Low Renin And Low Aldosterone

[lotsicker]

I have been confirmed a dysautonomic but, it is a secondary result of the Herpes Virus attacking the spinal column at the base of my neck. I have struggled with this virus my whole life and have a rare form that my body cannot fight off. I am now taking Famvir and BB and paxil.

What was not explained was why I have low renin and low aldosterone yet not the high BP that goes with it.

Anyone else have this issue??

[nunntrio]

I am not sure that I can help with your question. I actually thought low aldosterone was caused by sluggish adrenal glands which caused low BP. I can be wrong thought,

I'm not a hormone expert.

I was wondering how you discovered the primary cause of the virus attacking you spine? Are there any tests for that? I have had some unusual infections and sometime wonder about them being the cause.

Wish I could help you more.

Laurie

[ramakentesh]

Low renin and aldosterone responses are a sign of inappropriate hypovolumia - read Dr Stewart's work on angiotensin II and low flow POTS.

[TXPOTS]

Low renin and aldosterone responses are a sign of inappropriate hypovolumia - read Dr Stewart's work on angiotensin II and low flow POTS.

Dr. Stewart's work confuses me. For example, I have low renin, low aldosterone, and low ADH release (thought to be due to denervation of the kidney and failure of the renin-angiotensin-aldsosterone system per my endocrinologist and POTS specialist). Angiotensin II promotes the release of aldosterone from the adrenals and release of ADH from the pituitary. I am confused as to how an elevation of angiotensin II would lead to a decrease in aldosterone. Anyone understand that mechanism? His theory here seems to be a paradox, but I must be missing something.

[firewatcher]

Have you read the Renin/Aldosterone Paradox article by Dr. Raj? It sort of explains it. I'd love to get your take on it.

[TXPOTS]

Yes, the article in Circulation. Interesting article. Someone please correct me if I am wrong. The renin aldosterone paradox is a state of low renin and low aldosterone despite the POTS patient having hypovolemia. In a normal patient, when circulating blood volume is low, the juxtaglomerular apparatus in the kidney senses this and triggers the renin-aldosterone-angiotensin system. Renin triggers the conversion of angiotensin I to II via angiotensin converting enzyme. Angiotensin II then triggers the adrenals to release aldosterone which causing sodium and water retention. It also facilitates release of ADH in the pituitary. Angiotensin II also causes sodium reabsorption and is a vasoconstrictor. The paradox is that blood volume is low, but this vital system is not being triggered to its full capacity. I don't think even the top POTS researchers understand why as of yet. There are theories such as denervation of the kidney or a structural problem with the juxtaglomerular apparatus itself. There is a part of the puzzle I am not grasping yet from Dr. Stewart's research on low flow POTS, angiotensin II and nitric oxide. Perhaps, this only applies to a subset of patients WITH low renin and aldosterone. Still trying to learn... I wish we had a better grasp on POTS. Hopefully, the future will bring more research and understanding. Is that what you got from the Raj article?

[vemee]

That is what I got from the article. I wonder how people in this category respond to the acth stimulation test?

[firewatcher]

Yes, the article in Circulation. Interesting article. Someone please correct me if I am wrong. The renin aldosterone paradox is a state of low renin and low aldosterone despite the POTS patient having hypovolemia. In a normal patient, when circulating blood volume is low, the juxtaglomerular apparatus in the kidney senses this and triggers the renin-aldosterone-angiotensin system. Renin triggers the conversion of angiotensin I to II via angiotensin converting enzyme. Angiotensin II then triggers the adrenals to release aldosterone which causing sodium and water retention. It also facilitates release of ADH in the pituitary. Angiotensin II also causes sodium reabsorption and is a vasoconstrictor. The paradox is that blood volume is low, but this vital system is not being triggered to its full capacity. I don't think even the top POTS researchers understand why as of yet. There are theories such as denervation of the kidney or a structural problem with the juxtaglomerular apparatus itself. There is a part of the puzzle I am not grasping yet from Dr. Stewart's research on low flow POTS, angiotensin II and nitric oxide. Perhaps, this only applies to a subset of patients WITH low renin and aldosterone. Still trying to learn... I wish we had a better grasp on POTS. Hopefully, the future will bring more research and understanding. Is that what you got from the Raj article?

I'm a little fuzzy headed today (post workout crash) but yes, that is what I got from the article. This is where I think the endocrine, hypothalamic, ADH abnormalities may come it. Either to hypoperfusion or negative feedback from inappropriate vasoconstriction, the whole endocrine shebang is blunted. Just a personal theory though. I had my renin/aldosterone tested by my endo and my numbers fit just above the POTS patients and just below "normals," and I have no measurable ADH secretion during any test.

