Mortality in CKD is dominated by the cardiovascular domain. We will more likely die of a cardio related issue than anything else. We are the highest risk group of all groups for cardio related death. Death for cardio reasons is more likely than our progressing to end stages of the disease: "Expressed another way, persons with mild to moderate (stages 1 to 3) CKD are at higher risk of CV events and CV mortality than they are for progression to ESKD (9,10)."
Here's how one paper title describes vascular calcification:
"The Killer of Patients with Chronic Kidney Disease"
Vascular Calcification is the main cardio disease that kills us. There are others, but this is by far the most significant. We need to prevent / limit VC.
Obviously, calcification requires calcium but whilst we need not to over consume (from whence VC), under consumption leads to bone disorder / fragility. Carbon balance is the term. And like climate change we need to be calcium neutral aka balanced. But how that is achieved??
I figured to open a thread on this specific subject(s) so as to start accumulating current information in one place.
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SOME RANDOM BITS OF INFO I've picked up as I go:
Vascular calcification (VC) is influenced by, amongst things, vit K2 levels. We don't want to be deficient in it. A significant cause of vitK2 deficiency in CKD is ... diet. We tend to lower consumption of or go off animal products altogether as the disease progresses. Animal products are comparatively high in vitK2 and is where the general population gets it's K2. We also tend to limit green leaf veg (due to higher potassium levels) which also contains comparatively high levels of vitK2. Hence deficiency is common in the CKD population. There is a blood marker that infers/correlates with vitamin K2 status. It's called dp-ucMGP which is a protein that combats vascular calcification when it is activated by vitK2. High levels of dp-ucMGP indicate low levels of vitK2. High because it's not been activated by K2 and therefore isn't doing the anti-calcification job intended for it. Thus can we be potentially serum checked for K2 levels. I gather it not something routinely checked
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The general population (not CKD) would have a level of dp-ucMGP of something like 300-500 pmol/L. CKD can produce levels in the multiple thousands
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Link 6 below discusses the various ways in which CV occurs. Here's an interesting piece of it. "Uremic Toxins: compared with serum from nonuremic individuals, uremic serum increases the mineralization (aka calcification) of VSMCs (vascular smooth muscle cells > aka blood vessels) and upregulates the expression of Cbfa1/Runx2 and its target protein OPN". The low/very low protein diet regime aims to reduce serum urea levels. But it's not just urea, it's the other toxins not being filtered out which aren't measured. This is another reason why we need to eliminate uremia - it contributes to VC.
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Interesting but requiring translating
"Importantly, as shown by Shanahan and colleagues,19,20,74 changes in VSMC matrix vesicle metabolism induced by hyperphosphatemia and uremia profoundly impair the arterial surveillance normally provided by mural smooth muscle, such as the phagocytic removal of procalcified matrix vesicles and apoptotic bodies."
There are cells that gobble up the crap that would lodge on our blood vessels. Phagocyte - gobbling cell. These cells are the cleaning crew and their work is hindered by hyperphosphatemia and uremia. High phosphorous might be tackled with a med (but it might be allowed to run a bit on the high side). But uremia is tolerated and just goes up and up until you hit the point where the patent side effects of uremia become unbearable/dangerous and you are put on dialysis. But what about the latent work of uremia. Years and years of uremia without manifest symptom = years of uremia hindering the work of the cleaning crew cells protecting your blood vessels. No wonder cardio kills so many before kidneys do.
THE way to tackle uremia is to cut the amount of protein you eat. And so, the pointers towards a low (or supplemented very low ,if need be) protein diet.
Just scanned the 2021 KDIGO guidelines for BP. I was under the impression that systolic was to be managed to <130 (the 2012 KDIGO target as it happens)
Whereas the 2021 guideline has systolic target management at <120. Can't easily see what diastolic ought to be (as I read the 2012 KDIGO and they urged not less than 70, even if it meant letting systolic run higher than optimal (then target was <130)). I imagine diastolic still is important??
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Lee Hull's "Stopping Kidney Disease" is lite on calcium / VC. The papers he cites talks of VC in the context of its occurance in dialysis. That doesn't illuminate us for early stage approaches. He suggests ( but doesn't show adequately) dietary calcium as harmless irrespective of intake whereas calcium supplements do the harm. This may be the result of absorbability?? Lastly, the role of magnesium levels in offsetting calcium effects. Worth exploring that.
