TextbookRenal MedicineAcute Kidney Injury

Acute Kidney Injury

Rapid decline in kidney function over hours to days, defined by KDIGO criteria as a rise in serum creatinine of ≥26.5 µmol/L within 48 hours or ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/hr for 6 hours. Common causes include sepsis, hypovolaemia, nephrotoxins, and obstruction.

Key Facts

AKI affects 13-18% of hospitalised patients and carries an in-hospital mortality of 20-30% in severe cases KDIGO staging: Stage 1 (creatinine 1.5-1.9× baseline), Stage 2 (2.0-2.9×), Stage 3 (≥3.0× or ≥353.6 µmol/L or RRT) Classified as pre-renal (55-60%), intrinsic renal (35-40%), or post-renal/obstructive (5-10%) NICE NG148 recommends risk assessment using NEWS2 score and detection via NHS AKI e-alert system First-line investigation: urinalysis, renal USS within 24 hours if obstruction suspected, and U&Es with serial monitoring Management: IV fluid resuscitation (crystalloid, typically 0.9% NaCl), stop nephrotoxins (NSAIDs, ACEi, ARBs, aminoglycosides), treat underlying cause Indications for urgent dialysis: refractory hyperkalaemia, severe metabolic acidosis (pH <7.1), pulmonary oedema, uraemic pericarditis/encephalopathy 50% of AKI is preventable with early recognition and intervention

Overview

Key Facts

AKI is a common and serious condition with significant morbidity and mortality. Early detection via the NHS AKI e-alert system and prompt management substantially improve outcomes. Prevention is key, particularly in high-risk groups.

Epidemiology

  • Affects 13-18% of hospital admissions in the UK
  • Community-acquired AKI accounts for ~50% of cases
  • In-hospital mortality: 20-30% for severe AKI (stage 3); overall mortality 10-15%
  • ICU incidence: up to 50% of critically ill patients develop AKI
  • Survivors have increased long-term risk of CKD progression

Aetiology

Pre-renal (55-60%):

  • Hypovolaemia: haemorrhage, dehydration, burns, diarrhoea/vomiting
  • Reduced cardiac output: heart failure, cardiogenic shock
  • Systemic vasodilation: sepsis, anaphylaxis, liver failure
  • Renal vasoconstriction: NSAIDs (block afferent arteriolar dilation), ACEi/ARBs (block efferent arteriolar constriction), hepatorenal syndrome

Intrinsic renal (35-40%):

  • Acute tubular necrosis (ATN): ischaemic (prolonged pre-renal) or nephrotoxic (aminoglycosides, contrast, cisplatin)
  • Acute interstitial nephritis: drugs (NSAIDs, PPIs, penicillins), autoimmune
  • Glomerulonephritis: RPGN, anti-GBM, lupus nephritis
  • Vascular: renal artery stenosis/thrombosis, HUS/TTP

Post-renal/Obstructive (5-10%):

  • Prostatic hypertrophy, prostate cancer
  • Renal/ureteric calculi
  • Pelvic malignancy, retroperitoneal fibrosis

Pathophysiology

  • Pre-renal: reduced renal perfusion leads to decreased GFR; reversible if corrected early, but prolonged hypoperfusion causes ATN
  • ATN: ischaemic or toxic injury to tubular epithelial cells; characterised by muddy brown granular casts
  • Post-renal: bilateral obstruction (or unilateral in single kidney) causes back-pressure and reduced GFR

Clinical Presentation

General Presentation

  • Oliguria (<0.5 mL/kg/hr) or anuria
  • Fluid overload: peripheral oedema, pulmonary oedema, raised JVP
  • Nausea, vomiting, anorexia
  • Lethargy, confusion (uraemic encephalopathy)
  • Pruritus and uraemic frost (severe)

Pre-renal Features

  • Thirst, postural hypotension, tachycardia, dry mucous membranes
  • Low urine sodium (<20 mmol/L), high urine osmolality (>500 mOsm/kg)
  • Responds to fluid resuscitation

Intrinsic Renal Features

  • Haematuria, proteinuria (glomerulonephritis)
  • Rash, fever, eosinophilia (interstitial nephritis)
  • Muddy brown casts on urinalysis (ATN)

Post-renal Features

  • Suprapubic fullness, palpable bladder
  • Loin pain, anuria alternating with polyuria
  • History of prostatic symptoms or pelvic malignancy

Red Flags

  • Pulmonary oedema unresponsive to diuretics → urgent dialysis
  • K+ >6.5 mmol/L with ECG changes → emergency treatment
  • Uraemic pericarditis (friction rub) → dialysis indication
  • Rapidly rising creatinine with active sediment → consider RPGN (renal biopsy urgently)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
CKDSmall kidneys on USS, normocytic anaemia, raised PTHRenal USS, previous creatinine trend
AKI on CKDAcute deterioration on chronic baselinePrevious blood results, renal USS
Hepatorenal syndromeCirrhosis, ascites, progressive renal failureHepatic function, urine sodium <10
Urinary obstructionBilateral hydronephrosis, bladder distensionRenal USS, bladder scan
RhabdomyolysisMuscle pain, dark urine, massively raised CKCK, urine myoglobin
GlomerulonephritisActive urine sediment, systemic featuresUrine protein:creatinine, immunology

