title: Involvement of arginine vasopressin and renal sodium handling in pathogenesis of hyponatremia in elderly patients.
abstract: The present study was undertaken to determine the pathophysiological role of arginine vasopressin (AVP) in elderly patients with hyponatremia, and the efficacy of fludrocortisone acetate in treating their hyponatremia. Eleven hospitalized patients aged 65 years or older whose serum sodium levels were less than 130 mEq/l were examined. The hyponatremic patients included two groups of patients: syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and central salt-wasting syndrome. And 24 healthy, young subjects aged 20 to 34 years, and 24 healthy, elderly subjects age 65 to 80 years were recruited by community announcement. The elderly subjects had decreased urinary concentrating ability and exaggerated response of AVP secretion to osmotic and nonosmotic stimuli, as compared to the young subjects. All the patients had hyponatremia, with the exaggerated urinary loss of Na. Plasma AVP levels were elevated despite hypoosmolality in all the 2 groups of hyponatremic, elderly patients. Plasma renin activity and plasma aldosterone concentrations were low in the patients with SIADH and central salt-wasting syndrome. Fludrocortisone acetate therapy was effective in the patients with central salt-wasting syndrome and 3 patients with SIADH whose hyponatremia remained unchanged after water restriction. Water restriction therapy normalized serum Na levels in only 3 patients with SIADH. These results indicate that AVP is involved in the mechanism for hyponatremia in the elderly patients with SIADH and central salt-wasting syndrome. Severe hyponatremia associated with SIADH and central salt-wasting syndrome responds well to mineralocorticoid therapy. Both the secretion of AVP and renal sodium handling may be involved in the mechanism of action of the disorders. The diagnostic criteria for SIADH in the elderly patients may have to be reevaluated and should be considered to indicate fludrocortisone acetate therapy.
authors.affiliation: Department of Medicine, Jichi Medical School, Tochigi, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Ishikawa
authors.forename: N
authors.initials: N
authors.lastname: Fujita
authors.forename: G
authors.initials: G
authors.lastname: Fujisawa
authors.forename: Y
authors.initials: Y
authors.lastname: Tsuboi
authors.forename: N
authors.initials: N
authors.lastname: Sakuma
authors.forename: K
authors.initials: K
authors.lastname: Okada
authors.forename: T
authors.initials: T
authors.lastname: Saito
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001127:Arginine Vasopressin / Q000378:metabolism*; D001769:Blood; D001794:Blood Pressure; D005260:Female; D005438:Fludrocortisone / Q000627:therapeutic use; D006339:Heart Rate; D006801:Humans; D007010:Hyponatremia / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D009318:Natriuresis; D009994:Osmolar Concentration; D012462:Saline Solution, Hypertonic; D012964:Sodium / Q000378:metabolism*; D018667:Tilt-Table Test
chemical_list: D012462:Saline Solution, Hypertonic; D001127:Arginine Vasopressin; D012964:Sodium; D005438:Fludrocortisone