Acute Kidney Injury — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr David Thompson, 73 years old. ^[1]

Presenting complaint: Three-day history of worsening breathlessness, reduced urine output, and confusion. His wife reports he has had a "chest cold" for a week and has been taking ibuprofen for body aches. ^[1]

Past history:

• Type 2 diabetes (22 years) — HbA1c 72 mmol/mol. Complications: diabetic nephropathy (baseline creatinine 155, eGFR 38), diabetic neuropathy, background retinopathy
• Ischaemic heart disease — NSTEMI 2020, DES to LAD
• Hypertension — 15 years
• Heart failure with preserved ejection fraction (LVEF 52%), NYHA II
• Benign prostatic hyperplasia
• Gout ^[1]

Current medications:

• Metformin 1g BD
• Empagliflozin 10mg OD
• Perindopril 10mg OD
• Frusemide 40mg OD
• Atorvastatin 80mg
• Aspirin 100mg
• Allopurinol 300mg
• Ibuprofen 400mg TDS (over-the-counter, started 1 week ago)
• Tamsulosin 400mcg OD ^[1]

Examination findings (trainee elicits):

• Alert but mildly confused, GCS 14, febrile 38.6, RR 28, SpO2 91% on room air
• HR 108 irregular (AF), BP 94/58 lying (84/50 standing)
• JVP flat — trace visible at 30 degrees
• Cool peripheries, capillary refill 4 seconds, dry mucous membranes
• Reduced skin turgor over the clavicle
• Right basal crackles to mid-zone, increased work of breathing
• Soft abdomen, bladder not palpable
• No peripheral oedema ^[1]

Investigations:

• Creatinine 365 (baseline 155 — 2.4 times baseline), Urea 28.5, K+ 6.5, Na+ 134
• pH 7.20, bicarbonate 12, lactate 3.2, base excess minus 14
• FBC: Hb 126, WCC 17.8, neutrophils 14.2
• CRP 195
• CK 280 (normal)
• Glucose 14.2
• Venous lactate 3.2
• Troponin 45 (chronically elevated, no acute rise)
• Urinalysis: leucocytes++, nitrites+, protein+, blood trace, ketones+
• Urine microscopy: WBC 50/hpf, no casts, no eosinophils
• ECG: AF, HR 108, peaked T waves diffusely, QRS 110ms
• CXR: right lower lobe consolidation with small right pleural effusion
• Renal ultrasound: normal-sized kidneys, no hydronephrosis ^[1]

Candidate's structured presentation (model)

Opening statement: ^[1]

"Mr Thompson is a 73-year-old man with type 2 diabetes, ischaemic heart disease, HFpEF, and stage 3b CKD who presents with a 3-day history of worsening breathlessness, oliguria, and confusion, on a background of a one-week respiratory illness treated with over-the-counter ibuprofen. ^[1]

His main problems are:

1. Sepsis — right lower lobe pneumonia with septic shock (qSOFA 3: RR 28, SBP 94, confused)
2. Acute kidney injury, KDIGO stage 2, multifactorial — sepsis-associated AKI compounded by nephrotoxicity (NSAIDs, ACE inhibitor) on diabetic CKD
3. Hyperkalaemia K+ 6.5 with peaked T waves — medical emergency
4. Severe metabolic acidosis (pH 7.20, bicarbonate 12) with raised lactate
5. New atrial fibrillation — likely secondary to sepsis and electrolyte disturbance
6. Polypharmacy with multiple nephrotoxins and sick-day-rule contraindicated drugs ^[1]

Investigation summary: ^[1]

"His creatinine has risen from a baseline of 155 to 365 — a 2.4-fold rise, consistent with KDIGO stage 2 AKI. The urine shows leucocytes and nitrites with WBC on microscopy, suggesting a urinary tract infection may be contributing alongside the pneumonia. The renal ultrasound shows normal-sized kidneys with no obstruction. His hyperkalaemia at 6.5 with peaked T waves and his metabolic acidosis at pH 7.20 are both severe and require emergency management. His ECG shows new atrial fibrillation, likely precipitated by sepsis and his electrolyte derangement." ^[1]

Management plan: ^[1]

1. Emergency hyperkalaemia management:

   • Calcium gluconate 10 mL of 10% IV immediately (peaked T waves present)
   • Insulin 10 units with 25 g IV dextrose
   • Nebulised salbutamol 20 mg
   • Recheck K+ at 1 hour; if refractory, RRT ^[1]

