Acute Kidney Injury

Acute Kidney Injury (AKI) is a clinical syndrome involving a sudden decrease in kidney function, typically occurring over hours or days. It is identified by an Absolute increase in serum creatinine of ≥26.5 µmol/L within 48 hours, a ≥1.5-fold increase from baseline within 7 days, or urine output <0.5 mL/kg/h for 6 consecutive hours. AKI represents a common and serious complication in hospitalised patients, affecting up to 15% of admissions. Most cases are pre-renal, due to Hypovolaemia or hypotension reducing renal perfusion. However, intrinsic causes such as Acute Tubular Necrosis (ATN) and Acute Interstitial Nephritis (AIN), or post-renal causes such as obstructive uropathy, must be excluded. Management focuses on identifying the cause, optimizing fluid status, and avoiding nephrotoxic drugs. Monitoring for life-threatening complications—specifically hyperkalaemia, pulmonary oedema, and metabolic acidosis—is paramount. The KDIGO staging system (Stages 1-3) provides a standardised assessment of severity. Stage 1 is a 1.5-1.9x increase in creatinine; Stage 2 is 2.0-2.9x; Stage 3 is a 3.0x increase or creatinine ≥354 µmol/L or initiation of Renal Replacement Therapy (RRT).

The pathophysiology of AKI depends on the anatomical site of injury. Pre-renal AKI involves reduced renal blood flow without structural damage to the parenchyma. This triggers the Renin-Angiotensin-Aldosterone System (RAAS) to maintain Glomerular Filtration Rate (GFR); failure of these compensatory mechanisms leads to ischaemia. Intrinsic AKI involves damage to the kidney itself. Acute Tubular Necrosis (ATN) is the most frequent intrinsic cause, resulting from prolonged ischaemia or nephrotoxins (e.g., aminoglycosides, radiocontrast). This leads to epithelial cell death and sloughing into the tubular lumen, forming 'muddy brown' granular casts. Acute Interstitial Nephritis (AIN) is often an inflammatory/allergic reaction to drugs (e.g., penicillins, PPIs), characterized by interstitial eosinophilic infiltration. Glomerulonephritis represents an immunological attack on the basement membrane. Post-renal AKI occurs when urinary flow is obstructed (e.g., prostatic hypertrophy, stones, tumours), leading to retrograde pressure that reduces GFR and eventual hydronephrosis and parenchymal atrophy if unresolved.

AKI often presents non-specifically, frequently occurring alongside sepsis or acute illness. Patients may report oliguria (reduced urine output) or anuria (no urine output), though many remain non-oliguric. Symptoms of the underlying cause include thirst, dizziness (pre-renal), or loin pain and lower urinary tract symptoms (post-renal). Clinical signs focus on fluid status: dry mucous membranes and reduced skin turgor suggest hypovolaemia, while raised JVP and peripheral oedema suggest fluid overload (often a complication of AKI). Complications are critical to recognize: Hyperkalaemia can cause cardiac arrhythmias; Uraemia can lead to encephalopathy, pericarditis, or platelet dysfunction; Metabolic Acidosis occurs due to failure of acid excretion; and Pulmonary Oedema results from fluid overload. Uraemic frost and asterixis (flapping tremor) are late signs of severe renal failure. Clinicians must monitor for 'red flags' such as a rapid rise in creatinine despite fluid resuscitation or signs of systemic vasculitis (e.g., purpuric rashes, haemoptysis).

Bedside: Fluid balance chart and daily weights; Urinalysis (leucocytes/nitrites for UTI, blood/protein for GN). Bloods: U&Es (Creatinine rise, Urea rise), FBC (anaemia/leucocytosis), CRP, Bone profile (phosphate rise, calcium fall), Bicarbonate (acidosis). Imaging: Renal Ultrasound (first-line for suspected obstruction or unknown cause) to check for hydronephrosis and kidney size. Special tests: Vasculitic screen (ANA, ANCA, anti-GBM) if intrinsic disease suspected; Myoglobin/CK if rhabdomyolysis suspected.

Management follows the 'ABC' and 'STOP' approach. Conservative: Daily weights, fluid restriction if overloaded, or fluid resuscitation if hypovolaemic (0.9% Saline or Hartmann's). Medical: Treat underlying causes (sepsis). STOP nephrotoxics: NSAIDs, ACE inhibitors, ARBs, Diuretics, Metformin, Aminoglycosides. Treatment of complications: Hyperkalaemia management (Calcium gluconate, Insulin/Dextrose), Pulmonary oedema (Oxygen, Loop diuretics). Post-renal: Catheterization or nephrostomy if obstructed. Surgical: Urgent urological intervention for stones or tumours causing obstruction. Indications for RRT (AEIOU): Acidosis (pH <7.2), Electrolytes (K+ >6.5), Intoxicants (ethylene glycol), Overload (refractory), Uraemia (pericarditis/encephalopathy).