Acute Kidney Injury
By the end of this post you will be able to:
- Recognize acute kidney injury from a creatinine trend or the urine output, using the KDIGO criteria.
- Distinguish pre-renal, intrinsic and post-renal injury using the bedside assessment and the urine.
- Initiate first-line ward management — fluids, nephrotoxin review, relief of obstruction — and recognize the triggers for calling nephrology.
TL;DR
What you need to know before seeing your first patient on your IM rotation with this condition
Estimated read time: 3 minutes
Criteria: a rise of ≥26.5 µmol/L in 48 hours or to ≥1.5× baseline within 7 days. Ultrasound is selective, not routine. Biopsy is nephrology’s decision. Dialysis starts when an indication is present, not as a last resort. Fluid is for volume depletion, not the heart failure, cirrhosis or nephrotic syndrome listed as pre-renal.
- What it is: An abrupt fall in kidney function over hours to days. Any one diagnoses it: a creatinine rise of ≥26.5 µmol/L within 48 hours, a rise to ≥1.5× the usual baseline within 7 days, or urine output under 0.5 mL/kg/h for 6 hours.
- How it presents: Usually found on bloodwork, not symptoms. At the bedside: volume status, a palpable bladder, the medication list. No single examination finding reliably identifies hypovolemia (JAMA Rational Clinical Examination); weigh several.
- Initial tests to order: Labs — creatinine, CBC, electrolytes, urea; CK, SPEP/SFLC if suggested. Bedside — bladder scan. Imaging — ultrasound KUB only if no cause is found or obstruction is possible. Urine — urinalysis with microscopy. Unexplained AKI with a suspected renal cause: refer to nephrology, who may biopsy.
- If unstable — indications for renal replacement, AEIOU: Acidosis · Electrolytes · Intoxication · Overload · Uremia. A, E, O when refractory to medical therapy; U with pericarditis or encephalopathy; I for dialysable toxins. No single number triggers dialysis. Who to call: section 5.
- If stable — stabilize first, then treat by category: Pre-renal — if volume-depleted, 500 mL of crystalloid over less than 15 minutes, reassessing after each. Congested or cirrhotic: no bolus — see sections 1–2. Renal — treat the cause. Post-renal — catheterize if retained; if catheterized, check it drains. Across all three: stop NSAIDs; hold ACE inhibitors, ARBs and metformin; avoid aminoglycosides where an alternative exists; dose vancomycin by levels.
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Read Around the Case
Based on KDIGO 2012 Clinical Practice Guideline for Acute Kidney Injury, Canadian Association of Radiologists Guidance on Contrast-Associated AKI (2022) and NICE NG148 (acute kidney injury, updated 2024). No Canadian guideline is dedicated to acute kidney injury; the Canadian Society of Nephrology has published a commentary on the KDIGO recommendations.
Estimated read time: 21 minutes
The AKI Sequence
Confirm it, and stage it against a baseline
Volume status · bladder scan · the medication list
The cheapest high-yield test, and the one most often skipped
Scan first. Ultrasound if no cause is found, or obstruction is likely
Strict intake/output, daily weight, creatinine and electrolytes daily. Call if output stays under 0.5 mL/kg/h or creatinine keeps rising
1. Is It Acute, and Where Is the Injury?
Estimated read time: 6 minutes
Staging is arithmetic, and it needs a denominator. Find a previous creatinine — a prior admission, family physician bloodwork, a pre-operative panel. Where none exists, the lowest value this admission is the usual stand-in; say so in the chart.
KDIGO set these criteria in 2012; an update went to public review in March 2026.
Two things the table does not say out loud:
- Creatinine lags filtration. A normal value on the day of the insult does not mean normal kidneys; a plateau is not recovery.
- The urine criterion is unusable unless somebody measures. A patient can meet stage 1 on output alone and be recorded normal because nobody charted it
A rising creatinine during decongestion is not automatically AKI
Week 0 Day 3 met the heart failure patient whose creatinine climbs during diuresis. In a secondary analysis of DOSE, a creatinine rise over 26.5 µmol/L during decongestion did not predict death, readmission or emergency visits at 60 days.
- A creatinine rising while the jugular venous pressure falls and breathing eases is behaving differently from one rising while the patient stays congested
- The question is not “has the creatinine gone up” but “is this patient still volume overloaded?” If so, the diuretic usually continues
Where is the injury?
Localizing the injury is a clinical judgement, not a single test. The history, volume assessment, bladder scan and medication list do most of the work. The urine is one input — cheap, quick, often not sent. NICE recommends a dipstick in everyone as soon as AKI is suspected; microscopy adds what a dipstick cannot.
Two caveats belong next to the finding, not in a footnote:
- Granular casts are not exclusive to acute tubular injury
- Scattered fine granular casts alone carry little diagnostic weight
2. Pre-Renal AKI
Estimated read time: 4 minutes
Fractional excretion of sodium and urea
What it is, and how to read it. The proportion of filtered sodium the kidney fails to reabsorb. Send a spot urine sodium and creatinine with paired serum values, drawn at the same time.
- FeNa below 1% — the tubules are conserving sodium, fitting a pre-renal picture. It also fits early obstruction and some glomerulonephritis, so it narrows rather than decides.
- FeNa above 2% — sodium is being wasted, which fits tubular injury. Between 1% and 2% is indeterminate.
- On a diuretic, use the fractional excretion of urea instead — below 35% suggests pre-renal, with the caveat below.
How well it performs:
- Best in the clean case. A 2022 meta-analysis found pooled sensitivity 90% and specificity 82% at the 1% threshold, rising to 95% and 91% in oliguric patients with no chronic kidney disease and no diuretics.
- Diuretics damage the specificity, not the sensitivity — 80% and 54% (95% CI 31–75) in that subgroup. Because specificity falls, it is a high FeNa — the tubular answer — that stops meaning much; a low FeNa despite a diuretic still suggests pre-renal.
- The workaround is weaker than taught. In a 2007 study the fractional excretion of urea had a specificity of 33% on diuretics — it “cannot be used as an alternative tool because it lacks specificity.” A 2026 meta-analysis is kinder at 87%, with heterogeneity over 90%.
The next three sections take the buckets in order.
- Which fluid — two separate questions. Outside hemorrhagic shock, KDIGO suggests an isotonic crystalloid (0.9% saline, Ringer’s lactate or Plasma-Lyte) over a colloid such as albumin or starch (grade 2B). Whether a balanced solution beats saline is a separate question.
- Prefer a balanced solution, on a modest signal. SMART is the only trial of the three with a kidney primary outcome and it favoured balanced — major adverse kidney events 14.3% vs 15.4% (OR 0.91, 95% CI 0.84–0.99) — though no individual component reached significance, and BaSICS and PLUS, powered on mortality, found none. Saline is not an error.
- How much, and when to stop. If the patient needs fluid resuscitation, NICE CG174 sets the bolus at 500 mL of crystalloid over less than 15 minutes, reassessing after each. Congested patients need section 1’s decongestion box or the hepatorenal box, not a bolus. Once perfusion is restored, more fluid is not a kidney treatment.
- Why the usual suspects matter here. NSAIDs and ACE inhibitors or ARBs blunt the autoregulation that protects filtration when perfusion falls — which is how a combination tolerated for years turns dangerous the week the patient gets dehydrated. Stop the NSAID and hold the ACE inhibitor or ARB; the drug table in section 5 has each class and its restart plan.
- Two things that are not treatments. KDIGO and NICE both advise against loop diuretics to treat AKI, except for volume overload. “Renal-dose” dopamine carries a 1A recommendation against it: it has been tested and does not work.
Hepatorenal syndrome — when more fluid is the wrong answer
- In advanced cirrhosis with ascites, a rising creatinine may be a functional, pre-renal-looking injury with a bland sediment and very low urinary sodium
- The pre-renal reflex misleads here. Terlipressin with albumin improves renal function in type 1 disease, at the cost of ischemic and respiratory adverse events
- For a clerk the job is recognition, not management — call for help
3. Renal (Intrinsic) AKI
Estimated read time: 4 minutes
Renal causes divide four ways — tubular, interstitial, glomerular, vascular — the same four the urine table above points to.