2. Sepsis management (Surviving Sepsis Bundle):

   • Blood, urine, and sputum cultures immediately
   • Antibiotics within 1 hour: ceftriaxone 2g IV plus azithromycin 500mg for CAP; add gentamicin if concern for urosepsis with resistant organism (dose-adjust and monitor levels)
   • 30 mL/kg balanced crystalloid bolus (about 2.1 L given his weight approximately 70 kg), reassess
   • Noradrenaline if MAP remains below 65 after fluid resuscitation
   • Source control: continue and assess for complications (empyema, abscess) ^[1]

3. Stop all nephrotoxic and contraindicated medications:

   • Ibuprofen — stop immediately (NSAID nephrotoxicity)
   • Perindopril — withhold (ACE inhibitor contributing to AKI in volume depletion)
   • Metformin — withhold (lactic acidosis risk)
   • Empagliflozin — withhold (sick day rules; ketoacidosis risk)
   • Frusemide — withhold during volume resuscitation; may restart for volume overload
   • Allopurinol — withhold during AKI ^[1]

4. Fluid strategy:

   • He is hypovolaemic (flat JVP, postural drop, cool peripheries) — give balanced crystalloid
   • Challenge with 500 mL boluses, reassess between
   • Monitor closely for pulmonary oedema given HFpEF history — this is the key tension
   • If he becomes volume overloaded with ongoing oliguria, trial IV frusemide; if refractory, RRT for fluid management ^[1]

5. Monitor and manage AF:

   • Rate control with beta-blocker if needed (bisoprolol cautious given hypotension)
   • Anticoagulate after initial stabilisation (CHA2DS2-VASc high, but balance with bleeding risk in AKI — use unfractionated heparin which can be rapidly reversed)
   • Correct electrolytes (potassium, magnesium) which may contribute to AF ^[1]

6. Drug dosing:

   • All renally-cleared drugs dose-adjusted to current eGFR (much lower than baseline 38)
   • Gentamicin if used: extended-interval with trough monitoring, avoid if possible
   • Vancomycin if needed: trough-guided ^[1]

Examiner discussion questions

Q: "His ibuprofen is over-the-counter. How do you prevent this happening again?" ^[1]

"This is a common and dangerous scenario. Over-the-counter NSAIDs are a leading cause of preventable AKI, especially in elderly patients with CKD. I would take three steps. First, I would counsel the patient and his wife explicitly that he must never take ibuprofen, naproxen, diclofenac, or any NSAID — including over-the-counter products — because of his diabetic kidney disease. I would explain that paracetamol is the safe alternative for pain. Second, I would document this prominently in his medical record and medication list, flagging NSAIDs as a documented allergy or contraindication. Third, I would inform his GP so this is reinforced at every visit. The pharmacist should also be alerted. Patient education is the single most effective intervention — many patients do not realise that ibuprofen from the supermarket can be dangerous." ^[1]

Q: "Should you be worried about the troponin of 45?" ^[1]

"In this context, the troponin is likely a type 2 myocardial injury — demand ischaemia from septic shock and hypoperfusion — rather than a type 1 MI (plaque rupture). His chronically elevated troponin from his prior NSTEMI and heart failure provides a baseline. I would not treat this as an acute coronary syndrome. My priority is treating the sepsis and restoring perfusion, which will address the supply-demand mismatch. I would trend the troponin rather than acting on a single value. If it shows a clear rising trend with chest pain or dynamic ECG changes, I would involve cardiology for consideration of ACS management." ^[1]

Q: "When would you involve nephrology?" ^[1]

"I would involve nephrology early — within the first 24 hours — for any patient with stage 2 or worse AKI, especially with the complexity of this patient. Specifically, I would call immediately if: he meets absolute indications for RRT (refractory hyperkalaemia, acidosis, or volume overload); his AKI is not responding to standard management within 48 hours; the diagnosis is unclear and intrinsic renal disease is possible; or he has persistent oliguria with rising creatinine. In this case, if his hyperkalaemia does not respond to initial medical therapy, I would call nephrology and ICU for RRT planning without delay." ^[1]

Q: "He is on an SGLT2 inhibitor. When would you restart it?" ^[1]

"I would withhold it during this acute illness as part of sick day rules. I would restart it after his AKI has recovered — when his creatinine has returned to near baseline (around 155) and he is clinically stable, eating and drinking normally, and not volume-depleted. SGLT2 inhibitors have powerful renoprotective and cardioprotective benefits in diabetic CKD and heart failure (DAPA-CKD, EMPEROR-Reduced, EMPA-KIDNEY), and long-term he should be on it. But during acute illness, the risks of volume depletion and euglycaemic ketoacidosis outweigh the benefits. I would document the plan to reinstate it so it is not forgotten at discharge." ^[1]