OBJECTIVE: The objective of the present study was to investigate the renin-aldosterone axis in neurogenic diabetes insipidus in man, in view of the fact that profound abnormalities of this axis have been described in experimental animals with congenital neurogenic diabetes insipidus. DESIGN AND PATIENTS: Nine patients with neurogenic diabetes insipidus and 11 healthy subjects (controls) were examined under basal conditions, following the standard 8-hour water deprivation test and 1 hour after a subsequent oral rehydration. MEASUREMENTS: Plasma and urine osmolalities were determined by freezing point depression, plasma sodium and potassium by a method using an ion-selective electrode, plasma AVP, cortisol, aldosterone and plasma renin activity by radioimmunoassay. RESULTS: Plasma renin activities under basal conditions were significantly higher in patients with diabetes insipidus than in controls (mean +/- SEM 23.4 +/- 6.6 vs 7.8 +/- 1.2 ng/l min). In the diabetes insipidus group, water deprivation caused a twofold increase in plasma renin activities (48 +/- 13.8 ng/l min) while in the control group plasma renin activity levels were not significantly altered (10.2 +/- 1.2 ng/l min). Rehydration did not alter plasma renin activity levels in either group (patients 50.4 +/- 13.2, controls 9.0 +/- 2.4 ng/l min). Plasma aldosterone concentrations under basal conditions did not differ between the two groups (patients 302.4 +/- 37, controls 326.4 +/- 36.5 pmol/l) and did not change in patients with diabetes insipidus after water deprivation or rehydration (307.5 +/- 67.2 and 385.5 +/- 91 pmol/l, respectively). Conversely, controls showed a significant decrease in plasma aldosterone levels after dehydration (201 +/- 27.9 pmol/l), which was attributed to the circardian variation in aldosterone secretion, as shown by a parallel decrease in plasma cortisol levels. CONCLUSIONS: Patients with diabetes insipidus are hyper-reninaemic, probably because of chronic volume contraction. There is a dissociation between renin and aldosterone in patients with diabetes insipidus under basal conditions, which is exaggerated during water deprivation.
OBJECTIVE: The objective of the present study was to investigate the renin-aldosterone axis in neurogenic diabetes insipidus in man, in view of the fact that profound abnormalities of this axis have been described in experimental animals with congenital neurogenic diabetes insipidus. DESIGN AND PATIENTS: Nine patients with neurogenic diabetes insipidus and 11 healthy subjects (controls) were examined under basal conditions, following the standard 8-hour water deprivation test and 1 hour after a subsequent oral rehydration. MEASUREMENTS: Plasma and urine osmolalities were determined by freezing point depression, plasma sodium and potassium by a method using an ion-selective electrode, plasma AVP, cortisol, aldosterone and plasma renin activity by radioimmunoassay. RESULTS: Plasma renin activities under basal conditions were significantly higher in patients with diabetes insipidus than in controls (mean +/- SEM 23.4 +/- 6.6 vs 7.8 +/- 1.2 ng/l min). In the diabetes insipidus group, water deprivation caused a twofold increase in plasma renin activities (48 +/- 13.8 ng/l min) while in the control group plasma renin activity levels were not significantly altered (10.2 +/- 1.2 ng/l min). Rehydration did not alter plasma renin activity levels in either group (patients 50.4 +/- 13.2, controls 9.0 +/- 2.4 ng/l min). Plasma aldosterone concentrations under basal conditions did not differ between the two groups (patients 302.4 +/- 37, controls 326.4 +/- 36.5 pmol/l) and did not change in patients with diabetes insipidus after water deprivation or rehydration (307.5 +/- 67.2 and 385.5 +/- 91 pmol/l, respectively). Conversely, controls showed a significant decrease in plasma aldosterone levels after dehydration (201 +/- 27.9 pmol/l), which was attributed to the circardian variation in aldosterone secretion, as shown by a parallel decrease in plasma cortisol levels. CONCLUSIONS:Patients with diabetes insipidus are hyper-reninaemic, probably because of chronic volume contraction. There is a dissociation between renin and aldosterone in patients with diabetes insipidus under basal conditions, which is exaggerated during water deprivation.
Authors: R Pivonello; A Faggiano; M Filippella; C Di Somma; M C De Martino; M Gaccione; G Lombardi; A Colao Journal: J Endocrinol Invest Date: 2002-12 Impact factor: 4.256