Why AKI Is a Core OSCE Topic
Acute kidney injury affects approximately 15% of hospital inpatients and is directly responsible for significant preventable mortality. It appears in OSCEs as: a deteriorating inpatient scenario (the creatinine has risen — what do you do?), a prescribing station (this patient has AKI — review their medications), and a data interpretation station. Examiners test systematic assessment, correct staging, cause identification, and safe management.
💡 Tip
AKI is not a disease — it is a syndrome. Always ask: what caused this? The treatment is determined by the cause, not the creatinine alone.
KDIGO Staging Criteria
| Stage | Serum creatinine | Urine output |
|---|---|---|
| 1 | Rise of 26 micromol/L or more within 48 hours, OR 1.5-1.9x baseline within 7 days | Below 0.5 mL/kg/hour for 6-12 hours |
| 2 | 2.0-2.9x baseline | Below 0.5 mL/kg/hour for 12 or more hours |
| 3 | 3.0x or more baseline, OR creatinine above 354 micromol/L, OR starting renal replacement therapy | Below 0.3 mL/kg/hour for 24 or more hours, or anuria for 12 or more hours |
💎 Clinical Pearl
Always compare to a baseline creatinine — ideally the most recent pre-morbid value, or a value from 3 months before if acutely unwell. A creatinine of 180 micromol/L in a patient with CKD stage 3 (baseline 160) is very different from the same reading in a previously healthy 25-year-old (baseline 70).
Causes of AKI — Pre-renal, Intrinsic, Post-renal
🧠 Mnemonic
Think in three compartments — PIP:
- P re-renal — reduced kidney perfusion
- I ntrinsic — damage within the kidney itself
- P ost-renal — obstruction to outflow
Most hospital AKI is pre-renal (60-70%) — inadequate fluid or circulatory failure.
Pre-renal (reduced perfusion)
- Hypovolaemia: vomiting, diarrhoea, haemorrhage, burns, poor intake
- Reduced cardiac output: heart failure, cardiogenic shock, MI
- Vasodilation: sepsis, anaphylaxis, liver failure (hepatorenal syndrome)
- Medications: NSAIDs (reduce renal prostaglandins), ACE inhibitors/ARBs (efferent arteriole dilation), diuretics
Intrinsic renal
- Acute tubular necrosis (ATN) — most common intrinsic cause; from prolonged ischaemia or nephrotoxins
- Glomerulonephritis (haematuria, proteinuria, hypertension)
- Interstitial nephritis — drug-induced (penicillins, NSAIDs, PPIs) or autoimmune
- Vascular: renal artery stenosis, vasculitis, thrombotic microangiopathy
Post-renal (obstruction)
- Benign prostatic hyperplasia (most common in older men)
- Ureteric calculi
- Pelvic/retroperitoneal malignancy
- Clot retention
- Bilateral ureteric obstruction (rare but important — pelvic cancer, retroperitoneal fibrosis)
Investigations
Bedside:
- Urine dipstick (blood/protein — glomerulonephritis; nitrites/leucocytes — sepsis/UTI as AKI cause)
- Urine output monitoring (catheterise if not already — allows hourly measurement)
- Fluid balance chart review
Blood tests:
- U&E, creatinine (compare to baseline)
- FBC, CRP (infection)
- LFTs (hepatorenal syndrome)
- Bone profile (calcium, phosphate — myeloma in the elderly)
- Clotting (DIC, hepatorenal)
- Blood cultures if sepsis suspected
- Urine protein:creatinine ratio (PCR) if glomerulonephritis suspected
Imaging:
- Renal ultrasound within 24 hours (NICE recommendation) in all unexplained AKI — identifies obstruction (hydronephrosis), bilateral renal artery stenosis, and chronic kidney disease (small, echogenic kidneys)
- CXR — pulmonary oedema, fluid overload
Management
Step 1: Identify and treat the cause
This is the most important step. Correct hypovolaemia, stop nephrotoxins, treat sepsis, relieve obstruction.
