ECE2018 Poster Presentations: Adrenal and Neuroendocrine Tumours Adrenal cortex (to include Cushing's) (70 abstracts)
Renin: a possible novel marker for the efficacy of pharmacological treatment of primary aldosteronism
Nikolaos Voulgaris 1 , Sofia Vlachou 1 , Evangelia Kyriazi 1 , Eleni Papaoikonomou 1 , Ernestini Tyfoxylou 1 , Nikoletta Monastirioti 1 , Chara Kapsali 1 , Aglaia Zachaki 1 , Liana Charalampidou 1 , Theodora Kounadi 1 , Athina Markou 1 , Labrini Papanastasiou 1 , Eirini Giagourta 1 , Eva Kassi 2 , Gregory Kaltsas 3 & George Piaditis 1
1Department of Endocrinology and Diabetes Center, ‘G Gennimatas’ General Hospital, Athens, Greece; 2Department of Biological Chemistry, Medical Scholl, National and Kapodistrian University of Athens, Athens, Greece; 3Department of Pathophysiology, Laikon Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Introduction: Primary aldosteronism (PA) treatment is either pharmacological with aldosterone receptor antagonists (MRAs) or surgical with the resection of the responsible adenoma. The efficacy of MRAs treatment is based on the normalization of blood pressure (BP) in relation to potassium levels. However, it remains unclear whether the stimulation of renin levels during treatment could serve as an additional marker of adequate MR blockade.
Aim: To investigate prospectively the effectiveness of MRAs on BP control in PA patients in correlation with renin levels.
Methods: Thirty eight patients diagnosed with PA, were treated with MRAs and were prospectively followed –up at regular intervals ranging from 3 to 12 months. All patients were instructed to have 2 consecutive BP measurements twice daily. Systolic (SBP) and diastolic (DBP) BP target were <135 and <85 mmHg respectively. Renin levels >7.8 μU/ml were considered as unsuppressed. In patients with raised BP (SBP or DBP) or renin levels <7.8 μU/ml MRAs dose was gradually increased.
Results: At the first follow up visit, 10 of 38 (26.3%) PA patients had normal SBP, DBP and unsuppressed renin levels. The initial MRAs dose ranged from 25 to 100 mg (mean 57.2 mg). Patients with unsuppressed renin levels had lower DBP compared to patients with suppressed renin levels (77.6±7.3 mmHg vs 83.15±8.7 mmHg, P=0.04). Patients with either elevated BP or suppressed renin levels received higher MRAs dose, which ranged from 50 to 200 mg (mean 104.5 mg). At the last follow-up 24 of 33 (72.7%) patients had normal BP and unsuppressed renin levels. Compared to the 1st follow-up, at the last follow up visit the PA patients improved SBP (136.9±9.9 mmHg vs 127.8±9.14 mmHg, P<0.001), DBP (80.2±8.9 mmHg vs 75.6±5.6 mmHg, P=0.04), raised renin (9.9±8.1 μU/ml vs 16.3±9.8 μU/ml, P<0.001) and potassium levels (4.2±0.5 vs 4.4±0.3 mEq/L, P=0.024). In addition, there was a negative correlation between mean MRAs doses and renin levels (r-0.42, P 0.014) at the last follow-up indicating that the higher MRA doses were needed in patients with supressed renin levels at the beginning of the study.
Conclusion: The targeted MRAs pharmacological treatment leads to an increase of renin levels and more effective BP control. According to our data, unsuppressed renin levels in combination with BP could be used as a novel marker of adequate MR blockade and can predict BP control.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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