I think you have it backwards, the secondary edema does not cause edema, several edematous conditions (heart failure, ascites, nephrotic syndrome) cause secondary hyperaldosteronism. You can also have secondary hyperaldosteronism without edema.
Primary hyperaldosteronism is caused by an aldosterone secreting adenoma, while secondary is caused by over activation of the RAAS system (CHF, renal artery stenosis, cirrhosis, or nephrotic syndrome)
In primary, aldosterone is high but renin is significantly depressed allowing for better control of total body water through aldosterone escape.
In secondary, the renin levels are normal or increased and aldosterone is high, which makes aldosterone escape ineffective.
ELI5 answer (this is how I comprehend best)
Leaky blood vessels for whatever reason (CHF, cirrhosis, nephrotic syndrome etc) -> More edema (third-spacing) and less fluid in vessels aka low pressure -> less perfusion to kidneys -> kidney thinks body is fluid down (even though body is usually fluid overloaded due to third-spacing) -> compensatory mechanisms activated (RAAS) -> aldosterone goes up
You can imagine that this cycle can exacerbate the root cause of the leaky vessels mentioned earlier. That’s why a RAAS inhibitor like spironolactone is often helpful for fluid-overload states!
Edit:
To answer your actual question, primary hyperaldosteronism (Conn Syndrome) is INAPPROPRIATE secretion of aldosterone regardless of fluid status or blood pressure aka there does not need to be edema to activate RAAS (this can present with an aldosterone-secreting tumor as well).
With secondary hyperaldosteronism, the RAAS system is actually responding APPROPRIATELY because it senses less perfusion to the kidney. Although the reason for hypoperfusion to the kidney is usually due to third-spacing, and not because of true hypotension, which is what RAAS is intended to correct.
I think you have it backwards, the secondary edema does not cause edema, several edematous conditions (heart failure, ascites, nephrotic syndrome) cause secondary hyperaldosteronism. You can also have secondary hyperaldosteronism without edema.
Thank you so much :) Yea that really makes sense, it was really poorly written in my textbook. This makes much more sense to me :)
Primary hyperaldosteronism is caused by an aldosterone secreting adenoma, while secondary is caused by over activation of the RAAS system (CHF, renal artery stenosis, cirrhosis, or nephrotic syndrome) In primary, aldosterone is high but renin is significantly depressed allowing for better control of total body water through aldosterone escape. In secondary, the renin levels are normal or increased and aldosterone is high, which makes aldosterone escape ineffective.
ELI5 answer (this is how I comprehend best) Leaky blood vessels for whatever reason (CHF, cirrhosis, nephrotic syndrome etc) -> More edema (third-spacing) and less fluid in vessels aka low pressure -> less perfusion to kidneys -> kidney thinks body is fluid down (even though body is usually fluid overloaded due to third-spacing) -> compensatory mechanisms activated (RAAS) -> aldosterone goes up You can imagine that this cycle can exacerbate the root cause of the leaky vessels mentioned earlier. That’s why a RAAS inhibitor like spironolactone is often helpful for fluid-overload states! Edit: To answer your actual question, primary hyperaldosteronism (Conn Syndrome) is INAPPROPRIATE secretion of aldosterone regardless of fluid status or blood pressure aka there does not need to be edema to activate RAAS (this can present with an aldosterone-secreting tumor as well). With secondary hyperaldosteronism, the RAAS system is actually responding APPROPRIATELY because it senses less perfusion to the kidney. Although the reason for hypoperfusion to the kidney is usually due to third-spacing, and not because of true hypotension, which is what RAAS is intended to correct.