Anyone got any further insights into cardiovascular calcification / bone health whether from dietary, supplement, exercise or drug, etc?
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LINK 0
A readable enough paper covering the various elements involved and showing the paucity of progress in this area. Indeed, progress in CKD treatment isn't noteworthy. Dialysis has been around since the 60's I gather. ACE/ARB? That it??
(Note: oldmangreenes link, the one directly below) is an article written by a naturopath who is also selling a book. Neither is necessarily a mark against but you ought to be aware)
If K2 is beneficial then is naturally there's a kicker (there's always a kicker with CKD). If you're on a plant based diet then some of the sources of K2 will now be denied you (my local Tescos always seems to be clean out of natto) and so, perhaps, deficiency.
Deatiled paper on the various mechanisms at play that lead to vascular calcification. Bit of a teckkie read but it can be skimmed to get an idea. Interesting info therein
A readable paper on calcium balance and the downsides of too much (vascular calcification) or too little (bone disorder / oesteoporosis). Found by member 'whats'
I've done quite a bit of reading into K2 over the past year, primarily because of a coeliac diagnosis and implications for bone health.
My understanding is that we used to get enough K2 from grass fed beef/butter as grass fed cows make healthy amounts of K2 in the stomach, but now most commercially kept cows are grain fed we don't get enough from food....that's aside from needing a plant based diet... ....which fortunately I don't......yet.
I have also read everywhere that if we have limited amounts of K2, then the body prioritises using it to transport calcium to do things like repairing artery walls (hence the plaque build up) rather than directing the calcium to bones and teeth, and that some trials show that supplementing is beneficial. I had a heart attack in 2012 due to blocked LAD, so it was a no-brainer for me.
A word of caution though. Because of the coeliac, I was very low on basic nutrients, and amongst other things I was prescribed loading doses of vit D (20,000iu X 2 per week for 7 wks). A few weeks into this regime I bought some K2-MK7. Now, I had read a few articles stating that 100mcg K2 was sufficient for 10,000iu D3, so I took 200mcg. It had a big impact. Within a short space of time my heart and the whole area around it was racing/raging. I was saying out loud "Oh sh*t, oh sh*t, oh sh*t", I've never felt anything like it, and don't want to ever again. It lasted about an hour. I stopped taking the K2.
I've been on a maintenance dose of 2000iu D3 every other day for months now, and re-introduced the K2 at 25mcg (I cut 100mcg tablets), and that hasn't caused me any problems at all. My advice would be to take it slowly.
This was recommended by one of the admins on the thyroid forum (and they are quite well informed regarding excipients and bio available forms etc)
Whilst mentioning thyroid........Have you had your thyroid levels checked. I've done a lot of reading on thyroid/ckd, and there is much about low FT3 levels in the latter stages (with or without having a proper functioning thyroid.......... and whether they tell the patients???). Might be a good idea to get baseline checked now.
Mum (CKD3) supplements with a D3/K2 spray at 2000iu/dy D3 so that is 500mcg K2.
Re fT3, we wrote to her GP a year ago for it's measurement as a possible cause for increased cholesterol (there's a note from Thyroid UK on that, I can send if you wish). The doc agreed but nurse still followed "TSH OK so stop testing" approach 2-3 times since, despite that. We will try again soon otherwise go private.
500 mcg? What I've read indicates its fairly safe to supplement K2. What is this thing with D tied with K2 - the two being supplemented to gether. Can you not just supplement K2?
I was figuring to see about "dephosphorylated and uncarboxylated matrix Gla protein (dp-ucMGP) is considered to be an indicator of vitamin K2 status" to see whether dpucMGP is high first. If not then no need to supplement
Yes, I know your tag from the thyroid forum. I am Hashi's since 2007, but only found the forum when I was knocked off my feet by coeliac last year, without enough energy to do anything but sit in front of my laptop. I wish I'd found it years ago.
I think most people are good with K2, but after what happened to me I looked at reviews on Amazon, and I wasn't the only one. I have wondered if the coeliac was a factor.
