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 (1.5 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]

DCE Short Case — Volume Status Examination

Instruction

"Assess this patient's volume status. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates (hypovolaemic model)

• Hands: Cool peripherally, capillary refill 4 seconds (delayed), no peripheral oedema
• Pulse: Regular, 104 bpm, reduced volume (thready)
• Blood pressure: 96/62 lying, 84/55 standing — postural drop of 12 mmHg systolic
• JVP: Flat — not visible above sternal angle at 45 degrees
• Mucous membranes: Dry tongue, furrowed
• Skin turgor: Reduced over clavicle — persistent tenting
• Lungs: Clear — no crackles
• Heart: Dual heart sounds, no gallop, no murmurs
• Abdomen: Soft, no ascites, bladder not distended
• Legs: No ankle or sacral oedema [1]

Presentation template

"I assessed this patient's volume status. Beginning with the hands, the peripheries are cool with a capillary refill time of 4 seconds, indicating delayed perfusion. There is no peripheral oedema. The pulse is regular at 104 beats per minute, of reduced volume. Blood pressure is 96 over 62 lying, dropping to 84 over 55 on standing — a postural systolic drop of 12 mmHg. The JVP is flat, not visible above the sternal angle at 45 degrees. The mucous membranes are dry with a furrowed tongue. Skin turgor over the clavicle is reduced with persistent tenting. Examination of the chest reveals clear lung bases with no crackles. Heart sounds are dual with no gallop rhythm. There is no sacral or peripheral oedema. [1]

In summary, these findings are consistent with intravascular volume depletion. I would manage this patient with intravenous balanced crystalloid resuscitation." [1]

Discussion

1. Summarise findings and conclusion: "The constellation of flat JVP, postural hypotension, delayed capillary refill, dry mucous membranes, and reduced skin turgor is diagnostic of significant volume depletion — estimated at least 10 to 15% reduction in circulating volume." [1]

2. What is the significance of the JVP? "The JVP is the only bedside sign that directly reflects right atrial pressure. A flat JVP at 45 degrees indicates right atrial pressure close to zero, consistent with low intravascular volume. In contrast, a JVP elevated more than 3 cm above the sternal angle suggests elevated right atrial pressure from volume overload, right heart failure, or tricuspid regurgitation." [1]

3. What fluid would you give and how much? "I would give balanced crystalloid (Plasma-Lyte or Hartmann's) in 500 mL boluses, reassessing JVP, blood pressure, capillary refill, and oxygen saturation between each. I would continue until the JVP is visible, the postural drop resolves, capillary refill normalises, and MAP exceeds 65 mmHg. I would stop if the patient develops pulmonary crackles or a rising JVP suggesting overload." [1]

4. How does this differ if the patient were volume-overloaded? "If the patient were volume-overloaded — elevated JVP, basal crackles, peripheral oedema — I would not give fluids. I would treat with IV frusemide for fluid removal, and if refractory, discuss RRT for fluid management. The key principle is that AKI management requires accurate volume assessment before deciding whether to give or remove fluid." [1]

5. What is the role of point-of-care ultrasound in volume assessment? "POCUS complements the physical examination. IVC assessment gives a dynamic measure of volume status and responsiveness — a small, collapsible IVC (less than 1.5 cm with greater than 50% collapse on sniff) suggests low volume, while a dilated, non-collapsible IVC suggests volume overload. Lung ultrasound for B-lines detects interstitial pulmonary oedema before it is clinically apparent as crackles. These tools are particularly useful in obese patients where the JVP is difficult to assess, and in ventilated patients where positional assessment is limited." [1]