Nocturia due to nocturnal polyuria is a prevalent problem in middle-aged and elderly patients. The mechanism of nocturnal polyuria is believed to be multifactorial, including a change in the circadian release of natriuretic peptides and anti-diuretic hormone, and blunting of the normal nocturnal dip in blood pressure (which can drive pressure-natriuresis and thus nocturnal polyuria). This study attempts to identify an association between the intensity of anti-hypertensive (AHT) drug therapy required and nocturnal polyuria.

We performed a retrospective analysis of voiding diaries taken from men at a Veterans-Affairs based urology clinic. Inclusion criteria were patients with a baseline actual nocturnal voids (ANV) ≥1 and age ≥ 50. Patients were excluded who had a diagnosis of obstructive sleep apnea, diabetes insipidus, congestive heart failure, or chronic renal failure. Patients were split into 3 groups based on number of AHT's taken (0, 1, or 2 or more), which were limited to thiazide diuretics, calcium-channel blockers, and ACE-I's/ARB's. One-way ANOVA on ranks was used to determine significance between groups, and two-way ANOVA was used to detect interactions.

A total of 184 voiding diaries completed by 184 men were used in the present analysis. Patients taking 0, 1, or 2 or more AHT's had: (1) a nocturnal polyuria index (NPi) of 38% (n=96), 40% (n=59), and 47% (n=29), respectively (p= 0.03, Table); (2) an ANV of 2.5, 2.5, and 3.0 (p=0.02); and a nocturnal bladder capacity index (NBCi) of 1.10, 1.23, and 1.53 respectively (p=0.04). No interaction was found between age for ANV (p=0.73), NBCi (p=0.52), or NPi (p=0.79).

Combination drug therapy for hypertension, compared with untreated hypertension or monotherapy, was shown to be associated with much more nocturia and nocturnal polyuria. Nocturnal bladder capacity also progressively diminished as compared with MVV, manifesting as the increasing NBCi in patients taking combination therapy.

Patients requiring multiple antihypertensive drugs are likely to have more severe and long-standing hypertension, with impairment of both nocturnal dipping of blood pressure and renal tubular sodium and water transport. Further research is warranted.

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