BP Meds possibly linked to kidney damage

[MyNameIsJeff]

Question. What about those of us who take a ARB (eg Telmisartan 40mg) and a beta blocker (eg Inderal 60mg)? I love that my blood pressure is 120/80 but I don't want to crash my kidneys doing it right?

ARB plus beta blocker is also a great combination. However, non-selective and non-vasodilating beta blockers such as Propranolol are not ideal in terms of renal function:

The nonselective β-blocker propranolol diminishes renal perfusion by lowering cardiac output and renal perfusion pressure, thereby stimulating reflex α1-vasoconstrictor activity while blocking β2-mediated vasodilation. Most studies have shown that the chronic administration of propranolol results in the reduction of RBF and GFR.55

[...]

Lowering blood pressure with nonselective (propranolol) or selective (metoprolol, atenolol) β-blockers is associated with compensatory stimulation of the SNS and renin–angiotensin systems, leading to elevated NE and renin levels. Subsequent activation of vascular α-adrenergic receptors results in an increase in systemic as well as RVR. Vasoconstriction is further exacerbated with nonselective β-antagonists because of the blockade of β2-mediated vasodilation. It has been known for a long time that propranolol increases RVR and reduces RBF and GFR.59,82 Conversely, α1-blockers such as prazosin and doxazosin enhance renal perfusion.59 In addition, whereas β-blockers reduce insulin sensitivity and promote proatherogenic lipoprotein changes, α1-blockers have the opposite effect.46 Consequently, nonselective β-blockers with adjunctive α1-blocker activity have been developed that attenuate renal nerve activity and could preserve RBF and GFR. Two such agents, labetalol and carvedilol, have been evaluated in hypertensive patients with and without renal impairment.

https://www.sciencedirect.com/science/article/pii/S0085253815518735

Further problems with Propranolol are the relatively short half-life and potential adverse effects such as reduced insulin sensitivity, ED, etc. So rather than Propranolol, I would favor cardio-selective and vasodilating beta blockers such as Carvedilol or Nebivolol. With that being said, I also love Propranolol for its psychological effects (I take it before important meetings/presentations), and it's very far from crashing your kidneys. Just not the ideal drug for this particular purpose.

 

[tornquad201]

Obviously we know that PEDS raise BP am curious to how many have a problem with caffeine , energy drinks I read a study from a cardiologist that said caffeine cause you to be vascular resistant.

 

[Muay Thai]

ARB plus beta blocker is also a great combination. However, non-selective and non-vasodilating beta blockers such as Propranolol are not ideal in terms of renal function:

https://www.sciencedirect.com/science/article/pii/S0085253815518735

Further problems with Propranolol are the relatively short half-life and potential adverse effects such as reduced insulin sensitivity, ED, etc. So rather than Propranolol, I would favor cardio-selective and vasodilating beta blockers such as Carvedilol or Nebivolol. With that being said, I also love Propranolol for its psychological effects (I take it before important meetings/presentations), and it's very far from crashing your kidneys. Just not the ideal drug for this particular purpose.

doc had me taking prazosin and PROPRANOLOL. quit prazosin a while ago. supposed to help with my psycho nightmares. I had kidney failure recently

 

[trackstar19]

This thread is very much in my wheelhouse/interests.

Backstory:
2020 diagnosed with stage 3B/stage 4 CKD due to rare (1/1,000,000) autoimmune disease called c3g. Gfr was 40 and I was spilling 17,000mg protein in my 24 hour urine. Renal biopsy showed ~70% scarring … top nephrologists advised dialysis was imminent and if I get a transplant the disease returns in 85% of cases and destroys new kidney typically within 18 months. Told I could never workout again.

2021: Got a horrid case of Covid and at ER discovered my ejaction fraction was down to 26%.

Fast forward to now:
Gfr: 110 (up from 40)
24 hour protein spillage: 450mg (Down from 17,000mg)
EF: 55% (up from 26%)
BP: 110/65
Heart Rate: 50

Physique: In the middle of prep for a classic physique show 215lbs 7-8% BF.

The only two western medicines I utilize in my daily stack is an arb (100mg losartan), and a beta blocker (25mg metoprolol) everything else is a combination of supplements, diet, peptides, lifestyle, etc.

I dove heavy into figuring out how to heal the kidneys and heart - I refused to take the prognosis given by the doctors and, more so, trust myself to be able to heal myself better than these inept doctors. I’m considering doing a second kidney biopsy when I am finished what I’m doing to prove I regenerated my 70% scarred kidneys in a meaningful way.

