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Title:
Primary aldosteronism and salt | Pflügers Archiv - European Journal of Physiology
Description:
For many years, primary aldosteronism was thought (and taught) to be a relatively rare (<1 %) and benign form of high blood pressure: now we know that neither is the case. Currently, the prevalence is considered to be 5–10 % of hypertensives, on the basis of more or less stringent cutoffs for the aldosterone/renin ratio and plasma aldosterone concentration: increasingly, evidence is mounting that the true prevalence of (relatively) autonomous aldosterone secretion may be ∼30 % of hypertensives. There is, in addition, a consensus that the risk profile for patients with primary aldosteronism is substantially higher than in age-, sex-, and blood pressure-matched essential hypertensives; the cardiovascular/renal damage in primary aldosteronism is thus not a primary effect of raised blood pressure. The nexus between salt and primary aldosteronism is clear, as equivalently raised or even higher levels of plasma aldosterone in chronic sodium deficiency are homeostatic and do not cause cardiovascular damage, thus ruling out deleterious effects of aldosterone acting alone. In primary aldosteronism the normal homeostatic feedback loops between sodium status and aldosterone levels are disturbed, so that cardiovascular/renal damage reflects inappropriate aldosterone levels for sodium status. One possible actor in such a scenario is endogenous ouabain (or similar compounds), which is elevated in the sodium-loaded state and a vasoconstrictor, and thus potentially be able both to raise blood pressure and to cause cardiovascular/renal damage. A second consideration is that of the epidemiologic data linking a chronically high salt intake to a raised blood pressure. If autonomous aldosterone secretion is in fact present in ∼30 % of hypertensives, this may be the group sensitive to the pressor effects of high salt, with the remainder much less affected. Finally, at a practical level given even the currently accepted prevalence of primary aldosteronism, a radical reconsideration of first-line antihypertensive therapy is proposed.
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Topics {✒️}

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Funder JW (2012) Primary aldosteronism: are we missing the wood for the trees?

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         description:For many years, primary aldosteronism was thought (and taught) to be a relatively rare (<1 %) and benign form of high blood pressure: now we know that neither is the case. Currently, the prevalence is considered to be 5–10 % of hypertensives, on the basis of more or less stringent cutoffs for the aldosterone/renin ratio and plasma aldosterone concentration: increasingly, evidence is mounting that the true prevalence of (relatively) autonomous aldosterone secretion may be ∼30 % of hypertensives. There is, in addition, a consensus that the risk profile for patients with primary aldosteronism is substantially higher than in age-, sex-, and blood pressure-matched essential hypertensives; the cardiovascular/renal damage in primary aldosteronism is thus not a primary effect of raised blood pressure. The nexus between salt and primary aldosteronism is clear, as equivalently raised or even higher levels of plasma aldosterone in chronic sodium deficiency are homeostatic and do not cause cardiovascular damage, thus ruling out deleterious effects of aldosterone acting alone. In primary aldosteronism the normal homeostatic feedback loops between sodium status and aldosterone levels are disturbed, so that cardiovascular/renal damage reflects inappropriate aldosterone levels for sodium status. One possible actor in such a scenario is endogenous ouabain (or similar compounds), which is elevated in the sodium-loaded state and a vasoconstrictor, and thus potentially be able both to raise blood pressure and to cause cardiovascular/renal damage. A second consideration is that of the epidemiologic data linking a chronically high salt intake to a raised blood pressure. If autonomous aldosterone secretion is in fact present in ∼30 % of hypertensives, this may be the group sensitive to the pressor effects of high salt, with the remainder much less affected. Finally, at a practical level given even the currently accepted prevalence of primary aldosteronism, a radical reconsideration of first-line antihypertensive therapy is proposed.
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      description:For many years, primary aldosteronism was thought (and taught) to be a relatively rare (<1 %) and benign form of high blood pressure: now we know that neither is the case. Currently, the prevalence is considered to be 5–10 % of hypertensives, on the basis of more or less stringent cutoffs for the aldosterone/renin ratio and plasma aldosterone concentration: increasingly, evidence is mounting that the true prevalence of (relatively) autonomous aldosterone secretion may be ∼30 % of hypertensives. There is, in addition, a consensus that the risk profile for patients with primary aldosteronism is substantially higher than in age-, sex-, and blood pressure-matched essential hypertensives; the cardiovascular/renal damage in primary aldosteronism is thus not a primary effect of raised blood pressure. The nexus between salt and primary aldosteronism is clear, as equivalently raised or even higher levels of plasma aldosterone in chronic sodium deficiency are homeostatic and do not cause cardiovascular damage, thus ruling out deleterious effects of aldosterone acting alone. In primary aldosteronism the normal homeostatic feedback loops between sodium status and aldosterone levels are disturbed, so that cardiovascular/renal damage reflects inappropriate aldosterone levels for sodium status. One possible actor in such a scenario is endogenous ouabain (or similar compounds), which is elevated in the sodium-loaded state and a vasoconstrictor, and thus potentially be able both to raise blood pressure and to cause cardiovascular/renal damage. A second consideration is that of the epidemiologic data linking a chronically high salt intake to a raised blood pressure. If autonomous aldosterone secretion is in fact present in ∼30 % of hypertensives, this may be the group sensitive to the pressor effects of high salt, with the remainder much less affected. Finally, at a practical level given even the currently accepted prevalence of primary aldosteronism, a radical reconsideration of first-line antihypertensive therapy is proposed.
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