Acute kidney injury

Overview

Causes of AKI by category

Feature	Pre-renal	Intrinsic	Post-renal
Mechanism	Reduced renal perfusion	Direct kidney damage (ATN, AIN, HUS, glomerulonephritis)	Obstruction (e.g. posterior urethral valves)
FENa	<1%	>2%	Variable
Urine osmolality	>500 mOsm/kg	Low	Variable

•Acute interstitial nephritis (AIN): drug exposure (most commonly penicillins) → T-lymphocyte infiltration of renal interstitium → cytokine release → interstitial oedema and tubular dysfunction → impaired potassium secretion → hyperkalaemia

•HUS in children: Shiga toxin-producing E. coli O157:H7 → microangiopathic haemolytic anaemia + thrombocytopenia + AKI

⚠️

NSAIDs and ACE inhibitors are particularly dangerous in hypovolaemia - they remove compensatory afferent/efferent arteriolar mechanisms that maintain GFR.

Presentation

•Oliguria/anuria - urine output <0.5 mL/kg/hour; abrupt anuria suggests obstruction or severe glomerulonephritis

•Oedema and hypertension - fluid overload; particularly in intrinsic causes

•Rash, fever, arthralgia - triad suggesting AIN or systemic vasculitis

•Pallor with bloody diarrhoea in a young child - classic HUS presentation

•Haematuria - suggests glomerulonephritis, HUS, or renal vein thrombosis

Investigations

🥇 First-line

•Serum U&Es - confirm AKI, stage severity, detect hyperkalaemia and acidosis

•Urine dipstick - blood/protein → glomerulonephritis; leucocytes → infection or AIN; sterile pyuria + eosinophiluria → AIN

•FBC and blood film - eosinophilia → AIN; anaemia + thrombocytopenia + schistocytes → HUS

•VBG - assess metabolic acidosis

•Renal ultrasound - mandatory if obstruction suspected; identifies hydronephrosis

🥈 Second-line

•FENa - <1% pre-renal; >2% ATN/intrinsic

•Immunological screen (ANCA, anti-GBM, complement C3/C4, ANA) - if glomerulonephritis or vasculitis suspected

🏆 Gold standard

•Renal biopsy - unexplained AKI with normal imaging, suspected glomerulonephritis/vasculitis

Management

🥇 First-line

•Identify and treat underlying cause - treat sepsis, relieve obstruction, withhold nephrotoxic drugs (NSAIDs, ACE inhibitors, ARBs, aminoglycosides)

•Fluid resuscitation in hypovolaemia - IV isotonic crystalloid 10 mL/kg bolus; reassess frequently

•Treat hyperkalaemia urgently - calcium gluconate (cardioprotection), insulin/dextrose (drive K⁺ into cells), salbutamol nebulised

🥈 Second-line

•Furosemide - ONLY for fluid overload; do NOT use routinely to treat AKI or increase urine output

🥉 Third-line

•Renal replacement therapy (RRT) - haemodialysis or CVVHF in PICU for refractory hyperkalaemia, severe acidosis, pulmonary oedema unresponsive to diuretics, or Stage 3 AKI with oligoanuria

⚠️

Low-dose dopamine to increase renal perfusion - NICE explicitly advises AGAINST this. It does not improve renal outcomes and risks arrhythmia.

Complications

•Hyperkalaemia - most common and most urgent electrolyte complication; risk of life-threatening arrhythmia

•Metabolic acidosis - worsens hyperkalaemia by driving K⁺ out of cells

•Pulmonary oedema - fluid overload; may cause respiratory failure

•Uraemia - encephalopathy, pericarditis, coagulopathy; indicates need for RRT

•CKD - particularly after severe or recurrent AKI

Acute Interstitial Nephritis - Exam-Favourite Pattern

•Presents 7-10 days after starting the culprit drug

•Classic triad: fever, rash, arthralgia

•Eosinophilia on FBC

•Sterile pyuria (raised urinary white cells) on dipstick

•Rising creatinine without obvious pre-renal or post-renal cause

•Most common culprit drugs: penicillins (especially amoxicillin), NSAIDs, PPIs, sulfonamides

🎯

AIN is the most tested AKI pattern: triad of fever/rash/arthralgia + eosinophilia + sterile pyuria + recent penicillin/NSAID/PPI = AIN until proven otherwise.

Indications for Immediate Nephrology Referral

•K⁺ ≥6.5 mmol/L

•Oliguria with serum sodium ≤125 mmol/L

•Pulmonary oedema or hypertension unresponsive to diuretics

•Plasma urea >40 mmol/L unresponsive to fluid challenge