Primary Hyperaldosteronism (Conn’s disease).
- Aldosterone-secreting adrenal adenomas are the most common cause of Conn's syndrome, accounting for 65% of cases. Idiopathic hyperaldosteronism, which includes primary adrenal hyperplasia, makes up 30-40% of Conn's syndrome cases.
- The main effect of aldosterone is to stimulate the absorption of sodium and the excretion of potassium and hydrogen ions at the distal renal tubule. Thus, overproduction of aldosterone by tumors or hyperplastic zona glomerulosa cells can result in sodium retention, hypertension, hypokalemia, and metabolic alkalosis.
- Despite the increase in sodium absorption, hypernatremia in primary hyperaldosteronism is mild and rarely observed with mineralocorticoid excess. This can be explained by the phenomenon of "aldosterone escape". High aldosterone levels cause increased renal sodium and water absorption, thus raising renal blood flow and GFR, which in turn increase the rate of sodium excretion from the renal tubules. Moreover, the increase in intravascular volume stimulates the release of atrial natriuretic peptide, which causes natriuresis (aldosterone scape phenomenon). This counteracts the increase in Na reabsorption induced by aldosterone, leading to only a mild increase in extracellular fluid volume that manifests clinically as hypertension without significant edema or hypernatremia.
- Also, there is increased secretion of K and H from tubular cells leading to increased excretion of urinary K and H. As a result, hypokalemia (manifested by weakness and paresthesias) is common in states of aldosterone excess. Increased H excretion by intercalated cells leads to
a reactive increase in HCO3 production and absorption into the interstitium, resulting in
metabolic alkalosis.
- Renin levels are typically very low, due to the hypervolemia.
- SO, hypertension, mild hypernatremia, hypokalemia, metabolic alkalosis, suppressed plasma renin, weakness and paresthesias are highly suggestive of primary mineralocorticoid excess (Conn's syndrome).
- The question may ask you about the electrolyte pattern most likely be seen in Conn's syndrome?
Normal Na, ↓ k, ↑ Bicarbonate.
- Treatment: surgery to remove the tumor and spironolactone (a K sparing diuretic that works
by acting as an aldosterone antagonist).
Secondary Hyperaldosteronism.
- An overactive renin-angiotensin system is often due to the kidney's perception of low intravascular volume.
- In many cases, this is due to a primary over-secretion of renin, which is secondary to a decrease in renal blood flow and/or pressure.
- Examples include renal arterial stenosis, narrowing via atherosclerosis, fibromuscular hyperplasia, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome.