Acute kidney injury (AKI)
The creatinine tells you there is a problem. The potassium, the lungs and the acid tell you how dangerous it is. Find out if the patient is dry, blocked or poisoned.
A 72-year-old woman admitted with diarrhoea and vomiting for 4 days has passed 80 mL of urine in 6 hours. She takes ramipril, furosemide and a diclofenac injection she gets from a local clinic for knee pain. Creatinine 3.1 mg/dL (274 µmol/L), last month 0.9 mg/dL (80 µmol/L). Potassium 6.2 mmol/L.
What stage is this, what is causing it, and what do you do first?
- Potassium and ECG firstA blood gas potassium is fine to act on. Treat high potassium now if needed.
- Fluid statusPulse, BP, capillary refill, JVP, chest, oedema, fluid chart, weight.
- Bladder scanOr a catheter if retention is likely. Blocked bladders are common and easy to fix.
- Stop the harmful drugsNSAIDs, ACE inhibitors, ARBs, diuretics, metformin, gentamicin. Adjust doses of others.
- Find the baselineOld creatinine from records or labs to stage the AKI.
- Urine dipstickBlood and protein suggest a kidney inflammation (glomerulonephritis).
- Hourly urine outputCatheter if needed to measure it accurately.
- Ultrasound within 24 hoursIf no obvious cause, or suspected blockage. Sooner if infection with blockage.
- Potassium 6.5 mmol/L or more, or any ECG change
- Breathless with crackles and low oxygen
- pH below 7.15 or very low bicarbonate
- No urine
- Fever and loin pain with AKI (infected blocked kidney)
- Blood and protein in the urine with AKI
- High potassium
- Pulmonary oedema
- Blocked or infected blocked kidney
- Rapidly progressive glomerulonephritis
- Rhabdomyolysis
| Stage 1 | Creatinine rise of 0.3 mg/dL (26 µmol/L) in 48 hours, or 1.5–1.9 times baseline, or urine below 0.5 mL/kg/hour for 6–12 hours |
| Stage 2 | 2–2.9 times baseline, or urine below 0.5 mL/kg/hour for 12 hours or more |
| Stage 3 | 3 times baseline, or creatinine 4 mg/dL (354 µmol/L) or more, or urine below 0.3 mL/kg/hour for 24 hours, or anuria for 12 hours, or dialysis |
| Fluid challenge | 500 mL crystalloid over 15 minutes if dry, then reassess |
| Potassium 6.5 or ECG changes | Treat as an emergency: see High potassium |
Check every dose against a current drug reference and your hospital protocol.
On this page
What it is
AKI is a sudden fall in kidney function over hours to days. The creatinine rises and the urine output often falls. AKI is common, often preventable, and dangerous: it causes high potassium, acid build-up, fluid overload and drug toxicity.
- Not enough blood reaching the kidneys
- Dehydration, diarrhoea, vomiting, bleeding, sepsis, heart failure
- Made worse by NSAIDs, ACE inhibitors, ARBs, diuretics
- Damage to the kidney itself
- Acute tubular necrosis after prolonged low BP or toxins (gentamicin, contrast)
- Glomerulonephritis, rhabdomyolysis, snake bite, malaria, dengue
- Blocked outflow
- Enlarged prostate, stones, pelvic cancer, blocked catheter
- Both kidneys (or a single kidney) must be blocked
Common in Pakistan: diarrhoea in summer, painkiller injections (diclofenac), herbal remedies, gentamicin, snake bites (Russell's viper), dengue, malaria and sepsis.
Assess the patient
- Dry? Thirst, low BP, fast pulse, dry mouth, low JVP, postural drop, negative fluid balance.
- Overloaded? Crackles, raised JVP, swollen legs, low SpO₂.
- Blocked? Palpable bladder, prostate symptoms, loin pain, previous stones, catheter not draining.
- Septic? Fever, source.
- Kidney inflammation? Rash, joint pains, coughing blood, blood and protein on urine dipstick.
- Drug chart: every drug that harms the kidney or builds up in AKI.
