risk of AKI significantly due to reduced renal perfusion and altered autoregulation.

Management After AKI Recovery

1. Blood Pressure Control

   • Avoid restarting ACEi/ARB immediately post-AKI; typically wait 2–4 weeks until stable renal function is demonstrated.

   • If hypertension persists, consider alternative antihypertensives such as calcium channel blockers or beta-blockers.

   • Reintroduce ACEi/ARB cautiously if needed for cardiovascular or diabetic indications.

2. Medication Review

   • Reassess all nephrotoxic drugs.

   • Restart SADMANS medications only if renal function has clearly recovered and there are compelling indications (e.g. heart failure, diabetic nephropathy).

3. Renal Function Monitoring

   • Check eGFR & electrolytes:

     • 1–2 weeks post-discharge or post-AKI episode.

     • Monthly if ongoing chronic kidney disease (CKD) risk.

   • Monitor for proteinuria or haematuria (urinalysis, ACR) as signs of progressive CKD.

4. Assess for CKD Progression

   • If eGFR decline or persistent albuminuria (>3 months), consider referral to nephrology.

   • Patients with diabetes, hypertension, or recurrent AKI are at higher risk of CKD progression.

5. Lifestyle Advice

   • Ensure adequate hydration (unless fluid-restriction indicated for heart failure).

   • Reduce sodium intake if hypertensive or fluid-overloaded.

   • Consider protein intake moderation in established CKD, though individualised advice is needed.

   • Maintain a healthy weight and manage comorbidities (diabetes, hypertension, dyslipidaemia).

6. Follow-Up Imaging (If Required)

   • Renal ultrasound to assess for structural abnormalities if persistent deranged renal function or recurrent UTIs.

   • Repeat imaging in cases of high suspicion of obstruction or complex renal pathology.

Notes

• Many AKI cases are reversible with prompt identification and management of the underlying cause (e.g. volume replacement, stopping nephrotoxic agents).

• Monitor for progression to chronic kidney disease (CKD), especially after multiple AKI episodes.

• Avoid or minimise IV contrast in high-risk patients (eGFR <30 mL/min/1.73m^2, diabetic nephropathy) or consider prophylactic IV fluids if contrast is essential.

• Early nephrology referral is indicated if there is persistent eGFR decline, resistant electrolyte issues (e.g. hyperkalaemia), or diagnostic uncertainty.