Wed3November0919PM 7

A 52-year-old man presented with acute dyspnoea.

His past medical history includes three vessel coronary artery bypass surgery for ischaemic heart disease and hypertension.

Examination revealed widespread expiratory crackles with chest x ray confirming pulmonary oedema. He was treated with intravenous nitrates and furosemide with symptomatic improvement.

Investigations at this stage revealed:

Serum sodium 138 mmol/L (137-144)

Serum potassium 4.2 mmol/L (3.5-4.9)

Serum urea 8.7 mmol/L (2.5-7.5)

Serum creatinine 170 µmol/L (60-110)

Random plasma glucose 10.1 mmol/L (<11.1)

Urinalysis Protein++

The following day he was switched to oral furosemide at a dose of 80 mg daily and began captopril 12.5 mg twice daily, increased to 25 mg twice daily. Repeat investigations one week later revealed:

Serum sodium 134 mmol/L (137-144)

Serum potassium 5.1 mmol/L (3.5-4.9)

Serum urea 15.7 mmol/L (2.5-7.5)

Serum creatinine 220 µmol/L (60-110)

Fasting plasma glucose 6.0 mmol/L (3.0-6.0)

Which of the following is most likely to be responsible for the deterioration in renal function?

(Please select 1 option)

Captopril Correct

Cholesterol emboli

Diabetic nephropathy

Furosemide

Hypertension

Explanation

This patient has coronary artery atheroma and therefore could have a renal artery stenosis by the same pathophysiological mechanism.

A rise in serum creatinine more than 20% above the baseline after starting an angiotensin-converting enzyme inhibitor (ACEI) should prompt the clinician to hold the drug, monitor renal function and investigate for renal artery stenosis.

The patient does not have diabetes based upon a fasting plasma glucose of only 6 mmol/L (3.0-6.0).

Answer Statistics

1

85%

2

1%

3

1%

4

14%

5

1%

Times answered: 294