Investigations
| Test | Why |
|---|---|
| Potassium (gas first), urea, creatinine, sodium, bicarbonate | Severity and dangers |
| ECG | High potassium effects |
| CBC, CRP | Infection, anaemia |
| Blood gas | Acidosis |
| Urine dipstick (before a catheter if possible) | Blood and protein suggest glomerulonephritis |
| Bladder scan | Retention |
| Kidney ultrasound | Blockage (hydronephrosis), kidney size (small = chronic disease) |
| CK | Rhabdomyolysis after crush injury, fits, immobility |
| Blood cultures, malaria test, dengue tests | Infections that cause AKI |
| Further tests on senior advice | ANCA, anti-GBM, complement, ANA, if glomerulonephritis is possible |
Treatment
- SepsisLook for and treat infection.
- ToxinsStop NSAIDs, ACE inhibitors, ARBs, diuretics, metformin, gentamicin. Avoid contrast if possible.
- Optimise BP and volumeFluids if dry, in 500 mL boluses with reassessment. Stop if overloaded.
- Prevent harmTreat high potassium, dose-adjust drugs, catheter if blocked, monitor.
- Blocked bladder: catheter. Expect a large urine output for a day or two afterwards (post-obstructive diuresis): replace losses.
- Blocked kidney with infection: urology now for drainage (stent or nephrostomy).
- Glomerulonephritis: nephrology the same day.
- Rhabdomyolysis: generous IV fluids, aiming for urine 200–300 mL/hour, if no overload.
- Daily: weight, fluid balance, creatinine, potassium. Review the drug chart every day.
When dialysis is needed
- Acidosis: severe (pH below 7.15) not responding to treatment.
- Electrolytes: potassium high despite medical treatment.
- Intoxication: some poisons (lithium, methanol, ethylene glycol, salicylates).
- Overload: pulmonary oedema not responding to diuretics.
- Uraemia: confusion, pericarditis, bleeding.
Common mistakes
- Not checking the potassium and ECG first.
- Giving furosemide to "make urine" in a dry patient.
- Pouring in fluid until the lungs fill.
- Missing a full bladder.
- Leaving NSAIDs, ACE inhibitors, metformin or gentamicin on the chart.
- Not dipping the urine before catheterisation.
Frequently asked questions
How is AKI staged?
KDIGO stage 1: creatinine rise of 0.3 mg/dL (26 µmol/L) in 48 hours or 1.5–1.9 times baseline. Stage 2: 2–2.9 times baseline. Stage 3: 3 times baseline, creatinine 4 mg/dL (354 µmol/L) or more, or dialysis. Urine output criteria also apply.
Which drugs should be stopped in AKI?
NSAIDs, ACE inhibitors, ARBs, diuretics, metformin and nephrotoxic antibiotics such as gentamicin. Other drugs need dose adjustment.
What are the indications for dialysis in AKI?
Severe acidosis, high potassium not responding to treatment, certain poisonings, fluid overload not responding to diuretics, and uraemic complications such as confusion, pericarditis or bleeding.
What is the first line treatment for AKI?
Treat the cause and prevent harm: check potassium and the ECG, give fluid if the patient is dry, relieve any blockage (catheter or drainage), stop drugs that harm the kidney, and treat sepsis.
Test yourself
Exam-style questions on this guide, from our two question banks. Choose an answer to see why each option is right or wrong.
1. A patient's baseline creatinine was 0.9 mg/dL (80 µmol/L). It is now 3.1 mg/dL (274 µmol/L). What KDIGO stage of AKI is this?
Answer: Stage 3. A rise to 3 or more times baseline (or creatinine 4.0 mg/dL / 354 µmol/L or more, or dialysis) is stage 3 AKI.
- Chronic kidney disease: The rise is acute.
- Stage 2: Stage 2 is 2.0–2.9 times baseline.
- Not AKI: It clearly is.
- Stage 1: Stage 1 is 1.5–1.9 times baseline.
2. An elderly man with AKI has a bladder scan showing 1100 mL. What is the next step?
Answer: Urinary catheter. Urinary retention is a reversible cause of AKI. After catheterisation, watch for a large diuresis and replace fluid losses.
- Restrict fluids: He may diurese heavily after catheterisation.
- IV furosemide: Doesn't relieve obstruction.
- Tamsulosin and observe: Retention with AKI needs a catheter.
- CT abdomen before anything else: Relieve the retention first.
