Abstract
Tani and his colleagues divided elderly patients with nocturia into four groups according to their 24-h urine output per body weight and concluded that nocturnal polyuria was due to the impaired function of arginine-vasopressin (AVP) in the kidney as the secretion of AVP did not change between groups.1 But if we look at data presented in the paper, the secretion of AVP decreased with the increase of urine output, however it was not statistically significant, probably because of the wide standard deviation in the value of AVP. Thus, there is still the plausible possibility that nocturnal polyuria was simply caused by increased fluid intake with resultant decreased AVP secretion in the central nervous system. A study to determine whether the restriction of fluid intake in patients with high urine output causes elevation in the AVP level, together with the diminution of urine volume, would be interesting.
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