Acute kidney injury

Acute kidney injury: KDIGO criteria, pre-renal, renal and post-renal causes, investigations with the question each answers, dialysis red flags, management, nephritic presentations and practice questions.

Clinical reasoning notes. Drug choices and thresholds follow common guidelines; always check your local protocol before prescribing.

The reasoning chain: confirm it is AKI → stage it → decide where the problem is (pre-renal, renal, post-renal) → find the cause → investigate with a question for every test → look for the complications that can kill → treat the cause and support the patient.

"Acute kidney injury" is a finding, not an answer. The examiner wants to hear what is causing it, how bad it is and what you will do about it.

1. Define and confirm: KDIGO criteria

AKI is present if any one of these is met:

  • Creatinine rise of 26.5 µmol/L (0.3 mg/dL) or more within 48 hours
  • Creatinine 1.5 times baseline or more within the last 7 days
  • Urine output below 0.5 mL/kg/h for 6 hours

RIFLE (older, still examined): Risk → Injury → Failure → Loss → End-stage kidney disease.

2. Stage the severity

KDIGO stages 1 to 3 rise with the creatinine multiple (1.5×, 2×, 3× baseline or a need for dialysis) and with falling urine output. Stage 3 means dialysis-range disease. Always ask for the baseline creatinine: without it you cannot tell AKI from chronic kidney disease.

3. Localise: where is the problem?

LevelMeaningExamples
Pre-renalNot enough blood reaches a healthy kidneyDehydration (vomiting, diarrhoea), sepsis, haemorrhage, heart failure, cirrhosis, NSAIDs and ACE inhibitors
Renal (intrinsic)The kidney itself is damagedAcute tubular necrosis (ATN) from ischaemia or toxins (aminoglycosides, contrast, herbal remedies); glomerulonephritis; interstitial nephritis (drugs, infection); blackwater fever in malaria; rhabdomyolysis
Post-renalUrine cannot leaveProstate enlargement, stones, schistosomiasis, cervical or prostate cancer, blocked catheter

Think local: sepsis, malaria, HIV-related kidney disease, herbal remedies and obstruction from schistosomiasis or cervical cancer are common causes where resources are limited.

4. Investigate with purpose

Every test must answer a question.

TestThe question it answers
Urea, creatinine, electrolytesHow severe is it? Is the potassium dangerous?
Cystatin C / eGFRIs there kidney damage before the creatinine has risen? (Creatinine lags behind injury.)
Urinalysis and urine microscopyMuddy brown (epithelial) casts point to ATN; red cell casts to glomerulonephritis; white cell casts to interstitial nephritis or pyelonephritis
FeNa (fractional excretion of sodium)Below 1% suggests pre-renal; above 2% suggests intrinsic. Unreliable on diuretics
Full haemogramRaised white cells (sepsis), anaemia, haemolysis
Blood cultures, malaria testIs there an infective cause?
Toxicology and drug historyNephrotoxins, NSAIDs, aminoglycosides, herbal remedies
Kidney, ureter and bladder ultrasoundObstruction? Kidney size: small kidneys mean chronic disease
Autoimmune tests: ANCA, anti-GBM, ANA, C3/C4, ASOIs this a glomerulonephritis?
Epithelial cell cast in urine, the muddy brown cast of acute tubular necrosis. Ajay Kumar Chaurasiya, CC BY-SA 4.0, Wikimedia Commons
Epithelial cell cast in urine, the muddy brown cast of acute tubular necrosis. Ajay Kumar Chaurasiya, CC BY-SA 4.0, Wikimedia Commons
White cell cast in urine, seen in interstitial nephritis and pyelonephritis. Ajay Kumar Chaurasiya, CC BY-SA 4.0, Wikimedia Commons
White cell cast in urine, seen in interstitial nephritis and pyelonephritis. Ajay Kumar Chaurasiya, CC BY-SA 4.0, Wikimedia Commons
Ultrasound of a hydronephrotic kidney with a dilated pelvis and calyces: look for this in post-renal AKI. Hansen, Nielsen and Ewertsen, CC BY 4.0, Wikimedia Commons
Ultrasound of a hydronephrotic kidney with a dilated pelvis and calyces: look for this in post-renal AKI. Hansen, Nielsen and Ewertsen, CC BY 4.0, Wikimedia Commons

Where results can mislead: the creatinine can still be normal early in kidney damage; FeNa is unreliable in a patient on diuretics; a patient who is oliguric may still have a "normal" urea if they are young and well-nourished.

