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Published on: September 15, 2017
Deciphering the Role of Vasopressin in Primary Aldosteronism
Luis Nogueira-Silva1, Anne Blanchard1, Emmanuel Curis1
1Department of Internal Medicine (L.N.), Centro Hospitalar São João, 4200-319 Porto, Portugal; Center for Health Technology and Services Research, Faculty of Medicine (L.N.), University of Porto, 4099-002 Porto, Portugal; Université Paris Descartes, Faculté de Médecine (A.B., A.L., V.Z., S.B., L.A., P.-F.P., J.M., M.A.), Sorbonne Paris Cité F-75006 Paris, France; Assistance Publique Hôpitaux de Paris (A.B., E.C., A.L. V.Z., M.A.), Hôpital Européen Georges Pompidou, Centre d'Investigation Clinique, F-75015 Paris, France; INSERM, CIC 1418 (A.B., D.B., M.A.), F-75015 Paris, France; Laboratoire de Biomathématiques, Faculté de Pharmacie (E.C.), Université Paris Descartes, Sorbonne Paris Cité, F-75005 Paris, INSERM, UMR 1144 (E.C.), F-75015 Paris, France; and Département de Physiologie-Explorations Fonctionnelles (S.B.), and Unité d'Hypertension Artérielle (L.A., G.B., P.-F.P., M.A.), Assistance Publique Hôpitaux de Paris, Hôpital Européen Georges Pompidou, 75015 Paris, France.
Context:
The role of vasopressin (AVP) in the pathophysiology of primary aldosteronism (PA) remains unclear.
Objectives:
The primary aim of this study was to investigate AVP secretion in PA by measuring the plasma concentration of copeptin (PCop), the C-terminal portion of provasopressin. The secondary aim was to assess renal sensitivity to AVP.
Design And Setting:
This was a cross-sectional study in a tertiary-care hospital.
Protocol:
We recruited 115 patients with PA, 48 patients with essential hypertension (EH), and 108 normotensive healthy subjects (HS). Blood was sampled for biochemical and hormonal evaluations in fasting condition after 1-h rest in supine position. Osmolality was determined in 24-h urine. PCop was determined by immunoassay.
Main Outcome Measure:
The main outcome measure was adjusted difference in PCop between groups.
Results:
After adjustment for sex, body mass index, systolic blood pressure, natremia, and kalemia, PCop was significantly higher in patients with PA than in HS (geometric mean ratio, 1.61; 95% confidence interval [CI], 1.26-2.06; P < .0001) and patients with EH (1.40; 95% CI, 1.08-1.82; P = .0070) PCop was positively correlated with natremia (P = .0094). Urine osmolality was significantly lower in patients with PA than in HS (0.82; 95% CI, 0.74-0.92; P = .0002) and 24-h urinary output was significantly higher in patients with PA than in HS (1.32; 95% CI, 1.11-1.56; P = .0005). The relationship between urine osmolality and PCop was shifted downward in patients with PA but was similar in patients with EH and HS, indicating peripheral resistance to AVP.
Conclusion:
PCop increases in patients with PA in response to an increase in natremia and a renal resistance phenomenon, indicating that AVP release is chronically stimulated in PA.
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