Renal and urology · Moderate
This case is fictional and exists for study. It describes no real patient.
72 years · male
A 72-year-old man presents to the emergency department with a 3-day history of worsening fatigue, nausea, and poor oral intake. He has a history of hypertension and osteoarthritis. One week ago, he started taking high-dose naproxen for knee pain. On examination, he appears lethargic and dehydrated with reduced skin turgor. Abdominal examination is unremarkable with no palpable urinary bladder. Urine output has been less than 200 mL in the last 24 hours. An electrocardiogram (ECG) shows tall, peaked T waves across multiple leads and widening of the QRS complex.
Vital signs
- HR
- 108 bpm
- BP
- 98/62 mmHg
- RR
- 20/min
- Temp
- 36.8 °C
- SpO₂
- 96%
Examination findings
- Decreased skin turgor and dry mucous membranes
- No suprapubic tenderness or palpable urinary bladder
Investigations
| Serum urea | 24.5 mmol/L | reference: 2.5-7.8 |
| Serum creatinine | 340 µmol/L | reference: 60-110 |
| Serum potassium | 6.9 mmol/L | reference: 3.5-5.0 |
| Serum sodium | 132 mmol/L | reference: 135-145 |
| Serum bicarbonate | 16 mmol/L | reference: 22-29 |
Question 1 of 3
Which of the following is the single most appropriate initial management step for this patient?
In severe hyperkalaemia associated with ECG changes (such as tall peaked T waves and QRS widening), the immediate priority is myocardial cell membrane stabilization using IV calcium gluconate (or calcium chloride) to prevent life-threatening cardiac arrhythmias. Intravenous insulin with glucose effectively shifts potassium intracellularly to reduce serum concentrations, but its effect takes 15-30 minutes and it does not directly protect the cardiac membrane. Fluid resuscitation and haemodialysis are important subsequent management steps once membrane stabilization is achieved.
Teaching point: Intravenous calcium gluconate must be given immediately in severe hyperkalaemia when ECG changes are present to stabilize the myocardium.
Question 2 of 3
What is the primary underlying renal pathophysiological mechanism caused by the patient's new medication?
Non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen inhibit cyclooxygenase enzymes, preventing the synthesis of renal prostaglandins (e.g., PGE2 and PGI2). Prostaglandins normally dilate the afferent arteriole to maintain glomerular filtration rate (GFR), particularly in volume-depleted states. Inhibiting prostaglandins leads to unchecked afferent arteriolar vasoconstriction, causing pre-renal acute kidney injury. ACE inhibitors cause efferent arteriolar dilation. While NSAIDs can cause interstitial nephritis, the acute onset following dehydration and high-dose intake primarily leads to functional haemodynamic pre-renal AKI.
Teaching point: NSAIDs impair renal autoregulation by blocking prostaglandin-mediated afferent arteriolar vasodilation, resulting in pre-renal acute kidney injury.
Question 3 of 3
After stabilizing the potassium level and starting IV fluids, which initial imaging investigation is most appropriate to rule out structural urinary tract obstruction?
Renal ultrasound is the standard, non-invasive initial imaging modality used to evaluate acute kidney injury and rule out post-renal urinary tract obstruction (hydronephrosis). Non-contrast CT KUB is primarily used for suspected nephrolithiasis rather than initial evaluation of unexplained AKI. Intravenous urography is outdated and involves iodinated contrast, which is contraindicated in AKI. Renal MRA evaluates vascular stenoses, not structural tract obstruction.
Teaching point: Renal ultrasound is the first-line imaging investigation to exclude obstructive post-renal causes in patients presenting with acute kidney injury.
Key learning points
- Severe hyperkalaemia with ECG changes requires immediate cardiac membrane stabilization with intravenous calcium gluconate.
- NSAIDs induce pre-renal acute kidney injury by inhibiting prostaglandin-mediated afferent arteriolar vasodilation.
- Renal ultrasound is the diagnostic imaging modality of choice to exclude urinary tract obstruction in acute kidney injury.
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