Renal & Urology

Acute kidney injury

Acute kidney injury is a measurable fall in kidney filtration or urine output caused by reduced perfusion, intrinsic renal disease or obstruction; identify the cause early, protect the kidneys, monitor complications and escalate for refractory life-threatening physiology.

In a nutshell

AKI is a change in creatinine or urine output from baseline. Find the cause in parallel: perfusion/sepsis, medicines and toxins, intrinsic renal disease and obstruction. Protect the kidneys, monitor potassium and fluid status, and escalate urgently for refractory hyperkalaemia, acidosis, uraemic complications, fluid overload or pulmonary oedema.

Classic presentation

An acutely unwell patient has a rising creatinine or oliguria after vomiting, sepsis, hypotension, surgery, nephrotoxic medicines or possible obstruction, with or without hyperkalaemia or fluid overload.

Key points

AKI criteria include a creatinine rise of at least 26 micromol/L within 48 hours, a 50% rise within 7 days or oliguria below 0.5 ml/kg/hour for more than 6 hours in adults.
Check fluid status, sepsis, medication exposure, intrinsic renal features and obstruction at the same time; pre-renal and intrinsic causes can coexist.
Perform urine dipstick for blood, protein, leucocytes, nitrites and glucose as soon as AKI is suspected.
Do not routinely give loop diuretics to treat AKI and never use low-dose dopamine; consider a loop diuretic only for fluid overload or while awaiting RRT.
Stage 3 AKI, unclear cause, inadequate response, complications, transplant or CKD stage 4/5 needs nephrology discussion within 24 hours.
RRT indications are refractory hyperkalaemia, acidosis, uraemic complications, fluid overload or pulmonary oedema; do not use an isolated creatinine or potassium number.
After AKI, monitor recovery and longer-term CKD risk; NICE recommends at least 3 years of CKD monitoring, longer after stage 3, even if eGFR recovers.

First-line investigation

Compare creatinine with baseline, measure urine output, assess fluid status and perform urine dipstick plus complication blood tests.

Management

Stabilise and monitor

Use ABCDE, treat shock/sepsis and complications, monitor urine output and fluid balance, and escalate for refractory hyperkalaemia, acidosis, uraemia or pulmonary oedema.^1,2

Identify the mechanism

Search for hypoperfusion, sepsis, nephrotoxins, intrinsic renal disease and obstruction in parallel; perform urine dipstick and ultrasound when the cause is unclear or obstruction is possible.^1,2,3

Protect renal function

Give fluids only for hypovolaemia, review renal dosing and temporary medicine cessation, avoid routine diuretics and monitor creatinine, electrolytes, urine output and fluid status.^1,3,4,5,6

Refer and consider RRT

Discuss stage 3, unclear or non-responsive AKI and suspected nephritis with nephrology; start urgent RRT discussion for complications not responding to medical management.^1,2

Protect the patient after discharge

Document the AKI, medicines stopped and restart plan, repeat renal function and monitor for CKD, hypertension and proteinuria over the recommended follow-up period.^1,7,2

Exam traps

A normal-looking creatinine does not exclude AKI without a baseline comparison.
Do not give repeated fluid boluses without reassessing for congestion or pulmonary oedema.
Do not use eGFR to stage rapidly changing AKI as if it were stable CKD.
Do not delay emergency contrast when the risk of delaying diagnosis or treatment is clinically significant.
Do not routinely give furosemide to make urine or use low-dose dopamine as a renal-protective treatment.
A patient with haematuria and proteinuria without UTI or catheter trauma may have nephritis and needs renal discussion.
Do not wait for severe creatinine elevation before treating refractory potassium, acidosis, uraemia or pulmonary oedema.

Illustrations

Pre-renal, intrinsic and post-renal AKIThree-column diagram linking hypoperfusion, intrinsic renal injury and urinary obstruction to typical clues, urine findings and first actions.PassFinals · original

AKI detection and escalation pathwayFlow diagram from creatinine or oliguria detection through cause search, complication management, nephrology referral and renal replacement therapy.PassFinals · original

Renal replacement therapy indicationsClinical red-flag diagram showing refractory hyperkalaemia, acidosis, uraemic complications, fluid overload and pulmonary oedema.PassFinals · original

Key sources

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.