BACKGROUND: Poor blood pressure control in renal artery disease patients after percutaneous renal angioplasty (PTRA), with or without stenting (PTRAS), may be due to pre-existing hypertension. Primary hyperaldosteronism is much more frequent than was previously suspected. We hypothesized that residual hypertension observed in some renal artery disease patients after technically successful endovascular treatment may be due to primary hyperaldosteronism. METHODS: Only patients free of significant residual artery stenosis were included in the study. Aldosterone and renin were measured in 52 renal artery disease patients (8 with fibrodysplastic and 44 with atherosclerotic lesions), in whom successful PTRA/PTRAS had been performed previously. An aldosterone-to-renin ratio > or = 23 pg/ml per pg/ml was considered as the cut-off value for performing tests to confirm the diagnosis of primary hyperaldosteronism. RESULTS: Residual hypertension (blood pressure > or = 160/90 mmHg) was observed in 24/52 patients (46%) after revascularization. A raised aldosterone-to-renin ratio was found in nine subjects (17.3%), eight of whom had poor blood pressure control (33% of patients with residual hypertension). A diagnosis of primary hyperaldosteronism was confirmed in seven patients (four atherosclerotic, three fibrodysplastic). All fibrodysplastic subjects with unresponsive blood pressure after PTRA were affected by primary hyperaldosteronism. Primary hyperaldosteronism was confirmed in 9% (4/44) of the atherosclerotic patients (19% of subjects with residual hypertension). No specific clinical features were associated with the subsequent blood pressure control. CONCLUSIONS: Primary hyperaldosteronism is a frequently neglected cause of residual hypertension despite technically successful endovascular treatment of renal artery disease.

Primary aldosteronism is a frequent cause of poor blood pressure control despite techically successful endovascular treatment of renal artery stenosis

PIZZOLO, Francesca;PAVAN, Chiara;GUARINI, Patrizia;GIRELLI, Domenico;CORROCHER, Roberto;OLIVIERI, Oliviero
2005-01-01

Abstract

BACKGROUND: Poor blood pressure control in renal artery disease patients after percutaneous renal angioplasty (PTRA), with or without stenting (PTRAS), may be due to pre-existing hypertension. Primary hyperaldosteronism is much more frequent than was previously suspected. We hypothesized that residual hypertension observed in some renal artery disease patients after technically successful endovascular treatment may be due to primary hyperaldosteronism. METHODS: Only patients free of significant residual artery stenosis were included in the study. Aldosterone and renin were measured in 52 renal artery disease patients (8 with fibrodysplastic and 44 with atherosclerotic lesions), in whom successful PTRA/PTRAS had been performed previously. An aldosterone-to-renin ratio > or = 23 pg/ml per pg/ml was considered as the cut-off value for performing tests to confirm the diagnosis of primary hyperaldosteronism. RESULTS: Residual hypertension (blood pressure > or = 160/90 mmHg) was observed in 24/52 patients (46%) after revascularization. A raised aldosterone-to-renin ratio was found in nine subjects (17.3%), eight of whom had poor blood pressure control (33% of patients with residual hypertension). A diagnosis of primary hyperaldosteronism was confirmed in seven patients (four atherosclerotic, three fibrodysplastic). All fibrodysplastic subjects with unresponsive blood pressure after PTRA were affected by primary hyperaldosteronism. Primary hyperaldosteronism was confirmed in 9% (4/44) of the atherosclerotic patients (19% of subjects with residual hypertension). No specific clinical features were associated with the subsequent blood pressure control. CONCLUSIONS: Primary hyperaldosteronism is a frequently neglected cause of residual hypertension despite technically successful endovascular treatment of renal artery disease.
2005
aldosterone-to-renin ratio, hypertension, primary hyperaldosteronism, renal artery disease
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/308444
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