Key result
Primary hyperaldosteronism was confirmed in 7 of 52 patients (13.5%) following successful endovascular treatment for renal artery disease, highlighting it as a frequent cause of residual hypertension.
Why the study?
Is primary hyperaldosteronism a frequent cause of residual hypertension in patients after successful endovascular treatment of renal artery disease?
Observational (n=52)
Is primary hyperaldosteronism a frequent cause of residual hypertension in patients after successful endovascular treatment of renal artery disease?
Primary hyperaldosteronism is a frequently neglected cause of residual hypertension in patients who have undergone technically successful endovascular treatment for renal artery disease.
May support screening for primary aldosteronism in residual hypertension post-revascularization; hypothesis-generating and should not yet change practice.
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.
No takes yet. Share an insight, caveat, or question.
Pizzolo et al. (2005) conducted an observational in Renal artery disease after successful percutaneous renal angioplasty (n=52). Primary hyperaldosteronism was evaluated on Confirmed diagnosis of primary hyperaldosteronism. Primary hyperaldosteronism was confirmed in 7 of 52 patients (13.5%) following successful endovascular treatment for renal artery disease, highlighting it as a frequent cause of residual hypertension.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: