Nocturia in the elderly. Aspects on epidemiology, pathogenesis, and antidiuretic treatment.

Analysis of nocturia questionnaires mailed to all persons aged 65 years or more in Tierp, a Swedish rural community, showed that the number of nocturnal voids was highly correlated with urge and incontinence. No correlation between nocturia and a known and treated hypertension, angina, congestive heart failure or diabetes mellitus was detected. Frequency-volume charts from elderly subjects with two or more voids per night (nocturics) were compared with those reporting <1 void/night (non-nocturics). Nocturics had a higher nocturnal urine production and lower volume per void than non-nocturics. The differences between nocturics and non-nocturics in urine production and largest voided volume did not follow the same pattern in men and women. Considerable overlap was found in all studied voiding parameters and nocturia was mainly due to a mismatch between nocturnal urine volume and largest voided volume rather than abnormal values in either. The results also indicated that, from a community-perspective, nocturnal polyuria was the dominant pathogenic factor. Elderly patients with nocturia were treated with 0.2 mg peroral desmopressin for three consecutive nights. The short-term treatment was well tolerated and the absolute majority of patients did not experience any serum sodium value below the normal range. Logistic regression searching for risk factors for hyponatraemia showed increased risk with increasing age, concomitant cardiac disease and increasing 24-hour urine output. A database study including over 600 patients exposed to desmopressin verified that increasing age and 24-hour urine output increase the risk of hyponatraemia. Desmopressin-induced hyponatraemia follows the model of SIADH. Re-challenge of 5 women who developed hyponatraemia showed recurrence of hyponatraemia on the same dose regimen. Hyponatraemia was due to failure to decrease fluid intake in proportion to the reduction in diuresis and antidiuresis lasting 24-hours or more. The findings suggest that the prolonged antidiuresis was secondary to slow elimination of desmopressin rather than to an endogenous source of antidiuresis.