unique1
InGodITrust
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We have adema in secondary hyperaldosteronism while there is no edema in primary hyperaldosteronism (Conn's syndrome ) . Aldosterone level is raised in both and salt and water retention takes place in both. Then why not edema in both ?
Does it have something to do with renin level? Please shed some light . Thanks in advance.
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| epica
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Yes, you right.
In Secondary Hyperaldost ( due to Renal artery stenosis or Nephrotic) kdney
PERCEPTION of low intravascular volume ---- results in overactive Renin-Agtensin system.
So, if u have low IV volume---- Renin is high and v.s.
Primary (Conn's)---- caused by Aldosterone secreting tumor ( Na is up, BP will be high, K is low hypertension) LOW PLASMA RENIN
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| epica
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Let me clarify and open our disccussion.
Why we don't have Edema?
Increase in Sodium and water retention is prevented by "Na escape" only in primary but not in secondary . Kaplan is telling that mechanism is not well understood but probably because of ANF.. So, in secondary, no"escape" of Na, MORE NA-----EDEMA
Guys, correct me and add your explanation.
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| me007
Forum Guru
Topics: 72
Posts: 803
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it is from Goljan's explanations
reason for the lack of pitting edema in prim hyperaldosteronism.
1. incr EABV from excess Na+ and water in ECF compartment
2.This lead to increased peritubulary hydrostatic pressure, what will prevent prox tub reabsorbtion of Na+.
Majority of Na is reabs in prox tubule.
Na/K aldosterone -enhanced pump is already max functioning and cannot reabs Na+ - called "escape mechanism"
increased Na loss from the prox tubule is almost equal the amount of Na reabsorbed by aldosterone.
Slight incr in TBNa present, but it is not detectable as pitting edema.
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| epica
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Very Good me 007!!!
I forgot to mention very important points. please tell me what happened with GFR and Renal blood flow ?
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| goodies
Forum Junior
Topics: 19
Posts: 39
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what is EABV?
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| epica
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Effective arterial blood volume (EABV)
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| new_n_lost
Politically InCorrect
Topics: 652
Posts: 6,066
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Primary aldosteronism or primary hyperaldosteronism refers to a renin-independent increase in the secretion of aldosterone. Approximately 99% of cases of primary aldosteronism are due to either an aldosterone-producing adenoma ([APA] approximately 40% of cases) or idiopathic hyperaldosteronism ([IHA] approximately 60% of cases, almost all of which are bilateral). Adrenocortical carcinomas that are purely aldosterone secreting are exceedingly rare and are usually large at the time of diagnosis. Unilateral adrenocortical hyperplasia is a rare occurrence.
That said its the reason why dont we have non pitting edma is that renin - angiotensin -aldosterone axis is not blunted we will have low renin activity as a response to high aldosterone levels.
Furthermore, Sec. Hyperaldosteronism this represents a diverse group of disorders characterized by physiologic activation of the renin-angiotensin-aldosterone (R-A-A) axis as a homeostatic mechanism designed to maintain serum electrolyte concentrations or fluid volume. In the presence of normal renal function, it may lead to hypokalemia. Secondary hyperaldosteronism can be divided into 2 categories depending on whether associated hypertension exists. The former category includes renovascular hypertension, which results from renal ischemia and hypoperfusion leading to activation of the R-A-A axis. The most common causes of renal artery stenosis in children are fibromuscular hyperplasia and neurofibromatosis. Hypokalemia may occur in up to 20% of patients.
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| new_n_lost
Politically InCorrect
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Me007 has done an excellent job of reproducing the facts mentioned by Goljan which truly isnt explained in any other book.
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FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."
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| unique1
InGodITrust
Topics: 19
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Thank you so much epica, me007 and nnl .
It is not explanined even in Robbins 
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