Biggest thing I can recommend is doing meaningful research and knowing exactly what you are taking and doing … choosing to be ignorant when it comes to your health and trusting the doctors is a fools route to death/poor health.

 

[Soalian]

Let explore why, despite their potential side effects, ARBs/ACEis are still superior to CCBs in terms renoprotection.

Effect of Ramipril vs Amlodipine on Renal Outcomes in Hypertensive Nephrosclerosis

Context Incidence of end-stage renal disease due to hypertension has increased in recent decades, but the optimal strategy for treatment of hypertension to prevent renal failure is unknown, especially among African Americans.Objective To compare the effects of an angiotensin-converting enzyme...

jamanetwork.com

The figure below (from the same paper) nicely illustrates how CCBs (like Amlodipine) lead to an increase in proteinuria. Proteinuria is one of the strongest predictors for, and potentially causes of, worsening kidney function.

In line with this finding, we can see that at least in the medium term (3 years after initiation of medication), end-stage renal disease and death were more frequent in those who receive a CCB (like Amlodipine) instead of an ACEi (like Ramipril). We know from Mann et al. (2008) that the deleterious effects of excess RAS suppression already occur after 3 years (see the red line in the graph in post#64).
So if these negative effects of reasonably-dosed RAS suppressing drugs (like an ACEi or an ARB) are real, then they are already baked into the cake in the below graph. However, despite those negative effects of RAS suppressing drugs, they are still superior to CCBs in terms of preventing death and progression to ESRD.

It is worth noting that the size of the advantage of the ACEi over the CCB depended on the state of the patients' kidney health when they started medication. The stronger the initial level of proteinuria, the higher the benefit of using an ACEi rather than a CCB. But even at low initial levels of proteinuria, the ACEi is likely superior:





As most readers will know, ACEis and ARBs have a very similar mechanism of action, and ARBs are generally considered equally effective as ACEis, but have better tolerability. Hence why the above results also apply to ARBs and not just ACEis. And among class of ARBs, Telmisartan is considered one of the best (for reasons that have been discussed on this forum at length).

thank you for this, I was actually looking into this issue as well, because as a result of low serum sodium level readings over my last two blood panel tests,

GP switch me from ramipril to amlodipine (have been 150/160-90/100 hypertensive for about two years before without meds, with lifestyle changes)

After a bit of research, I found out about the issue it might cause about four weeks into the 10mg ED Amlodipine treatment, aka, as you described, at any given mean arterial blood pressure level, the amlodipine-induced afferent arteriole vasodilation will increase the intraglomerular pressure overall,

and that, despite the overall BP-lowering effects of the amlodipine.

Moreover, alongside the amlodipine I've been upping my dietary sodium intake significantly (diet was poor in salt overall before).

Now daily BP stands at about 140-150/90-95 average on the daily, and this is WITH the amlodipine, and reducing salt intake again as well,

which would mean, from that same hypothesis, that the corresponding renal perfusion pressure would actually correspond to what you would get at HIGHER BP levels, if not on the amlodipine, like the actual glomerular pressure I get while on the CCB could be equivalent to that of a 160-170/100-110 without meds, maybe, maybe more?)

(Amlodipine increase RPP, because it dilates the afferent arteriole, while having little effect on the efferent arteriole, therefore increasing intraglomerular pressure, as you also described).

Knowing that, I asked my GP to run new blood tests to see where sodium levels are at, but still, with sodium levels now in range, she won't switch me to an ACEi/ARB instead for now, told me to keep going with the amlodipine because four weeks isn't long enough to assess effects of the drug on BP levels, according to her.

As a result, I stopped taking the amlodipine anyway; I'd rather have slighlty higher BP levels without it, than going through with it for any longer.

From following the above hypothesis, I cannot allow myself to run the amlodipine without a strong justification anymore; the benefits simply aren't there, worse, it might be impairing my renal function on the whole, because of the increase of the renal perfusion pressure from the increased arteriolar vasodilation, without any corresponding dilation of the efferent arterioles.

 

[Ranchhand]

From following the above hypothesis, I cannot allow myself to run the amlodipine without a strong justification anymore; the benefits simply aren't there, worse, it might be impairing my renal function on the whole, because of the increase of the renal perfusion pressure from the increased arteriolar vasodilation, without any corresponding dilation of the efferent arterioles.

In the last couple of years I threw in Amlodipine with Telmisartan. Amlodipine definitely helped lower my BP, not quite as much as Telmisartan has, been it did make an impact. But earlier this year I did stop using Amlodipine, wasn't comfortable with the potential sides like renal impairment and the fact that it's a CCB.

 

[Ruhlfreak55]

This thread is very much in my wheelhouse/interests.

Backstory:
2020 diagnosed with stage 3B/stage 4 CKD due to rare (1/1,000,000) autoimmune disease called c3g. Gfr was 40 and I was spilling 17,000mg protein in my 24 hour urine. Renal biopsy showed ~70% scarring … top nephrologists advised dialysis was imminent and if I get a transplant the disease returns in 85% of cases and destroys new kidney typically within 18 months. Told I could never workout again.

2021: Got a horrid case of Covid and at ER discovered my ejaction fraction was down to 26%.

Fast forward to now:
Gfr: 110 (up from 40)
24 hour protein spillage: 450mg (Down from 17,000mg)
EF: 55% (up from 26%)
BP: 110/65
Heart Rate: 50

Physique: In the middle of prep for a classic physique show 215lbs 7-8% BF.

The only two western medicines I utilize in my daily stack is an arb (100mg losartan), and a beta blocker (25mg metoprolol) everything else is a combination of supplements, diet, peptides, lifestyle, etc.

I dove heavy into figuring out how to heal the kidneys and heart - I refused to take the prognosis given by the doctors and, more so, trust myself to be able to heal myself better than these inept doctors. I’m considering doing a second kidney biopsy when I am finished what I’m doing to prove I regenerated my 70% scarred kidneys in a meaningful way.

Biggest thing I can recommend is doing meaningful research and knowing exactly what you are taking and doing … choosing to be ignorant when it comes to your health and trusting the doctors is a fools route to death/poor health.

I'd be curious as to an update from you. What caused the heart situation to begin with? Is it also the c3g?

 

[OuchThatHurts]

ARB plus beta blocker is also a great combination. However, non-selective and non-vasodilating beta blockers such as Propranolol are not ideal in terms of renal function:

https://www.sciencedirect.com/science/article/pii/S0085253815518735

Further problems with Propranolol are the relatively short half-life and potential adverse effects such as reduced insulin sensitivity, ED, etc. So rather than Propranolol, I would favor cardio-selective and vasodilating beta blockers such as Carvedilol or Nebivolol. With that being said, I also love Propranolol for its psychological effects (I take it before important meetings/presentations), and it's very far from crashing your kidneys. Just not the ideal drug for this particular purpose.

Thanks for the info. I asked my doc about prescribing nebivolol instead of propranolol and he asked incredulously, “Why would you want to do that?” I said, “I’m not really sure.” He just laughed.

But yes, before any big talk I have to make, this destroys the butterflies you get right beforehand. I take it on a PRN basis. Maybe 3 or 4 days a week.

Also, with these kids running around like monkeys, my nerves get on edge and even the telmisartan doesn’t keep it down where I want it. But I got the propranolol originally for the tachycardia (rapid heart beat). It works great. My kidneys seem fine. My renal values (which don’t tell the full story) but those are normal.

I use to do low salt for BP reasons but I need the electrolytes. Feel so much better increasing my salt intake. Seems counterintuitive to take in sodium which increases BP while taking Telmisartan to lower it but this is where I am.

edit: just thinking out loud but maybe the GH, tren, and propranolol combo (all lowering insulin sensitivity) is why Metformin and berberine does so well with me?

 

[OuchThatHurts]

Obviously we know that PEDS raise BP am curious to how many have a problem with caffeine , energy drinks I read a study from a cardiologist that said caffeine cause you to be vascular resistant.

Yes. Stims, even caffeine are almost all vasoconstrictors. That’s why caffeine drinks are not recommended on my bigger climbs (mountains). They’re constrictors and also many have a diuretic effect (dehydrating). Two things an athlete does NOT want.

*exception would be pre-contest but even then, use with caution alongside anther diuretics, e.g. thiazides, because of excess electrolyte loss. You don’t want to be mainlining pedialyte LOL.

 

[Soalian]

Thanks for the info. I asked my doc about prescribing nebivolol instead of propranolol and he asked incredulously, “Why would you want to do that?” I said, “I’m not really sure.” He just laughed.

But yes, before any big talk I have to make, this destroys the butterflies you get right beforehand. I take it on a PRN basis. Maybe 3 or 4 days a week.

Also, with these kids running around like monkeys, my nerves get on edge and even the telmisartan doesn’t keep it down where I want it. But I got the propranolol originally for the tachycardia (rapid heart beat). It works great. My kidneys seem fine. My renal values (which don’t tell the full story) but those are normal.

I use to do low salt for BP reasons but I need the electrolytes. Feel so much better increasing my salt intake. Seems counterintuitive to take in sodium which increases BP while taking Telmisartan to lower it but this is where I am.

edit: just thinking out loud but maybe the GH, tren, and propranolol combo (all lowering insulin sensitivity) is why Metformin and berberine does so well with me?

You just alluded to one crucial point regarding kidney health: barring overt proteinuria and confirmed decreased eGFR in successive blood tests over a period of months,

available kidney tests that are presently being done in medical settings are really poor at detecting mild kidney damage, instances of mild AKI, and incipient CKD (you get decreased eGFR further along into CKD, you can spend YEARS with ongoing kidney damage and early CKD, without any changes in eGFR/Cystatin C values, nor any amount of detectable proteinuria, nor any noticeable symptoms, and of course without anybody knowing what's really going on on the inside).

The glomeruli seems to be able to maintain adequate glomerular filtration, even in the presence of nephron loss, tubular damage, and glomerular sclerosis.

As regards kidney health, well, you'll most likely won't know about having overt kidney damage and CKD, until you know from available routine tests.

And at this point, CKD is a very specific condition in that, once the kidney damage manifestly shows through blood and urine tests and/or individual symptoms, it's likely the disease will be that far advanced, that the accumulated renal damage won't be reversible; you basically almost never know about evident kidney damage until its too late.

 

[whacked]

Guys try Irbesartan instead of telmisartan, it is kidney protective

I thought Telmi was too

Shoot me

 

[OuchThatHurts]

You just alluded to one crucial point regarding kidney health: barring overt proteinuria and confirmed decreased eGFR in successive blood tests over a period of months,

available kidney tests that are presently being done in medical settings are really poor at detecting mild kidney damage, instances of mild AKI, and incipient CKD (you get decreased eGFR further along into CKD, you can spend YEARS with ongoing kidney damage and early CKD, without any changes in eGFR/Cystatin C values, nor any amount of detectable proteinuria, nor any noticeable symptoms, and of course without anybody knowing what's really going on on the inside).

The glomeruli seems to be able to maintain adequate glomerular filtration, even in the presence of nephron loss, tubular damage, and glomerular sclerosis.

As regards kidney health, well, you'll most likely won't know about having overt kidney damage and CKD, until you know from available routine tests.

And at this point, CKD is a very specific condition in that, once the kidney damage manifestly shows through blood and urine tests and/or individual symptoms, it's likely the disease will be that far advanced, that the accumulated renal damage won't be reversible; you basically almost never know about evident kidney damage until its too late.

We’ve discussed this at length and you’re spot on. I currently have no reason to think I have kidney damage of any sort. I had my kidneys, liver, and gall bladder looked at via ultrasound and I’m told all is well.

 

[trackstar19]

I'd be curious as to an update from you. What caused the heart situation to begin with? Is it also the c3g?

I actually just had blood work and tests Friday ….. EF is still at 55% (up from 26%) GFR is still over 100 (up from 40) and 24 hour protein spillage is 418 presently (down from 17,000mg).

I’m currently finishing off season and transitioning into prep now. 5’10.5 235lbs in attached photos.

We never found an exact cause of my heart issues. The cardiologists hypothesized plenty (as did I) but essentially could be c3g related, they thought maybe sarcadosis, or (less likely) purely from Covid. My system has kept it at bay where the most recent echocardiogram showed the weakened damage parts of the heart (85% of the walls of my heart were infiltrated with something as per the MRI/scans) were no longer there. I effectively replaced the weakened parts with new healthy tissue and there aren’t any signs of it reoccurring presently. Cardiologist bumped me back to just yearly visits now to be safe but he thinks I fixed it and have kept it at bay.

Fingers crossed it stays this way - I had such a grim prognosis I am so wildly grateful I was born with the brain I was. Otherwise I’d likely be dead.

 

[whacked]

Not to derail but be careful or uric acid levels increasing on Beta Blockers, sadly, even Nebivolol.

