What is acute kidney injury and how does KDIGO define it?
Acute kidney injury (AKI) is an abrupt fall in kidney function measured by a rising serum creatinine, a falling urine output, or both. The older term 'acute renal failure' has been replaced because even small, short-lived rises in creatinine carry a worse outcome — the 'injury' label pushes clinicians to act early.
The definition used today comes from the KDIGO 2012 guideline, which merged the earlier RIFLE and AKIN systems. AKI is present if any one of the following is met:
- Serum creatinine rises by at least 0.3 mg/dL within 48 hours, or
- Serum creatinine rises to at least 1.5 times baseline, known or presumed to have occurred within the prior 7 days, or
- Urine volume below 0.5 mL/kg/h for 6 hours.
StatPearls also notes that newer KDIGO 2026 proposals add cystatin C (a rise to at least 1.5 times baseline) and a criterion based on structural kidney-damage biomarkers. For exam purposes, the 2012 creatinine and urine-output criteria are still the standard answer.
How is AKI staged under KDIGO?
Once AKI is diagnosed, KDIGO grades severity into three stages. The patient is placed in the highest stage reached by either the creatinine or the urine-output column.
| Stage | Serum creatinine | Urine output |
|---|---|---|
| 1 | 1.5–1.9 times baseline, or a rise of at least 0.3 mg/dL | Below 0.5 mL/kg/h for 6–12 hours |
| 2 | 2.0–2.9 times baseline | Below 0.5 mL/kg/h for 12 hours or more |
| 3 | 3.0 times baseline, or creatinine of at least 4.0 mg/dL, or start of renal replacement therapy | Below 0.3 mL/kg/h for 24 hours or more, or anuria for 12 hours or more |
RIFLE (Risk, Injury, Failure, Loss, End-stage) is the older five-tier system. Its first three tiers roughly correspond to KDIGO stages 1–3; Loss and End-stage describe outcome (persistent loss of function for more than 4 weeks and more than 3 months), not acute severity.
What are the prerenal, intrinsic and postrenal causes of AKI?
AKI is classified by where the problem lies relative to the kidney. The classification matters because it predicts the urine findings and the first step in treatment.
| Group | Mechanism | Typical causes |
|---|---|---|
| Prerenal | Reduced kidney perfusion; tubules are intact | Haemorrhage, vomiting, diarrhoea, burns, heart failure, sepsis, cirrhosis, NSAIDs and ACE inhibitors or ARBs (they blunt autoregulation) |
| Intrinsic (renal) | Damage to tubules, interstitium, glomeruli or vessels | Acute tubular necrosis (ischaemic or toxic), acute interstitial nephritis, glomerulonephritis, vasculitis, thrombotic microangiopathy |
| Postrenal | Obstruction to urine outflow | Prostatic enlargement, bilateral ureteric stones, pelvic tumours, blocked catheter |
Among patients who develop AKI in hospital, acute tubular necrosis (ATN) is the most common cause — about 45% in StatPearls. Prolonged prerenal hypoperfusion is the usual route into ischaemic ATN; aminoglycosides, amphotericin B, iodinated contrast, myoglobin (rhabdomyolysis) and haemoglobin are classic toxic causes.
How do you work up a patient with a rising creatinine?
A structured approach answers three questions in order: is it really acute (compare with an old creatinine), is the patient obstructed, and is the kidney under-perfused or intrinsically damaged?
- History and drug chart: fluid losses, sepsis, recent surgery or contrast, NSAIDs, ACE inhibitors or ARBs, aminoglycosides, prostatic symptoms.
- Volume status: pulse, blood pressure, postural drop, JVP, oedema and lung crackles decide whether to give fluid or restrict it.
- Exclude obstruction: palpable bladder, bladder scan, flush or replace a catheter, and a renal ultrasound for hydronephrosis.
- Urine dipstick and microscopy before treatment changes them: blood and protein point to glomerular disease; casts localise the lesion.
- Urine sodium, osmolality and FENa or FEurea to separate prerenal AKI from ATN.
- Bloods: potassium, bicarbonate or blood gas, calcium and phosphate, creatine kinase if rhabdomyolysis is possible.
How do urine indices separate prerenal AKI from ATN?
In prerenal AKI the tubules are healthy and respond to low perfusion by avidly holding on to sodium and water. In ATN the damaged tubules cannot do this, so sodium leaks into the urine and the urine cannot be concentrated. Every index below is built on that one idea.