"The doc agreed but nurse still followed "TSH OK so stop testing" This makes my blood boil. I don't think nurses are qualified to make decisions on what gets tested and what doesn't.
I'm plant based (although I do eat butter still) AAAWWGH!!!
What do you mean when you say X K2 is sufficient for Y D3?
I just checked the Lee Hull CKD-aimed multivitamin there and there's 50 mcg of K2 in it.. he must have figured on K2 as anti calcification but I'll take your point about overdoing it and run it by my RD.
Thanks for the tip on thyroid. Never heard of that. I'll check out that and vit K2 status next bloods
"What do you mean when you say X K2 is sufficient for Y D3?" I read this book for £1.24
Vitamin K2 And The Calcium Paradox: How a Little-Known Vitamin Could Save Your Life Kindle Edition by Kate Rheaume-Bleue.
"The secret to avoiding calcium-related osteoporosis and atherosclerosis While millions of people take calcium and Vitamin D supplements thinking they're helping their bones, the truth is, without the addition of Vitamin K2, such a health regimen could prove dangerous. Without Vitamin K2, the body cannot direct calcium to the bones where it's needed; instead, the calcium resides in soft tissue (like the arteries)—leading to a combination of osteoporosis and atherosclerosis, or the dreaded "calcium paradox."
It's very repetitive, and I skipped loads, but I then looked for any 'papers' I could find to confirm. I'm sorry I didn't keep them.
I think you probably will find that testing K2 is not available, apart from research studies. I'll be interested to learn if you can get it tested though.
Re Thyroid testing. You want TSH , F(ree) T4, and FT3, not T(otal)T4, or TT3 These tests are readily available.
SNAP on the Kerrygold. For years we were told butter was bad for us but that myth seems to have been busted thankfully.
On "What do you mean when you say X amount K2 is sufficient for Y amount D3?" I think I get you're saying: that supplementing with X amount of D (and/or Calcium) causes problems - you need Y amount of K2 to ensure the D goes to the right places.
I don't supplement D, so I suppose I need to measure K2 (or supplement a bit of it to be sure to be sure). I understand serum dp-ucMGP can be measured. Its a protein that is activated by K2 and prevents vascular calcification. If you've lots of dp-ucMGP (i.e. the unactivated protein) then that's a sign you've not enough activator (vit K2). Whether that can be added to the list for a regular punter like me is another question. No harm in asking.
Gotcha on the thyroid. I'll get that added to the panel next. Cheers Nellie.
I had seen an article on coronary calcification and a potential mitigation involving EDTA and tetracycline...mid 2000's I think, bit of and older paper.
I was reading that the general population has a level of dpucMGP (a marker from which to infer vit K2 status) is something like 300-500 pmol/litre. Whereas in CKders it can go 1500-4000.
So there's something there worth measuring.
Seems reasonably clear cut to measure and then supplement if found wanting.
Generally speaking, the vast majority of those with vascular calcification are diabetics. It results in feet and leg amputations, blindness, heart attacks, etc. When my hubby (with diabetes) was looking into getting on the kidney transplant list, the transplant center was exceptionally concerned about this as it affects veins and arteries where the organ is attached. So those without diabetes likely don't have to worry about it to the same extent that they do. A cure is desperately needed for diabetes of both types 1 and 2. Hope this eases your concerns a little bit. Blessings.
I've somehow chosen not to be concerned until I have good reason to be concerned
Ignorance is bliss. But reading around the subject did at least have me groan with the notion of yet another metric to convince my doc to take, perhaps another supplement to take and having to find out about it all first. For sure diabetes will be a big player - I used to think of it as a disease that merely meant you had to manage your blood sugar but now, having been exposed to folks experience of it, it appears to be cancer-like in its reach. A really ugly disease.