Ps. Uric acid levels are now considered far beyond what they used to be for overall health risks (research Dr Richard Johnson and Dr Perlmutter). It is not just for gout concerns….heart disease, kidney disease, increased mortality risk. Just to name a few concerns when uric acid is elevated.

 

[Ruhlfreak55]

I actually just had blood work and tests Friday ….. EF is still at 55% (up from 26%) GFR is still over 100 (up from 40) and 24 hour protein spillage is 418 presently (down from 17,000mg).

I’m currently finishing off season and transitioning into prep now. 5’10.5 235lbs in attached photos.

We never found an exact cause of my heart issues. The cardiologists hypothesized plenty (as did I) but essentially could be c3g related, they thought maybe sarcadosis, or (less likely) purely from Covid. My system has kept it at bay where the most recent echocardiogram showed the weakened damage parts of the heart (85% of the walls of my heart were infiltrated with something as per the MRI/scans) were no longer there. I effectively replaced the weakened parts with new healthy tissue and there aren’t any signs of it reoccurring presently. Cardiologist bumped me back to just yearly visits now to be safe but he thinks I fixed it and have kept it at bay.

I tend to agree with you about doctors. They have their use, but problem solving is really not part of their skillset per se. When presented with any kind of non-nominal situation they really lack the ability to critically think and SOLVE problems. At that point they're just treating symptoms and preparing you for 'living with it'.

Obviously not ALL doctors are this way, but on average it seems like they are. Good to hear you're still doing well.

 

[trackstar19]

I tend to agree with you about doctors. They have their use, but problem solving is really not part of their skillset per se. When presented with any kind of non-nominal situation they really lack the ability to critically think and SOLVE problems. At that point they're just treating symptoms and preparing you for 'living with it'.

Obviously not ALL doctors are this way, but on average it seems like they are. Good to hear you're still doing well.

Thanks man, I appreciate you asking. I agree there are some good doctors but most do not have the time (or care?) to problem solve for patients. Revolving door of trying to see as many patients as they can and it just is a shit system. Why I so strongly believe we must be our own biggest advocates and there is no excuse to not be read up and capable of problem solving our own health issues when warranted. Pubmed/google has so much great info - my disease is so rare but it had enough for me to make some hypothesis’s and a starting point for my self experimentations to find a solution. It’s half an issue with doctors not caring but also patients don’t care. Majority of population have shit diets, shit lifestyles, and zero care in bettering themselves or doing the readily available research to improve their situations. Society has gone to shit.

 

[Soalian]

thank you for this, I was actually looking into this issue as well, because as a result of low serum sodium level readings over my last two blood panel tests,

GP switch me from ramipril to amlodipine (have been 150/160-90/100 hypertensive for about two years before without meds, with lifestyle changes)

After a bit of research, I found out about the issue it might cause about four weeks into the 10mg ED Amlodipine treatment, aka, as you described, at any given mean arterial blood pressure level, the amlodipine-induced afferent arteriole vasodilation will increase the intraglomerular pressure overall,

and that, despite the overall BP-lowering effects of the amlodipine.

Moreover, alongside the amlodipine I've been upping my dietary sodium intake significantly (diet was poor in salt overall before).

Now daily BP stands at about 140-150/90-95 average on the daily, and this is WITH the amlodipine, and reducing salt intake again as well,

which would mean, from that same hypothesis, that the corresponding renal perfusion pressure would actually correspond to what you would get at HIGHER BP levels, if not on the amlodipine, like the actual glomerular pressure I get while on the CCB could be equivalent to that of a 160-170/100-110 without meds, maybe, maybe more?)

(Amlodipine increase RPP, because it dilates the afferent arteriole, while having little effect on the efferent arteriole, therefore increasing intraglomerular pressure, as you also described).

Knowing that, I asked my GP to run new blood tests to see where sodium levels are at, but still, with sodium levels now in range, she won't switch me to an ACEi/ARB instead for now, told me to keep going with the amlodipine because four weeks isn't long enough to assess effects of the drug on BP levels, according to her.

As a result, I stopped taking the amlodipine anyway; I'd rather have slighlty higher BP levels without it, than going through with it for any longer.

From following the above hypothesis, I cannot allow myself to run the amlodipine without a strong justification anymore; the benefits simply aren't there, worse, it might be impairing my renal function on the whole, because of the increase of the renal perfusion pressure from the increased arteriolar vasodilation, without any corresponding dilation of the efferent arterioles.

