Acute Kidney Injury (AKI)

Definition and Staging

•    Definition: Rapid deterioration in renal function, reflected by:

o    ↑ Serum creatinine (≥26 µmol/L within 48 hours or ≥1.5× baseline within 7 days)

o    Oliguria: urine output <0.5 mL/kg/hr for >6 hours

•    KDIGO Staging (Stages 1–3):

o    Stage 1: Cr rise ≥1.5–1.9× baseline or ≥26 µmol/L; urine output <0.5 mL/kg/hr for 6–12 h

o    Stage 2: Cr rise 2.0–2.9× baseline; urine output <0.5 mL/kg/hr for ≥12 h

o    Stage 3: Cr rise ≥3× baseline or ≥354 µmol/L or initiation of renal replacement therapy; 

                                                            urine output <0.3 mL/kg/hr for ≥24 h or anuria ≥12 h

Causes of AKI

•    Prerenal (most common):

o    Due to impaired renal perfusion

o    Causes: hypovolaemia, hypotension, heart failure, renal artery stenosis

o    Often reversible with fluid resuscitation

o    Urea:Creatinine ratio ↑, concentrated urine

•    Intrinsic (renal):

o    Structural damage to kidney parenchyma

o    Types:

    Acute Tubular Necrosis (ATN)

    Acute Interstitial Nephritis (AIN)

    Glomerulonephritis (GN)

    Vasculitis (e.g. ANCA-associated)

    Thrombotic microangiopathy (e.g. HUS, TTP)

•    Postrenal (obstructive):

o    Obstruction of urinary outflow

o    Causes: BPH, ureteric stones, tumours, retroperitoneal fibrosis

o    Requires imaging (bladder scan, renal US)

o    Bilateral obstruction → postrenal AKI

Specific Intrinsic Causes

•    Acute Tubular Necrosis (ATN)

o    Commonest intrinsic AKI

o    Causes: ischaemia (e.g. shock), toxins (aminoglycosides, contrast)

o    Muddy brown granular casts on urine microscopy

o    Usually self-limiting but may require dialysis

•    Acute Interstitial Nephritis (AIN)

o    Allergic hypersensitivity reaction

o    Causes: drugs (e.g. penicillins, NSAIDs, PPIs), infections

o    Features: fever, rash, arthralgia, eosinophiluria

•    Rhabdomyolysis

o    Myoglobin-induced tubular toxicity

o    Causes: crush injury, seizures, statins

o    ↑ CK, myoglobinuria (dark urine), hyperkalaemia, hypocalcaemia

o    Rx: aggressive IV fluids, correct electrolytes

•    Contrast-Induced Nephropathy

o    AKI within 48–72 hours of contrast exposure

o    Risk factors: CKD, diabetes, dehydration

o    Prevent with IV hydration ± N-acetylcysteine (controversial)

•    Tumour Lysis Syndrome

o    Rapid cell breakdown (e.g. lymphoma, leukaemia) → ↑ urate, phosphate, K⁺

o    Risk: high-grade malignancy, chemotherapy

o    Prophylaxis: IV fluids, allopurinol or rasburicase

Management of AKI

•    Initial Steps

o    Identify and treat underlying cause

o    Assess volume status (JVP, BP, urine output)

o    Stop nephrotoxins (NSAIDs, ACEi, aminoglycosides)

•    Supportive Measures

o    IV fluids for hypovolaemia

o    Monitor fluid balance, daily weights, U&Es

o    Avoid nephrotoxic agents

o    Adjust drug doses for renal function

•    Indications for Dialysis (AEIOU):

o    Acidosis (refractory)

o    Electrolyte imbalance (esp. hyperkalaemia)

o    Intoxication (certain toxins: lithium, ethylene glycol)

o    Overload (fluid, pulmonary oedema)

o    Uraemia (encephalopathy, pericarditis)