Nephrotic syndrome sits awkwardly: the lesion is glomerular, but the AKI is often pre-renal, through low oncotic pressure and depleted effective arterial volume. The Intern at Work episode covers it; section 2 treats the volume problem.
Vancomycin with piperacillin-tazobactam. Observational data linked the pair to AKI, and the episode below covers that signal. ACORN then tested it: in a randomized trial of 2,511 adults, most also on vancomycin, pip-tazo caused no more AKI or death than cefepime, which caused more delirium.
Contrast-associated AKI. The Canadian position, from the Canadian Association of Radiologists:
- Never delay an emergency scan for a creatinine
- Prophylaxis only at an eGFR of 30 or below, and even then the evidence for hydration is weak: CAR leaves it to local practice for intravenous contrast
- Existing AKI is its own risk group. The eGFR “is unreliable” in AKI, so the threshold of 30 does not apply; weigh what the scan will change
- Do not routinely stop drugs to reduce risk — except metformin in AKI or at an eGFR of 30 or below: hold it for 48 hours and restart only if function is stable
- N-acetylcysteine is not recommended, nor other prophylactic drugs. PRESERVE found no benefit from bicarbonate or acetylcysteine, and AMACING found withholding prophylactic hydration non-inferior in high-risk patients
- No routine follow-up creatinine, except 48–72 hours after intra-arterial contrast at an eGFR of 30 or below
- Other drugs to hold once AKI is established are in section 5
Acute interstitial nephritis:
- Suspect it when the sediment shows white cells without infection and a new drug started in the preceding weeks — antibiotics, proton pump inhibitors, NSAIDs, increasingly immune checkpoint inhibitors. Rash, fever and eosinophilia are frequently absent
- Stopping the drug is the least controversial intervention
- The steroid evidence is retrospective. A 2025 systematic review included 23 studies, only three randomized, and concluded high-quality trials are still needed
- What it agrees on is timing, not dose or duration. Delay of about a month was associated with failure to return to baseline and fibrosis on repeat biopsy; in 182 cases each day of delay carried an odds ratio of 1.02 for a worse creatinine at six months, while high-dose treatment beyond three weeks added nothing
- For a clerk: stop the drug, and if steroids are given the argument is for giving them early rather than long
4. Post-Renal AKI
Estimated read time: 3 minutes
- Scan the bladder first. Minutes, no radiology, and the one investigation a student can do alone at 2 a.m.
- A high residual means outlet obstruction, and a catheter is both test and treatment — the fastest intervention available
- Then image, selectively. NICE timings: ultrasound within 24 hours when no cause is identified or the patient is at risk of urinary tract obstruction, within 6 hours for suspected pyonephrosis
- Do not routinely scan when the cause is already identified
- Upper tract obstruction goes to urology — immediately for pyonephrosis, an obstructed solitary kidney or bilateral obstruction, with nephrostomy or stent within 12 hours
- Then watch for post-obstructive diuresis. Output can run to litres. Most is physiological; the pathological form causes dehydration, electrolyte derangement and, untreated, death. Incidence spans 0.5% to 52%, reflecting competing definitions
- This is where strict intake/output stops being paperwork — replacement is decided from the recorded output
Do not clamp the catheter. Staged drainage is widely taught, to prevent bleeding and hypotension. A 1997 review found hematuria in 2–16% after quick complete relief, rarely significant, blood pressure that usually normalized, and no studies supporting clamping at all. A randomized trial of 294 men then found hematuria in 11.3% with gradual drainage versus 10.5% with rapid. Drain the bladder.
5. Practical Considerations on the Ward
Estimated read time: 4 minutes
Every drug on the chart gets read again. Is it harming the kidney, and does the dose fit?
Calling about dialysis.
- Have these ready before you dial: potassium and whether the ECG has changed; pH and bicarbonate; the creatinine and urea trend, not one value; urine output over 24 hours; oxygen requirement and fluid status; and whether dialysis fits their goals of care.
- Say which AEIOU indication is met, and what you have already tried — name the treatment.
- Do not wait for a number. No creatinine or urea threshold triggers dialysis, and waiting for one is how the call gets made late. In AKIKI-2, delaying further in patients who already qualified was associated with higher mortality.
- Nor start early to get ahead of it. STARRT-AKI and AKIKI found no survival benefit, and STARRT-AKI more dialysis dependence at 90 days (10.4% vs 6.0%). ELAIN, smaller and single-centre, is the outlier. All four were in intensive care.
Who to call, and when. Tell your senior, then follow NICE:
- Nephrology or ICU immediately — an AEIOU indication not responding to treatment.
- Nephrology within 24 hours — possible vasculitis, glomerulonephritis, interstitial nephritis or myeloma; no clear cause; inadequate response; complications; stage 3; a kidney transplant; or CKD stage 4–5.
- Urology — upper tract obstruction (section 4).
- Not needed when the cause is clear and it is responding promptly, unless there is a kidney transplant.
Making the fluid record usable.
- A daily weight, same time and same scale, is often more reliable than a charted balance.
- The catheter is a decision with a downside. It relieves outlet obstruction and gives accurate hourly output; it also causes infection. Name the removal plan when you insert it — “for accurate output” is not an indefinite indication
Documenting it, and what happens after.
- Write the AKI into the discharge summary as a problem in its own right — peak creatinine, presumed cause, drugs held, which need restarting and when, and when function should next be checked
- A held ACE inhibitor with no restart plan is how a temporary hold becomes permanent. Week 0 Day 2 covers how to write it
- KDIGO advises review three months after an AKI for resolution, new chronic kidney disease, or worsening of existing disease — and that review is not automatic
- In AFTER AKI, an Alberta trial after stage 2–3 AKI, a risk-guided handover raised the share getting an ACE inhibitor or ARB, a statin and nephrology follow-up within 90 days from 3% to 28%, with more hyperkalemia.
Related Podcasts
Kidney topics this post points at rather than covers.
Test Yourself
Click on your answer to reveal the explanation.
A 72-year-old man is on day 3 of an admission for cellulitis. His creatinine six months ago was 80 µmol/L; this morning it is 160 µmol/L. He feels well. His blood pressure is 128/76 mmHg and has been stable, heart rate 84, and he is afebrile. He is clinically euvolemic. His medications include ramipril, naproxen for gout, and intravenous cefazolin.
What is the most appropriate next step?
A 78-year-old man with a long history of benign prostatic hyperplasia is admitted with delirium. His creatinine is 340 µmol/L, up from a baseline of 95. A bladder scan shows 900 mL. A urethral catheter is inserted and drains 1.2 L immediately. Over the next 8 hours he passes 3.2 L of urine. His blood pressure has fallen from 132/78 mmHg on admission to 104/60 mmHg, and his heart rate is 96.
What is the most appropriate next step?
Apply Your Learning
Your patient’s creatinine has risen from 78 to 145 µmol/L over two days. You stop the NSAID, give 1 L of saline, and plan to reassess in the morning. The next day the creatinine is 190 µmol/L and there is 200 mL of urine in the bag. What did yesterday’s plan assume, and what do you do now?
Please do not include patient identifying details — no names, initials, dates, medical record numbers, or any detail that could identify a specific patient or encounter. Write about your reasoning, not about a real person.
Further Reading
- GuidelineKDIGO Clinical Practice Guideline for Acute Kidney Injury (2012)
- GuidelineCanadian Association of Radiologists Guidance on Contrast-Associated Acute Kidney Injury (2022)
- GuidelineNICE NG148 — Acute kidney injury: assessment, prevention and management
- CommentaryCanadian Society of Nephrology commentary on the KDIGO AKI guideline (AJKD, 2013)
- Infographic and podcastAcute Kidney Injury — MedicinePods infographic and Intern at Work episode 190
Week 0