Diagnosis / Investigation

Bedside

  • Urinalysis: dipstick for blood/protein (active sediment suggests GN); leucocytes/nitrites (infection)
  • Bladder scan: post-void residual (exclude urinary retention)
  • Fluid balance chart: strict input/output monitoring
  • ECG: assess for hyperkalaemia changes
  • Blood gas: rapid potassium, pH, bicarbonate, lactate

Bloods

  • U&Es: creatinine, urea, potassium, sodium – serial monitoring
  • FBC: anaemia (may suggest chronicity), thrombocytopenia (HUS/TTP)
  • CRP: infection/sepsis
  • LFTs: hepatorenal syndrome
  • Calcium, phosphate, bone profile: deranged in established renal failure
  • CK: rhabdomyolysis
  • Blood cultures: if sepsis suspected
  • Immunology (if intrinsic renal cause suspected): ANA, ANCA, anti-GBM, complement (C3/C4), immunoglobulins

Imaging

  • Renal ultrasound: within 24 hours if obstruction suspected; assess kidney size (small = chronic), hydronephrosis
  • CT KUB: renal stones if suspected
  • CT abdomen/pelvis: retroperitoneal pathology, pelvic malignancy

Special Tests

  • Urine sodium and osmolality: pre-renal (<20 mmol/L, >500 mOsm/kg) vs ATN (>40 mmol/L, <350 mOsm/kg)
  • Fractional excretion of sodium (FENa): <1% pre-renal, >2% ATN
  • Urine protein:creatinine ratio (uPCR): quantify proteinuria
  • Renal biopsy: if intrinsic cause unclear, RPGN suspected, or unexplained AKI with active sediment

Management

Non-pharmacological

  • Fluid resuscitation: isotonic crystalloid (0.9% NaCl or Hartmann's) for pre-renal AKI; 250-500mL boluses with reassessment
  • Stop nephrotoxins: NSAIDs, ACE inhibitors, ARBs, aminoglycosides, metformin
  • Relieve obstruction: urinary catheter (urinary retention), nephrostomy or ureteric stent (ureteric obstruction)
  • Strict fluid balance and daily weights
  • Dietary modification: potassium and phosphate restriction if required

Pharmacological

  • Treat underlying cause: antibiotics for sepsis, immunosuppression for GN
  • IV fluids: guided by clinical assessment and fluid balance
  • Loop diuretics (furosemide 40-250mg IV): only for fluid overload, NOT to prevent or treat AKI itself
  • Hyperkalaemia management: insulin-dextrose, calcium gluconate, salbutamol as per protocol
  • Sodium bicarbonate 1.26%: for severe metabolic acidosis (pH <7.2)
  • Avoid contrast media; if essential, use lowest volume with pre-hydration (0.9% NaCl 1mL/kg/hr for 12 hours pre and post)

Renal Replacement Therapy (Indications)

Urgent dialysis indicated for refractory:

  • Hyperkalaemia (K+ >6.5 despite medical management)
  • Acidosis (pH <7.1 despite bicarbonate)
  • Pulmonary oedema (unresponsive to diuretics)
  • Uraemic complications: encephalopathy, pericarditis, neuropathy
  • Toxins: methanol, ethylene glycol, lithium, salicylate

Modes: CVVH/CVVHDF (ICU), intermittent haemodialysis (stable patients)

Referral Criteria

  • AKI stage 3 or requiring RRT → nephrology
  • Suspected GN or vasculitis → urgent nephrology
  • Obstruction requiring intervention → urology
  • ICU admission if haemodynamically unstable or requiring organ support

Prognosis

  • Overall in-hospital mortality: 10-15% for all AKI; 30-50% in ICU
  • Stage 1 AKI: mortality ~5-10%
  • Stage 3 AKI requiring dialysis: mortality 30-50%
  • Recovery: 50-70% of patients with AKI have full renal recovery
  • 20-50% of AKI survivors develop or progress to CKD within 5 years
  • 5-10% of severe AKI patients require long-term dialysis
  • AKI increases risk of future cardiovascular events by 40%
  • Prevention of a single AKI episode saves the NHS approximately £12,000-£25,000

Other Relevant Information

KDIGO AKI Staging

StageSerum CreatinineUrine Output
11.5-1.9× baseline or ≥26.5 µmol/L rise in 48h<0.5 mL/kg/h for 6-12h
22.0-2.9× baseline<0.5 mL/kg/h for ≥12h
3≥3.0× baseline or ≥353.6 µmol/L or RRT initiated<0.3 mL/kg/h for ≥24h or anuria ≥12h

Pre-renal vs ATN

FeaturePre-renalATN
Urine Na+<20 mmol/L>40 mmol/L
FENa<1%>2%
Urine osmolality>500 mOsm/kg<350 mOsm/kg
Urine:plasma urea>10:1<10:1
Urine sedimentBland/hyaline castsMuddy brown casts
Response to fluidsImprovesNo improvement

Indications for Urgent Dialysis (Mnemonic: AEIOU)

  • Acidosis (pH <7.1)
  • Electrolytes (refractory hyperkalaemia)
  • Intoxication (methanol, ethylene glycol, lithium)
  • Overload (pulmonary oedema refractory to diuretics)
  • Uraemia (encephalopathy, pericarditis)