Came across this, which doesn't disagree with you but points the finger at another number of elements outside diabetes:
"Cardiovascular complications are the leading cause of death in patients with chronic kidney disease (CKD). Vascular calcification is a common complication in CKD, and investigators have demonstrated that the extent and histoanatomic type of vascular calcification are predictors of subsequent vascular mortality. Although research efforts in the past decade have greatly improved our knowledge of the multiple factors and mechanisms involved in vascular calcification in patients with kidney disease, many questions remain unanswered. No longer can we accept the concept that vascular calcification in CKD is a passive process resulting from an elevated calcium-phosphate product. Rather, as a result of the metabolic insults of diabetes, dyslipidemia, oxidative stress, uremia, and hyperphosphatemia, “osteoblast-like” cells form in the vessel wall. These mineralizing cells as well as the recruitment of undifferentiated progenitors to the osteochondrocyte lineage play a critical role in the calcification process."
It's worth nothing that Lee Hull's book "Stopping Kidney Disease" talks of these lesser known items in the multitude of factors we ought to consider when tackling the disease: dyslipidemia, uremia, oxidative stress and hyperphosphatemia, etc. We need to tackle everything tackleable. In this case, to keep our blood vessels healthy as possible.
Oh, I don't disagree with this at all. I'm sure some do get vascular calcification who aren't diabetics. It's just that diabetics have many processes going on simultaneously - and those processes lead more quickly to things like vascular calcification than those without diabetes. It's very sobering when one realizes that the big majority of CKD and ESRD (dialysis and transplant) patients are diabetics. And then reality is often masked by poor data collection - for example, it's rare for a death certificate to list diabetes as the cause of death - it's generally a heart attack, a stroke, etc. Ugh. But, yes, if you have the opportunity to prevent things, by all means go for it. I do that, everyone should do it. After all, a person has only one life to live.
As mentioned by others, K2 is a recommended co-factor to take when supplementing with D3 to direct calcium to the bones rather than calcifying in unwanted places. However, K2 should not be taken by those with blood-clotting disorders or on medications such as warfarin, which is not always mentioned.
A particularly interesting piece. I added it to the OP but thought to highlight here too:
"Importantly, as shown by Shanahan and colleagues,19,20,74 changes in VSMC matrix vesicle metabolism induced by hyperphosphatemia and uremia profoundly impair the arterial surveillance normally provided by mural smooth muscle, such as the phagocytic removal of procalcified matrix vesicles and apoptotic bodies."
Rough Translation:
There are cells that gobble up the crap that would otherwise lodge on our blood vessel walls and narrow those vessels, e.g. calcification. Phagocyte translates as "gobbling cell". These cells are the cleaning crew for our vascular system and their work is hindered by hyperphosphatemia and uremia.
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High phosphorous might be tackled with a med (although it might be allowed to run a bit on the high side before medicating for it). But uremia is tolerated by the medics at early stages and just goes up and up until you hit the point where the patent side effects of uremia become unbearable/dangerous and you are put on dialysis.
But what about the latent work of uremia? Years and years of uremia without manifest symptom = years of uremia hindering the work of the cleaning crew cells protecting your blood vessels. I was stage 3a and 3b and had elevated urea and no symptoms. Nothing was being done about it until I decided to hit diet. No wonder cardio kills so many before they ever get to dialysis/transplant.
I found it interesting to come across something concrete attaching to uremia. We know its a toxin and that other toxins not measured are elevated if urea is. But this underlines the negative nature of uremia: we ought to consider any out of range urea as something damaging us years before we'd get to dialysis.
THE way to directly tackle uremia is to cut the amount of protein we eat. And so, the pointers again are towards a low protein diet. And if that doesn't bring urea in range, the only option left (that I'm aware of) is a supplemented (with ketoacidanalogues) very low protein diet. And that necessarily plant based, given the level of protein in animal produce.
The science behind the NKF KDOQI 2020 guidelines indicating supplemented very low protein diets usually just says that good results follow (re: mortality). It doesn't say why that is. Well, controlling uremia and so offsetting vascular calcification appears to be a contributor.
Another fascinating piece from the above cited paper:
"The hemodynamic consequences of vascular calcification are the loss of arterial elasticity, increase in pulse wave velocity, development of left ventricular hypertrophy, decrease in coronary artery perfusion, and myocardial ischemia and failure.2,34 These alterations are the main causes of mortality in the vast majority of patients with CKD."