3. A patient with AKI has crackles, SpO₂ 86% and potassium 7.1 mmol/L despite medical treatment. What is needed?
Answer: Urgent dialysis. Indications for urgent dialysis include refractory hyperkalaemia, refractory fluid overload, severe acidosis, uraemic complications and some poisonings.
- Oral calcium resonium only: Too slow for refractory hyperkalaemia.
- More IV fluids: Will worsen overload.
- IV sodium bicarbonate alone: Not sufficient.
- Repeat bloods tomorrow: Life-threatening now.
4. A man with CKD stage 5 needs long-term haemodialysis access. Which is the preferred first option?
Answer: Radiocephalic fistula. Vascular access for haemodialysis: native AV fistula preferred (lowest infection/thrombosis) — radiocephalic (wrist, Brescia–Cimino) in non-dominant arm first, then brachiocephalic, then brachiobasilic (transposed); AV graft if veins unsuitable; tunnelled central venous catheter as last resort/bridge. Create 3–6 months before dialysis to allow maturation. Protect the arm veins (no cannulas/blood tests) in CKD patients. Complications: steal syndrome, aneurysm, thrombosis, high-output heart failure.
- Tunnelled femoral catheter: Femoral catheters carry infection and thrombosis risk.
- Dominant-arm AV graft: Distal non-dominant fistulas come first.
- Subclavian dialysis line: Subclavian lines cause stenosis and are not long-term access.
5. On the evening after a laparotomy, a patient has passed 15 mL/h of urine for 3 hours. HR 110, BP 105/65, cool peripheries, catheter flushes well. What is the first step?
Answer: 500 mL fluid challenge. Post-operative oliguria (< 0.5 mL/kg/h): first exclude a blocked catheter (flush/replace), then assess volume status — most commonly hypovolaemia (bleeding, third-space losses, inadequate replacement). Give a fluid bolus (250–500 mL crystalloid) and reassess; look for bleeding. Consider sepsis, nephrotoxins, abdominal compartment syndrome, cardiac failure. Diuretics only once euvolaemic/overloaded.
- IV furosemide 40 mg: Furosemide worsens hypovolaemia.
- Low-dose dopamine: Dopamine gives no renal benefit.
- Wait until morning: Waiting risks AKI.
6. Which two mechanisms keep glomerular filtration rate steady when blood pressure changes?
Answer: Myogenic response and TGF. Autoregulation keeps GFR steady between mean pressures of about 80–180 mmHg. The afferent arteriole constricts when stretched (myogenic). The macula densa senses increased NaCl when GFR rises and triggers afferent constriction (tubuloglomerular feedback, via adenosine). Angiotensin II also constricts the efferent arteriole when pressure falls.
- ADH and aldosterone: Control water and sodium, not GFR autoregulation.
- ANP and BNP: Raise GFR and sodium excretion; not autoregulation.
- Sympathetic nerves and adrenaline: Reduce GFR in severe stress.
- Angiotensin II and prostaglandins alone: Help, but are not the two main mechanisms.
7. Red blood cell casts in the urine are most characteristic of:
Answer: Glomerulonephritis. Urinary casts form in tubules and reflect the site of disease: red cell casts — glomerular bleeding (nephritic syndrome); white cell casts — pyelonephritis or interstitial nephritis; muddy brown granular casts — acute tubular necrosis; fatty casts and oval fat bodies — nephrotic syndrome; hyaline casts — normal or dehydration; waxy casts — chronic kidney disease.
- Acute pyelonephritis: White cell casts.
- Acute tubular necrosis: Muddy brown granular casts.
- Nephrotic syndrome: Fatty casts.
- Renal stones: Haematuria without casts.
References and dose sources
- KDIGO clinical practice guideline for acute kidney injury
- NICE NG148: Acute kidney injury
- Think Kidneys (NHS AKI programme)
- UK Kidney Association — hyperkalaemia
- Ringer's lactate (Hartmann's solution) dosing: Drugs.com: Lactated Ringer's dosage (see also our ringer's lactate (hartmann's solution) dose page)
- Furosemide dosing: Drugs.com: Furosemide dosage (see also our furosemide dose page)
International guidance is linked where it reflects good practice. Where your hospital’s protocol differs, follow your hospital.