Case 1
A 64-year-old man presented with increasing nocturia and urinary frequency without dysuria. Physical examination was unremarkable. Bacteriological screening of the urine and renal function tests were normal. He had a long history of hypertension, well controlled on nifedipine 20 mg twice daily for the previous 6 months.

He was referred for urological assessment. Benign prostatic hypertrophy with an increased residual urine volume was found on ultrasonography. His prostate specific antigen was normal. He underwent a routine prostatectomy, but symptoms persisted after surgery.

A month after the operation he developed peripheral oedema that resolved when nifedipine was discontinued. His urinary symptoms disappeared two days after stopping nifedipine and the residual volume returned to normal on a subsequent ultrasound scan.

Case 2
A 78-year-old man with moderate essential hypertension was commenced on amlodipine 5 mg daily. He returned two weeks later, complaining of marked urinary frequency including nocturia, which he associated with the medication. Symptoms resolved two days after ceasing amlodipine.

Dihydropyridine calcium channel blockers are widely prescribed and generally have a low incidence of adverse effects apart from those related to vasodilatation. Symptoms due to altered bladder function are not well recognised, although polyuria is listed as an unusual adverse effect of nifedipine.

Nifedipine and other dihydropyridines affect urinary tract function to a variable extent. Mild diuretic and natriuretic effects are observed in some studies. Contraction of the detrusor muscle of the human bladder during micturition depends upon calcium entry into cells, and this is inhibited in vitro by low concentrations of dihydropyridines.1

Nifedipine has improved detrusor instability and neurogenic bladder symptoms in clinical trials producing a reduction in detrusor tone and an increase in residual volume. It is sometimes used to treat these symptoms.

Patients taking dihydropyridines may have adverse events affecting the urinary tract, particularly frequency, nocturia and increased residual volume. These adverse effects should be recognised since urological investigation is usually unnecessary. If these adverse events are suspected, suitable management is withdrawal of the suspect drug for several weeks. Symptoms should respond rapidly to this trial. Temporary cessation is relatively safe. The dihydropyridines are seldom essential and there is no recognised withdrawal syndrome.

These cases show the importance of taking a drug history when a patient is first assessed for prostatectomy.


D. Taverner

Senior Lecturer, Department of Clinical and Experimental Pharmacology, University of Adelaide, Adelaide