The alterations in plain, engineering, English, appear to be very much inter-related
- a layer of deposits builds up on the surface of your blood vessels. Its just like limescale building up in water pipework and narrowing the diameter of the pipe (vascular calcification).
- this layer of deposits reduces the flexibility of your vessels. It's obvious: apply a layer of hard, bone-like material onto the inner surface of a flexible, elastic tube and that tube will become a rigid pipe (arterial elasticity)
- because your now hardened vessels can't flex to absorb the peak-impacts of blood pressure (caused by each heartbeat), blood speed thro' your vessels increases (pulse wave velocity). In other words, if the blood pressure peak, caused by a heartbeat, isn't absorbed by your vessels expanding, then there's only one other place that pressure can dissipate and that's by pushing your blood at higher speeds though your blood vessels. That speed increase means more wear and tear on your vessels and heavier impact between blood on any deposits lining your blood vessels (thus bits of deposits falling off and blocking vessels - e.g. stroke). I don't imagine higher velocities do any good for your blood cells either - delicate cells bashed at high speed against rough calcium deposits lining the walls of your formerly smoothwalled vessels. We had a gentle meandering river flow of blood with our blood cells drifting along peacefully. Now, with vascular calcification, our blood cells are white water rafting!
- your heart develops a rippled 6 pack (hypertrophy). It has to work harder to get blood down narrowed, inflexible vessels. And so starts building muscle to do that job.
- decrease perfusion = lower rate of blood flow. Narrowed vessels can't transport the same amount of blood, obviously.
myocardial ishemia = blood starvation to the heart (and everything else) caused by the lowering of blood flow rates.
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If these are the main causes of mortality in CKD patients then vascsular calcification is the main cause of mortality in CKD patients via all the above inter-related mechanisms.
Doubtlessly there's other cardio related stuff contributing to high cardio mortality in CKD patients. But if this is the main one then that's kind of good news. Cardio, the Big Killer denying us the joys of dialysis/transplant boils down to a single issue.
A single target to zoom in on. There can be any number of ways to defend against VC, vit K, uremia, exercise, drugs. Break down the problem into smaller chunks and try to deal with as many as possible, I guess
I recall reading a book a number of years ago called "The Great Cholesterol Con" by a Scottish doctor, Malcolm Kendrick. I think he was a GP of all things. Anyway, the book called out statins and the whole notion of 'dietary cholesterol / saturated fat as heart damaging' a con. And a dangerous one at that.
I intended to read it again, given my nephro's recently desire to put me on statins for a 6.6 level of cholesterol. My recent low protein plant diet appears to have had impact and Chol. dropped significantly to 5.2, so statins thankfully abandoned. I figured it might have some relevance, given cardio important in CKD mortality, so thought to read it again
Trying to get a freebie Kindle copy of the book (which is buried in my attic somewhere) I came across this newpaper article detailing a recent scientific review paper from 2018
"There is no evidence that high levels of total cholesterol or of “bad” cholesterol cause heart disease, according to a new paper by 17 international physicians based on a review of patient data of almost 1.3 million people.
The authors include Galway-based Prof Sherif Sultan, professor of the International Society for Vascular Surgery; Scottish-based Dr Malcolm Kendrick, author of The Great Cholesterol Con; and Dr David M Diamond, a US-based neuroscientist and cardiovascular disease researcher.
...the paper said claims of benefit from statin trials have “virtually disappeared” since new regulations introduced in 2005 by health authorities in Europe and the US specified that all trial data had to be made public. "
Interesting bits in it I'm sure, not least the idea that lower levels of LDL (the baddie 'cholesterol' which isn't actually cholesterol) seems to be bunk. I plan to have a sit down a read sometime, but here's the hard hitting abstract.
ABSTRACT
Introduction: For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular
disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention.
However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.
Areas covered: The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis.
Expert commentary: Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.
I've yet to be convinced statins aren't evil. My PCP put me on one once and I suffered daily, excruciating. painful migraines for the three months I took them. Stopped and no migraines. I take Zetia now with no side effects but my entire family history has high cholesterol in it. I'd rather die of a heart attack than take statins. The way I figure it is: everyone dies and I'd rather not be in pain and enjoy every day I have.
Benefit and downsides are established by the science that reveals both. That is the hope at least.