Step 2: Stop nephrotoxic and renally-cleared medications
⚠️ Red Flag
In any patient with AKI, immediately review and stop or hold:
- NSAIDs (ibuprofen, naproxen, diclofenac)
- ACE inhibitors and ARBs
- Metformin (lactic acidosis risk in renal failure)
- Aminoglycosides (gentamicin — if possible)
- Contrast agents (avoid unless essential)
- Lithium (narrow therapeutic index, renally excreted)
- DOACs (renally cleared — dabigatran, edoxaban, rivaroxaban, apixaban)
- Digoxin (accumulates in renal failure)
Step 3: IV fluid resuscitation (if pre-renal)
- 500 mL sodium chloride 0.9% or Hartmann's solution over 15-30 minutes if volume-depleted
- Reassess after each bolus — repeat if clinical response
- Avoid aggressive fluid in patients with cardiac failure or oliguria not responding to fluid
Step 4: Treat complications
| Complication | Management |
|---|---|
| Hyperkalaemia | See below — ECG changes guide urgency |
| Pulmonary oedema | Fluid restriction, furosemide if not anuric, NIV, dialysis |
| Acidosis (pH below 7.2) | Treat cause; bicarbonate infusion rarely indicated; dialysis if severe |
| Uraemia (symptoms) | Nausea, encephalopathy, pericarditis — urgent dialysis |
Hyperkalaemia Management
| K+ level | ECG change | Action |
|---|---|---|
| 5.5-6.0 | None | Dietary restriction, treat cause, repeat in 2-4 hours |
| 6.0-6.5 | None or peaked T-waves | Calcium resonium PO, insulin-dextrose, salbutamol nebuliser |
| Over 6.5 or ECG changes | Peaked T, widened QRS, sine wave | Urgent: IV calcium gluconate 10% (10 mL), insulin-dextrose 10 units/50 mL 50%, consider dialysis |
Indications for Urgent Renal Replacement Therapy (Dialysis)
🧠 Mnemonic
AEIOU — dialysis indications:
- A cidosis — pH below 7.1 despite treatment
- E lectrolytes — refractory hyperkalaemia (K+ above 7.0 or ECG changes not responding)
- I ntoxication — dialysable toxins (metformin, lithium, aspirin, ethylene glycol)
- O verload — pulmonary oedema not responding to diuretics
- U raemia — symptomatic (encephalopathy, pericarditis, uraemic bleeding)
Frequently Asked Questions
"What is the difference between AKI and CKD?"
AKI is an acute decline in renal function over hours to days — it is potentially reversible. CKD is a chronic, progressive, irreversible reduction in GFR lasting more than 3 months, often with structural changes. AKI can be superimposed on CKD (acute on chronic), which carries a worse prognosis. The key distinguishing feature is timeline: look for a recent baseline creatinine compared to current values, and for features of chronicity on ultrasound (small kidneys, cortical thinning).
"Why do NSAIDs cause AKI?"
The kidneys rely on prostaglandins to maintain afferent arteriolar tone and glomerular filtration when renal perfusion is compromised (e.g., in dehydration, heart failure, or sepsis). NSAIDs inhibit cyclo-oxygenase, reducing prostaglandin synthesis. This is usually harmless in healthy patients but causes significant reduction in GFR in patients with pre-existing renal or haemodynamic compromise. They are particularly dangerous in combination with ACE inhibitors and diuretics — the "triple whammy."
"When should urine output rather than creatinine be used to stage AKI?"
Urine output criteria are particularly useful in the early stages of AKI before creatinine has had time to rise (creatinine lags by 24-48 hours). They are also important in patients with very low muscle mass (elderly, frail, amputees) where a creatinine in the normal range may mask significant GFR impairment. Oliguria (below 0.5 mL/kg/hour for 6 or more hours) is an early and sensitive sign.
"What is the triple whammy?"
The triple whammy refers to the combination of an ACE inhibitor or ARB, a diuretic, and an NSAID. ACE inhibitors/ARBs dilate the efferent arteriole (reducing filtration pressure), diuretics reduce circulating volume, and NSAIDs reduce afferent arteriolar prostaglandin-mediated dilation. Together, they can precipitate severe AKI even in previously healthy individuals. This combination should always be highlighted in a medication review.
"How do you assess fluid status in a patient with AKI?"
Clinically: skin turgor, mucous membranes, axillary moisture, capillary refill time (over 2 seconds suggests dehydration), pulse rate and character, lying and standing blood pressure (postural hypotension suggests hypovolaemia), JVP height and pitting oedema. A fluid balance chart and daily weights are essential. In complex cases (especially with AKI on background heart failure or sepsis), a urinary catheter for hourly output monitoring and early ITU/renal referral is appropriate.
Related Posts
- Blood Results Interpretation OSCE — interpreting the full biochemical picture in AKI
- Sepsis and NEWS Score OSCE — sepsis as the most common cause of hospital-acquired AKI
- Medication Review OSCE — identifying and stopping nephrotoxic medications