My GP finally agreed to put me on Irbesartan instead of a CCB;

I went off the Amlodipine anyway after researching the deleterious effects of L-type CCBs (which preferably dilate the afferent arteriole over the efferent arteriole, leading to increased Renal Perfusion Pressure) on glomerular hypertension (increased intraglomerular pressure, which over time might lead to hypertensive nephropathy in the form of consequent accumulated tubulointerstitial damage, overall nephron loss, and lead to glomerulosclerosis).

 

[Flex500]

Let explore why, despite their potential side effects, ARBs/ACEis are still superior to CCBs in terms renoprotection.

Effect of Ramipril vs Amlodipine on Renal Outcomes in Hypertensive Nephrosclerosis

Context Incidence of end-stage renal disease due to hypertension has increased in recent decades, but the optimal strategy for treatment of hypertension to prevent renal failure is unknown, especially among African Americans.Objective To compare the effects of an angiotensin-converting enzyme...

jamanetwork.com

The figure below (from the same paper) nicely illustrates how CCBs (like Amlodipine) lead to an increase in proteinuria. Proteinuria is one of the strongest predictors for, and potentially causes of, worsening kidney function.

In line with this finding, we can see that at least in the medium term (3 years after initiation of medication), end-stage renal disease and death were more frequent in those who receive a CCB (like Amlodipine) instead of an ACEi (like Ramipril). We know from Mann et al. (2008) that the deleterious effects of excess RAS suppression already occur after 3 years (see the red line in the graph in post#64).
So if these negative effects of reasonably-dosed RAS suppressing drugs (like an ACEi or an ARB) are real, then they are already baked into the cake in the below graph. However, despite those negative effects of RAS suppressing drugs, they are still superior to CCBs in terms of preventing death and progression to ESRD.

It is worth noting that the size of the advantage of the ACEi over the CCB depended on the state of the patients' kidney health when they started medication. The stronger the initial level of proteinuria, the higher the benefit of using an ACEi rather than a CCB. But even at low initial levels of proteinuria, the ACEi is likely superior:





As most readers will know, ACEis and ARBs have a very similar mechanism of action, and ARBs are generally considered equally effective as ACEis, but have better tolerability. Hence why the above results also apply to ARBs and not just ACEis. And among class of ARBs, Telmisartan is considered one of the best (for reasons that have been discussed on this forum at length).

I have always loved your posts sir! Thank you. I do have a question for you (I am not taking anything you say as medical advice and understand fully you do not present it as medical advice). I was on lisinopril for years and after about a decade it became less effective so my doc put me on amplodipine and it's been working "ok". No sides or anything, bloods are fine, but it isn't impacting my blood pressure as much as I hoped. My doc and I are pretty close and I'm wondering if trying telmisartan may be worth it?

I'm just curious overall as it seems many guys are in my shows where they did the old school lisinopril for a while, it lost effectiveness, and then moved to amlodipine. Just curious on your thoughts overall? For longterm overall health would it be better to move to telmisartan?

 

[Ranchhand]

my doc put me on amplodipine and it's been working "ok". No sides or anything, bloods are fine, but it isn't impacting my blood pressure as much as I hoped. My doc and I are pretty close and I'm wondering if trying telmisartan may be worth it?

Amlodipine and Telmisartan are frequently used together with great success at lower BP. For a little while I used both and it brought my BP down into the lower healthy range of 120/80. Sometimes I would get readings lower than both top and bottom numbers of 120/80. I did stop using Amlodipine though for health reasons associated with the known sides from it and the fact it's a CCB. Still using Telmisartan and it's been effective on its own, just not as much as the two combined together.

 

[Soalian]

Amlodipine and Telmisartan are frequently used together with great success at lower BP. For a little while I used both and it brought my BP down into the lower healthy range of 120/80. Sometimes I would get readings lower than both top and bottom numbers of 120/80. I did stop using Amlodipine though for health reasons associated with the known sides from it and the fact it's a CCB. Still using Telmisartan and it's been effective on its own, just not as much as the two combined together.

I'm curious, what side effects did you get with the amlodipine that made you stop?

When you write that you stopped it because of "the fact that it's a CCB", can you explain what you meant with that (known adverse mechanism from the drug?)? Is it related to the effects L-type CCBs have on increasing intraglomerular pressure, therefore putting one at risk for increased glomerular damage with time?

Thank you.