🩺 Acute Kidney Injury

Acute Kidney Injury (AKI) is defined by a rapid decline in renal excretory function, characterized by an increase in serum creatinine or a decrease in urine output. It is common in hospitalised patients and significantly increases morbidity and mortality. Traditionally divided into pre-renal (70%), intrinsic (20%), and post-renal (10%) causes. Most cases in the UK are caused by sepsis or hypovolaemia leading to Acute Tubular Necrosis (ATN). Management involves treating the underlying cause, stopping nephrotoxic drugs, and managing fluid and electrolyte imbalances.

Review the timeline of the illness: recent episodes of vomiting, diarrhoea, or sepsis are common pre-renal triggers. Ask about urinary symptoms: hesitancy, poor stream (prostatic obstruction), or 'cola-coloured' urine (glomerulonephritis). Perform a meticulous medication history looking for nephrotoxins (aminoglycosides, NSAIDs, contrast media). Enquire about risk factors: age >65, pre-existing CKD, heart failure, and diabetes. Screening for symptoms of uraemia (itching, hiccups, pericarditic chest pain) is essential in severe cases.

The priority is fluid status assessment: check JVP, mucous membranes, skin turgor, and capillary refill time to differentiate between hypovolaemia (pre-renal) and fluid overload (as a complication of AKI). Perform a bladder scan or check for a palpable bladder to rule out post-renal obstruction. Look for systemic clues: rashes (interstitial nephritis or vasculitis), signs of heart failure, or abdominal bruits. Monitor the respiratory rate and oxygen saturations as pulmonary oedema is a life-threatening complication.

Pre-renal (Hypovolaemia, Sepsis, Heart failure); Intrinsic (Acute Tubular Necrosis, Acute Interstitial Nephritis, Glomerulonephritis); Post-renal (BPH, Stones, Pelvic malignancy, Neurogenic bladder).

Refractory hyperkalaemia (>6.5 mmol/L); Pulmonary oedema non-responsive to diuretics; Severe metabolic acidosis (pH < 7.2); Uraemic complications (pericarditis, encephalopathy, or neuropathy); Anuria or severe oliguria persisting despite fluid resuscitation.

U&Es are the cornerstone (compare against baseline creatinine). Urinalysis is mandatory: 'bland' sediment suggests pre-renal or post-renal causes, while haematuria and proteinuria suggest intrinsic renal disease (e.g., GN). Renal ultrasound is recommended within 24 hours if the cause is unclear or if obstruction is suspected. Check blood gases for metabolic acidosis and hyperkalaemia. Further tests (ANA, ANCA, CK for rhabdomyolysis) are guided by clinical suspicion.

AKI is a syndrome, not a diagnosis—always search for the 'why'. High-risk medications (Triple Whammy: ACEi/ARB + Diuretic + NSAID) should be paused ('Sick Day Rules'). The staging of AKI (1, 2, or 3) is based on the rise in creatinine from baseline or the reduction in urine output. Note that creatinine is a lagging marker and may take 24 hours to rise after the initial insult.

Extremely high-yield MLA topic across 'Acute Medicine' and 'Renal'. Candidates must know the RIFLE/KDIGO staging and the life-threatening complications (Hyperkalaemia, Pulmonary Oedema, Acidosis, Uraemia).