[TXPOTS]

That is what I got from the article. I wonder how people in this category respond to the acth stimulation test?

Hi Vemee,

I don't know that I am in this low flow POTS category for sure, but I do have confirmed hypovolemia, low renin, and low aldosterone. I responded normally to the ACTH stimulation test. I was told my adrenals are perfectly healthy, but obviously something else is WAY off.

[vemee]

I responded normally to the stimulation test too but my aldosterone levels were low and from my other post it is because of the beta blocker and midodrine. However, I was looking at my blood work from Vanderbilt ( I think I was part of the study) that was taken several years ago and although my supine aldosterone was low, it jumped up to be in the high end of the normal response when I was standing. My blood volume was normal but pooling was severe so my take is that even though my supine aldosterone was at the low end of the pots group in the supine position it reacted correctly to the volume loss due to pooling. In short this is very confusing and if I had an answer I could do an infomercial.

[TXPOTS]

Good point Vemee,

My understanding is the best way to measure aldosterone and renin is in upright position. Also, my endocrinologist did not want me ingesting much salt prior to test.

[ramakentesh]

Remember that no one has demonstrated denervation of kidney receptors - its a theory and there is unpublished data from a few different research groups that suggest that this is not occuring in POTS.

To prove this point - Vandy arent examining this particular angle so much as they are now focusing on kidney dopamine release. Check out the clinical trials website.

In the low flow scheme of things angiotensin II appears to act paradoxically and blunting the normal renin aldosterine response to orthostatic hypovolumia. Angiotensin II decreases neuronal nitric oxide, causes vasomotor failure and excessive vasoconstriction.

if you could increase nitric oxide activity or increase angiotensin II catabolism in theory the problems would be rectified.

[TXPOTS]

Remember that no one has demonstrated denervation of kidney receptors - its a theory and there is unpublished data from a few different research groups that suggest that this is not occuring in POTS.

To prove this point - Vandy arent examining this particular angle so much as they are now focusing on kidney dopamine release. Check out the clinical trials website.

In the low flow scheme of things angiotensin II appears to act paradoxically and blunting the normal renin aldosterine response to orthostatic hypovolumia. Angiotensin II decreases neuronal nitric oxide, causes vasomotor failure and excessive vasoconstriction.

if you could increase nitric oxide activity or increase angiotensin II catabolism in theory the problems would be rectified.

An ACE inhibitor would technically decrease formation of angiotensin II. Anyone on an ACE inhibitor? It does appear to be yet another paradox, and one would think a patient's blood pressure would be high if angiotensin II were high, but maybe the drop in aldosterone compensates. This is very interesting. I'll look more into this. Thank you for the response

Quick edit... I just saw an article on the use of losartan, an angiotensin blocker, with good results in low flow POTS (but a small study and no long term prognosis follow up). I am grateful researchers are continuing to explore new theories.

[spaceorca]

I was really interested to see this thread because my son has both low aldosterone (almost non-existent) and low renin activity. Two separate tests demonstrated how low these were, but none of the doctors responded to them at the time. Later, after his POTS diagnosis, he started taking florinef and that helped him a little.

But here's an interesting point I discovered in following up on this research earlier today. UpToDate, which is the database that many doctors use for diagnoses, treatment protocols, etc., notes that many patients with low aldosterone and low renin (or even some with just low aldosterone) also are resistant to the action of aldosterone--so they need more than the usual replacement dose. For someone with impaired adrenal function, the "replacement" dose of aldosterone is 0.1 to 0.2 mg of florinef per day. But patients who are resistant to aldosterone need 0.2 to 1.0 mg of florinef per day according to this database.

This discussion did not refer to POTS--it was a general discussion of how to treat low aldosterone. But it made me wonder: Could some POTS patients benefit from higher doses of florinef than is usually prescribed? Is anyone here taking more than 0.2 mg/day? My son currently takes 0.15 mg/day and that amount seemed to help when he first started the florinef. I'm wondering if he's in the resistant category and if it would be worth increasing. Thanks again for the interesting thread, Debby

[ramakentesh]

Yeah Losarten was the medication being evaluated.

[ramakentesh]

http://www.clinicaltrials.gov/ct2/show/NCT...ral&rank=11

http://www.clinicaltrials.gov/ct2/show/NCT...ral&rank=13

[TXPOTS]

Yeah Losarten was the medication being evaluated.

I imagine an angiotensin II blocker may help a subtype of patients who have vasoconstriction at the level of the kidney from this dopamine mechanism they are researching or from impaired catabolism of angiotensin II. This is IF the theory proves true. Carbidopa should be effective in theory if excess dopamine is involved. Interesting, I'll be be watching and waiting to see how these studies go. Thank you for the links. I wonder why angiotensin II and EPO are not routinely measured in patients with low renin, aldosterone, and suspected hypovolemia. I also wonder why the study does not include measuring angiotensin II levels. I know the sample must be immediately frozen.

Spaceorca,

There are patients who take more. My POTS specialist has a few patients on 0.4mg. Doses over 0.4mg may cause adrenal suppression. Some patients (who can tolerate Florinef in the first place) can't tolerate higher doses because they get the "Florinef headache". I am also on 0.15mg/ day. I tried 0.2mg, but I got the dreaded headache. I do consume 6-8gm of sodium per day. I get my blood drawn periodically to test sodium and potassium levels and take my blood pressure from a home monitor. Some patients tolerate higher doses, so you may want to discuss this with his doctor if your son has found some benefit from the Florinef. If he has severe polyuria, DDAVP can also be a helpful drug to help patients hold on to more fluid. However, with a low aldosterone, he must be on Florinef, because DDAVP can cause low sodium levels. I actually was found to have diabetes insipidus, as well as very low renin and non-existent aldosterone. I had a formal water deprivation test in a hospital setting under close supervision. Just a few thoughts to consider.... the increased Florinef dose, salt, and DDAVP. I hope your son has a quick recovery.

[TXPOTS]

Kimi,

In a nutshell, good question. I think the researchers are trying to figure this out. Patients with pheochromocytoma have episodes of high blood pressure and low renin and low aldosterone. The treatment to reverse this is an alpha antagonist (the opposite of drugs like Midodrine, an alpha agonist) to restore the renin-angiotensin-aldosterone system. Many of us POTS patients have low renin and aldosterone, but have not experienced high blood pressure and are thought to have widespread vasodilation or pooling.. Some hyperadrenergic-POTS patients do have episodes of high blood pressure, but this is not so for all of us. I'd also love to know these answers. So many theories and subtypes of POTS...

[spaceorca]

Thanks, TXPots! My son also was diagnosed with diabetes insipidus through a water deprivation test: This was years ago, before anyone identified the POTS. He was placed on DDAVP, which he still takes, but his response has always been erratic. Sometimes it seems to help, other times it doesn't. And he finds that too much DDAVP creates unbearable urinary retention (i.e., he just can't force the urine out).

All of this, of course, mystified the doctors. If you have central diabetes insipidus, then DDAVP should cure it! If the DDAVP doesn't work, then there must be something wrong with you. (Or, as a nephrologist at Mayo suggested on one memorable occasion: Maybe the lab reported the wrong results from the water deprivation test. That was one of the more extreme examples we saw of a doctor trying to reason away a result that didn't fit with existing patterns.)

My son seems to have widespread endocrine failure along with his dysautonomia. He has hypogonadism (doesn't produce testosterone) and Addison's disease (no cortisol) along with the diabetes insipidus and lack of aldosterone (he had almost none, even when ambulatory, both times he was tested). Some doctors have hypothesized that his immune system or some other inflammatory process attacked a series of his organs (in addition to these endocrine and autonomic problems, he also suffers from Crohn's disease that has required several surgeries, so there's clearly an abnormal inflammatory process in his body). Whatever the underlying cause, it seems reasonable to supplement all of these hormones.

The other odd thing about my son is that he has never been able to hold onto either potassium or sodium. He needed those supplements even before taking DDAVP or florinef, and he takes significant amounts now just to have a normal concentration in his blood.

It's all very hard to figure out but I increasingly think a lot of it revolves around the hypovolemic status of POTS patients and the many factors that can cause that problem. A lot of research suggests that many POTS patients suffer from low blood volume--just not enough going around the veins and arteries! Water, salt, potassium, florinef, DDAVP, etc are all things that help increase blood volume in healthy humans. And if one of these is defective, there may be a good fix for a POTS patient. But there also seems to be a growing suspicion that there's something else wrong, something that's setting the blood volume too low in these patients. So the search for the right combinations or other contributing factors continues! Meanwhile, we'll watch out for that florinef headache--I hadn't heard about that. Best, Debby

[TXPOTS]

Thanks, TXPots! My son also was diagnosed with diabetes insipidus through a water deprivation test: This was years ago, before anyone identified the POTS. He was placed on DDAVP, which he still takes, but his response has always been erratic. Sometimes it seems to help, other times it doesn't. And he finds that too much DDAVP creates unbearable urinary retention (i.e., he just can't force the urine out).

All of this, of course, mystified the doctors. If you have central diabetes insipidus, then DDAVP should cure it! If the DDAVP doesn't work, then there must be something wrong with you. (Or, as a nephrologist at Mayo suggested on one memorable occasion: Maybe the lab reported the wrong results from the water deprivation test. That was one of the more extreme examples we saw of a doctor trying to reason away a result that didn't fit with existing patterns.)

My son seems to have widespread endocrine failure along with his dysautonomia. He has hypogonadism (doesn't produce testosterone) and Addison's disease (no cortisol) along with the diabetes insipidus and lack of aldosterone (he had almost none, even when ambulatory, both times he was tested). Some doctors have hypothesized that his immune system or some other inflammatory process attacked a series of his organs (in addition to these endocrine and autonomic problems, he also suffers from Crohn's disease that has required several surgeries, so there's clearly an abnormal inflammatory process in his body). Whatever the underlying cause, it seems reasonable to supplement all of these hormones.

The other odd thing about my son is that he has never been able to hold onto either potassium or sodium. He needed those supplements even before taking DDAVP or florinef, and he takes significant amounts now just to have a normal concentration in his blood.

It's all very hard to figure out but I increasingly think a lot of it revolves around the hypovolemic status of POTS patients and the many factors that can cause that problem. A lot of research suggests that many POTS patients suffer from low blood volume--just not enough going around the veins and arteries! Water, salt, potassium, florinef, DDAVP, etc are all things that help increase blood volume in healthy humans. And if one of these is defective, there may be a good fix for a POTS patient. But there also seems to be a growing suspicion that there's something else wrong, something that's setting the blood volume too low in these patients. So the search for the right combinations or other contributing factors continues! Meanwhile, we'll watch out for that florinef headache--I hadn't heard about that. Best, Debby

Wow, ME TOO, my response to DDAVP varies from day to day as well, and I get terrible bladder pressure if I try to increase the dose. I am on a tiny dose compared to the typical central DI patients. I am now 34, but my symptoms of DI started when I was 16. I was dismissed and lived with what I thought was an irritable bladder for 18 years! I started getting full blown symptoms of POTS May 2008. I have been struggling to get a diagnosis and recover since. You hit the nail on the head. Something is setting the blood volume in the body too low. It's as if the volume dial is stuck at 4, when it should be at 10. Simply replacing the aldosterone with Florinef and salt, and the ADH with DDAVP does not take the problem away. It does help, but it doesn't fix the underlying issue.

[sue1234]

I have been following this thread, but don't have alot to add. I have a low aldosterone(3) and a low ADH, and was prescribed DDAVP, but kind of scared to take it. Put it this way, I took a half a pill one day and waited all day to see how I felt, but no difference. I tend to get high b/p when standing, and normal when at rest, so I am afraid it will increase my b/p, so didn't continue. Plus, Firewatcher had told me they needed to check urine osmolar(l)ity at the same time, and my doctor had not done that. Just don't know which way to turn!

I just posted a thread on calcium(hypocalcemia) and one place I read says that low calcium can lower aldosterone. I would like some others to give me their take on it. I have had documented low calcium a couple of times over the last few years since developed POTS.

[TXPOTS]

I have been following this thread, but don't have alot to add. I have a low aldosterone(3) and a low ADH, and was prescribed DDAVP, but kind of scared to take it. Put it this way, I took a half a pill one day and waited all day to see how I felt, but no difference. I tend to get high b/p when standing, and normal when at rest, so I am afraid it will increase my b/p, so didn't continue. Plus, Firewatcher had told me they needed to check urine osmolar(l)ity at the same time, and my doctor had not done that. Just don't know which way to turn!

I just posted a thread on calcium(hypocalcemia) and one place I read says that low calcium can lower aldosterone. I would like some others to give me their take on it. I have had documented low calcium a couple of times over the last few years since developed POTS.

I learned the dangers of DDAVP the hard way. Before I met my current endocrinologist who actually has published studies on DI, I was diagnosed with DI without the formal water deprivation test, renin, and aldosterone. I was prescribed DDAVP and ended up in the hospital with hyponatriemia. However, I was on the more potent nasal spray twice a day. I know there are many patients with POTS who take the DDAVP tablet at bed time. I take a small amount in the morning and bed time, buy my dose is low, and I am under the care of a great endocrinologist who checks my chemistry every few weeks and more often in the beginning. She did check my urine osmos in the beginning as well. Maybe you can discuss a bed time dose and your blood pressure concerns with your physician.

[ramakentesh]

I wonder why angiotensin II and EPO are not routinely measured in patients with low renin, aldosterone, and suspected hypovolemia

You tell me ! EPO in particular - there are no studies that have examined this.

I have postural hypertension, low volume (low renin reponse to orthostatic stress) but I still spend most days dealing with cerebral hypoperfusion.

[issie]

This is a bump. Questions brought up in regard to Dopamine being low and the effect it can have on POTS - especially since noriephiprine comes from dopamine. We have started another topic under a question in regard to noriepi. Found this in my search. An old thread with some interesting info.

Issie

[ladyt]

Hello everyone....

I was going to recherarse somthing like aldosterone and i think renin... And then this tread meet me on the forum today

I did try to read and understand it. But i think my brain is gone away, not the normal brainfogg , but the same result...

The 12 of mars i got a sudden change in symtoms. I am uset to sudden changes and things never beibg the same. But this was somthing difrent all togetter...

Having had the pots diagnose since 98 and a worsening of symtoms and many non pots sytoms i have been very very frustraitd at times. And then at the sudden change my subtitut gp, was well usless. She didnt take any test the first week. The second sho took some bascic bloodwork, and after that she finaly referd me to the local hospital..

I was admitted and realeased the same day. But the doc made me take lots more blood than usuall.. Today I had my apionment whit here.. I was gettering all my strength, to be firm and demand some help, cause i knew the bloodwork would show nothing...

Entering the ofice i felt that i had to do what i could to not gett the usual brush of.. She asked some questions and i tryed to respond the best i could... Not always easy whan so many weird stuff in one lilte body

And then she asked me what hormone test i have had done before, and if any of them ever had come back off...

Then she said I had very very low aldosterone and renin (pretty sure that was it).. And the rest of the test of that part of the body (dont know the english name).

She had never seen anything like it. And wounders over wounders, usaly docs then demiss the find, she didnt... She said this was out of here leauge, but she had allreddy called (and probl anoid ) many other docs.. I was really thinking that a doc like this was ust of fairytails...

She whanted to refer me to a nero exam, cause many of my sytoms go that way. And she would try to gett me to a good nero etc. She even said i could come back to here in six mnths so if i was lost in the system again she would help me back... Thats ust , well i am lost for words... She seems to have called other docs the best she can. She said there where other docs, but she couldnt call them, becouse of the chain of comand. Think how many patiens that could gett better care if docs ust could gett over them self..?

But she, she didnt understand my illnes and symtoms, but she orded a bloodtest i never had done before (probl many i never have taken before)..

She had gone back in my medical history and gone trhough all the difrent meds and bloodtest i have taken.. that in it self is a mircal.. And I have never beofre cheched my renin and aldosteron, she didnt understand why, cause they regulate bloodpressure and i evedently have very much problems there...

After i left (feeling really happy, mosty ust cause i feelt the doc really had tryed), she called. She had talked whit this endo doc that spesialty is diabithis patient whit autonimc problems. And he whanted me to take some more tests and depending on what they showed gett an apointment whit him.. So I am not referd to the nero departm of the hosital now (i dont mind that at all)..

And tomorrow i am going early to the hospital to take lots more blood and a empty stomac... Finaly after all this years.. I am sort in shock right now. This might turn nothing up at all. But it seems like if it does so, its because that s right. Cause now i am getting somthimg better than the x-ray vison and standar bloodtests...

Sorry i didnt mean to start ranting about all this, I am very tierd and brain dead, but very happy also.. I whant to learn more about the renin and aldosterone thing...

But i am dens and not the best in englsh.. I didnt understand most whats in this tread, like the hypov somthing..

So can any of u in very very simple words explain what does low renin and low aldosterone meen? Speasly when the other test where fine..?

Sorry about the awfull spelling... I ust wish we all could meet docs like i meet to day.. She didnt have a clue, but she didnt brush me off or ust hide the weird bloodwork etc.. I belve she does here best... I ust hope that a am now on the rigth track to help and understanding... And even if this is another dead end, well I was proven wrong, there are docs that not only admittis to not knowing, but actually tryeds to talk to other docs and find the best solution for the patient....

For the first time my tears after the hospital apointment was happy ons

If any reads trough if u manage to understand tumbs up to u