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Renal abnormalities and vascular complications in primary hyperaldosteronism. Evidence on tertiary hyperaldosteronism
Insights
Primary hyperaldosteronism is not benign. This study found significant vascular complications in patients with primary hyperaldosteronism, necessitating prompt and effective treatment for hypertension management.
Area of Science:
- Endocrinology
- Nephrology
- Cardiovascular Medicine
Background:
- Primary hyperaldosteronism is often considered a benign form of hypertension.
- The potential for 'tertiary' hyperaldosteronism and its link to renal disease requires investigation.
Purpose of the Study:
- To review renal/renal artery disease and vascular complications in primary hyperaldosteronism.
- To assess if primary hyperaldosteronism is a benign condition.
- To investigate the possibility of 'tertiary' hyperaldosteronism.
Main Methods:
- Retrospective review of 136 primary hyperaldosteronism cases.
- Analysis of underlying renal or renal artery disease.
- Tracking of vascular complication incidence over a mean of 5.9 years.
Main Results:
- 7.4% had renal artery stenosis; 8.1% had parenchymatous renal disease, not exceeding general hypertensive populations.
- 2.9% showed malignant-phase hypertension.
- 22.8% developed vascular complications (39 events) over the observation period.
Conclusions:
- Primary hyperaldosteronism is associated with significant vascular complications, challenging the view of it being benign.
- No excess of underlying renal disease suggests tertiary hyperaldosteronism is unlikely.
- Early and effective treatment is crucial for managing hypertension and preventing complications.
Abstract:
The frequency of underlying renal or renal artery disease, and the incidence of vascular complications were reviewed in a series of 136 cases of primary hyperaldosteronism. This was in order to investigate the possible existence of 'tertiary' hyperaldosteronism, and to examine the commonly held view that primary hyperaldosteronism is a relatively benign form of hypertension. Ten cases (7-4 per cent) had evidence of renal artery stenosis and eleven (8-1 per cent) parenchymatous renal disease. In comparison with the reported frequency in large general series of hypertensives, these data show no evidence of an excess of underlying renal disease. It is unlikely, therefore, that autonomous aldosterone secreting adenomata occur commonly as a consequence of prolonged secondary hyperaldosteronism. Four cases (2-9 per cent) had evidence of the malignant-phase of hypertension, and over a mean observation time of 5-9 years, 31 cases (22-8 per cent) developed 39 vascular complications. It appears, therefore, that vascular complications are not rare in primary hyperaldosteronism, and early and effective treatment is thus necessary.