FENa (%) = (Urine Na × Plasma creatinine) ÷ (Plasma Na × Urine creatinine) × 100
Fractional excretion of sodium: the share of filtered sodium that ends up in the urine.
| Index | Prerenal | ATN (intrinsic) |
|---|---|---|
| FENa | Below 1% | Above 2% |
| Urine sodium (mEq/L) | Below 20 | Above 40–50 |
| BUN : creatinine | Above 20 : 1 | About 15 : 1 or lower |
| Urine osmolality (mOsm/kg) | Above 500 | Below 450 |
| FEurea | Below 35% | Above 50% |
| Urine sediment | Bland, hyaline casts | Muddy brown granular casts, tubular epithelial cell casts |
The high BUN-to-creatinine ratio in prerenal AKI comes from increased urea reabsorption in the proximal tubule, which follows the increased salt and water reabsorption; creatinine is not reabsorbed. Upper GI bleeding and steroids can also raise the ratio, so it supports, rather than proves, a prerenal cause.
What do urinary casts tell you in AKI?
Urine microscopy is cheap, quick and often decisive. Casts form in the tubules, so a cast tells you that the process is inside the kidney.
| Cast | Suggests |
|---|---|
| Muddy brown granular casts, renal tubular epithelial cell casts | Acute tubular necrosis |
| White blood cell casts | Acute interstitial nephritis (also pyelonephritis) |
| Red blood cell casts | Glomerulonephritis |
| Hyaline casts only | Non-specific; seen in prerenal states and concentrated urine |
How is AKI managed and when is dialysis indicated?
- Find and treat the cause: restore volume in prerenal AKI, relieve obstruction (catheter, nephrostomy) in postrenal AKI, treat sepsis.
- Stop nephrotoxins and review every drug dose for the current kidney function (NSAIDs, aminoglycosides, contrast; withhold ACE inhibitors or ARBs and metformin while unstable).
- Monitor fluid balance, urine output, creatinine, potassium and acid-base status.
- Treat complications: hyperkalaemia, metabolic acidosis, fluid overload and uraemia.
- Renal replacement therapy when complications cannot be controlled medically.
| Letter | Indication |
|---|---|
| A — Acidosis | Severe metabolic acidosis refractory to medical therapy (pH below 7.2) |
| E — Electrolytes | Hyperkalaemia above 6.5 mEq/L, or with ECG changes, not responding to treatment |
| I — Intoxication | Dialysable toxins: salicylates, ethylene glycol, methanol, lithium, metformin |
| O — Overload | Fluid overload (for example pulmonary oedema) refractory to diuretics |
| U — Uraemia | Uraemic complications: pericarditis, encephalopathy, bleeding |
What is contrast-induced nephropathy and how is it prevented?
Contrast-induced nephropathy is AKI after iodinated contrast. The StatPearls definition is a rise in serum creatinine of 25% or 0.5 mg/dL from baseline within 48–72 hours of contrast exposure. Pre-existing CKD, diabetes, dehydration and large contrast volumes raise the risk.
| Measure | KDIGO position |
|---|---|
| Contrast dose | Use the lowest possible dose |
| Type of contrast | Iso-osmolar or low-osmolar agents rather than high-osmolar |
| Volume expansion | IV isotonic saline or sodium bicarbonate; oral fluids alone are not enough |
| N-acetylcysteine | Oral NAC suggested (weak, grade 2D) — later trial evidence showed no benefit |
| Theophylline, fenoldopam | Not recommended |
| Prophylactic dialysis or haemofiltration | Not recommended |
Metformin is withheld on the day of contrast and for 48 hours afterwards, because metformin accumulates if contrast nephropathy develops and can cause lactic acidosis.
What are the common exam traps in AKI questions?
- FENa between 1% and 2% is indeterminate — read it together with urine osmolality, urine sodium and the sediment.
- Diuretics raise FENa — use FEurea instead.
- Creatinine lags behind injury — it can stay normal for the first day after a major insult, so urine output is the earlier signal.
- Muddy brown casts = ATN; WBC casts = interstitial nephritis; RBC casts = glomerulonephritis.
- Dialysis is driven by AEIOU complications, not by a creatinine number.
- ACE inhibitors and ARBs reduce efferent arteriolar tone and can tip a volume-depleted patient into prerenal AKI.