5. Nephritic presentations

Nephritic syndrome: haematuria, hypertension, oliguria and oedema.

  • Post-streptococcal glomerulonephritis (PSGN): follows a streptococcal throat or skin infection by 1 to 3 weeks; low C3, raised ASO; usually self-limiting in children.
  • Rapidly progressive glomerulonephritis (RPGN): the creatinine keeps rising over days to weeks; crescents on biopsy. Causes: anti-GBM disease (Goodpasture), ANCA vasculitis, immune-complex disease. This is an emergency: untreated, it leads to kidney failure.

Nephritic or nephrotic? Nephritic = blood (haematuria), pressure (hypertension), little urine. Nephrotic = heavy protein loss (over 3.5 g a day), low albumin, gross oedema, high cholesterol.

6. Red flags: when to think dialysis

Remember AEIOU:

  • Acidosis, severe and not responding to treatment
  • Electrolytes: potassium above 6.5 mmol/L or ECG changes
  • Intoxication (some poisonings)
  • Overload: pulmonary oedema not responding to diuretics
  • Uraemic complications: encephalopathy, pericarditis, bleeding

7. Management: treat the cause, support, monitor

  1. Find and stop the cause: treat sepsis, stop NSAIDs, ACE inhibitors, aminoglycosides and other nephrotoxins, relieve obstruction (catheter, nephrostomy).
  2. Fluids: resuscitate the dehydrated patient with balanced crystalloids and reassess often. Give fluid to the dry; do not push fluid into an overloaded patient.
  3. Hyperkalaemia first: protect the heart with IV calcium if there are ECG changes, shift potassium with insulin and dextrose (salbutamol nebulisers also help), remove it with a diuretic or dialysis.
  4. Monitor: strict fluid chart, daily weight, urine output (catheter if needed), daily electrolytes.
  5. Review every drug for dose adjustment in kidney failure.
  6. Refer early for dialysis if the red flags above are present.

8. Follow-up

Check the creatinine after discharge: AKI raises the risk of chronic kidney disease. Advise the patient to avoid NSAIDs and herbal remedies. Tell future prescribers.

Examiner questions

  1. Give the KDIGO criteria for AKI.
  2. A patient has muddy brown casts and a FeNa of 3%. What is the diagnosis, and what do you do?
  3. Why is creatinine a poor early marker, and what test can pick up injury sooner?

Practice questions

1. A 45-year-old man has vomited for 3 days and is on ibuprofen. His creatinine is double its baseline, urine is concentrated and FeNa is 0.5%. The level of the problem is: A. Post-renal · B. Pre-renal · C. Glomerular · D. Interstitial · E. Tubular necrosis Answer: B. Low FeNa and concentrated urine mean the kidney is still working hard to hold on to sodium and water.

2. Urine microscopy shows red cell casts. The most likely diagnosis is: A. Acute tubular necrosis · B. Interstitial nephritis · C. Glomerulonephritis · D. Pre-renal AKI · E. Urinary tract infection Answer: C.

3. Which finding is an indication for urgent dialysis? A. Creatinine of 200 µmol/L · B. Urine output of 0.4 mL/kg/h for 3 hours · C. Potassium of 7.0 mmol/L with peaked T waves not responding to treatment · D. Mild ankle swelling · E. FeNa above 2% Answer: C.

4. A child has haematuria and hypertension two weeks after a skin infection. Complement C3 is low. The most likely diagnosis is: A. IgA nephropathy · B. Minimal change disease · C. Post-streptococcal glomerulonephritis · D. Anti-GBM disease · E. Lupus nephritis Answer: C.

Compiled by Abongo Davis · Ompath Study · shared for MBChB students at Mount Kenya University and other universities.