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High renin states, and greater risks may be associated with the primary problem, leading to hyperreninemia.
End organ damage from long-standing Htn (e.g., chronic kidney disease, cardiomyopathy).
Abnormal glucose tolerance in up to 50% of pts with hyperaldosteronism.
Risks include hypernatremia and hypervolemia with high total body sodium.
Htn may be refractory to treatment, with increased risk of cardiovascular complications, including malignant hypertensive crisis.
Hypokalemia and hypomagnesaemia with low intracellular potassium and magnesium may cause cardiac arrhythmia and general muscle weakness.
The underlying primary medical disorder that leads to increased renin and, hence, increased aldosterone secretion.
Hypertensive response to intubation or surgical incision.
Hypokalemia and associated muscle weakness or potential for arrhythmia.
Metabolic alkalosis.
Secondary hyperaldosteronism is a renin-dependent oversecretion of the mineralocorticoid aldosterone secreted from the zona glomerulosa of the adrenal cortex.
Renin is released from the JGA as a response to decreased renal perfusion pressure. Osmoreceptors in the macula densa will also stimulate renin release in the presence of decreased sodium concentration in the distal tubule.
Renin enzymatically alters angiotensinogen to angiotensin I. ACE (found in the pulmonary and renal vascular endothelium) then converts angiotensin I to angiotensin II. Angiotensin II, a potent vasoconstrictor, then stimulates release of aldosterone from the zona glomerulosa of the adrenal medulla.
Aldosterone promotes restoration of circulating volume by correcting water and sodium depletion.
Diagnosis is suggested by increases in both plasma renin (>2 ng/mL) and aldosterone, but the ratio of plasma aldosterone concentration to renin activity is <10 ng/dL per ng/mL/h (ratio >35 strongly suggests primary hyperaldosteronism).
In some situations, such as pregnancy and chronic renal disease, increased aldosterone is an adaptive response and is not necessarily deleterious.
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