We have certainly been bombarded, for years, with the notion that cholesterol and saturated fats are bad for us. Lo-fat this, that and the other is a huge industry never mind the statins (which are apparently the most prescribed drug in the world).
If the science has either been corrupted (as the above review asserts) or, over time, develops on to alter initial evaluation as to benefit/harm, then so be it. We must go where it leads. That isn't always in the interests of business. Think of the Luddites reactions to better ways of doing things
It's not as if the problem of corruption isn't known.
"The truth about drug companies - how they deceive us and what to do about it" is a book written by Dr. Marcia Angell, former editor-in-chief of The New England Journal of Medicine, one of the most prestigious peer reviewed journals in the world. She had this to say about the trustworthiness of clinical research.
"It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of the New England Journal of Medicine".
Richard Horton, current editor of the equally prestigious The Lancet had this to say on the matter:
"The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue. Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness"
In the paper I linked, the authors note research in which 30 papers are cited (the body of trial research on the matter under consideration) by pro-statin advocates. But they only include date from about half the trials, which makes it look as if statins confer benefit. But when you include all the data from all trials, the benefit disappears. That's flagrant massaging to get the result you want.
It's hard to believe things could be that bad, but these notable, credible figures are shouting from the rooftops that it is that bad. Like Colin Powell told the world complete and utter lies on the matter of Saddam's weapons of mass destruction. We can be lied to to that extent by people with vested interests. I think we are fooled by their being authorities. And they know we can be fooled by their authority.
It's a real pickle. The advise to refer to our doctors doesn't solve the problem of which doctor do we refer to! Marcia Angell is a doctor. The people who did that review of the literature finding statins ineffective are doctors. If our own doctor (who is unlikely to be abreast of the issue but is merely following the establised paradigm) prescribes statins, ought we follow them.
Apologies if youve previously shown this link but this study indicates statins may enhance calcium accumulation in arterial walls by inhibition of vitamin K dependent proteins pubmed.ncbi.nlm.nih.gov/336...
No, hadn't seen that. Interesting though especially since I managed to dodge the statin bullet with a vegan diet. I'll add that link to the OP piece on the role of vit K in preventing vascular calcification. Cheers.
PS: you had any further thoughts on your mum's elevated urea and the role of protein intake re: same. Can't recall if I mentioned the role of (elevated) urea in vascular calcification but I linked stuff in the OP
Continually thinking of mums elevated urea and rapidly rising proteinuria with our strategy maintained including:
(i) Re-impose keto diet for at least 2 weeks then retest hba1c to see if still max normal
(ii) If hba1c reduced significantly after above period, retest urea & urinary protein
(iii) If """"not""""""""""""""""""""""""""""""""""""""""""""""""""""""", consider other natural options including ketoanalogues (protein already very low).
hba1c? Does your mum have diabetes (I understood hba1c to be a control measurement for diabetes). If so, apols I didn't pick that up.
Re: urea. What is the thinking behind (i). I understood protein intake to be the direct driver of urea levels
What was your mums g/kg protein intake from current dietary sources. Understood that if already low, then it's difficult to trim further. I'm haven't wrung the last out of it but 0.48g/kg is what I manage - that's about 30gr a day for a 65kg frame.
Not diabetic. Top of N range (141) is around prediabetic level though and consistently that. So low carb/keto is to try to address that on potential cause/effect basis.
Latest check indicates ~35-40gr protein/dy intake so circa. 0.6gr/kg for her ~61kg.
Understood. It's pain enough dieting for one thing bit when juggling a few things...
0.6g/kg isn't exactly going to town on protein and to trim it down to even my own 0.48 (and adding ketoacids) would take some management. Not quite eyes in the back of your head watching for protein sneaking in under the radar, but not far off that.
She's already tight without ketoacid supplementation but unless there is some other way to get urea down...
My own dramatic urea drop probably arose from my having a high enough protein intake pre diet. I was probably around 1.0gr/kg so the chop to 0.48 was going to impact.
Well here you go Skeptix, may need to change your meds…lol!
Alpha blocker use to control hypertension may be associated with a higher risk for kidney disease progression and a lower risk for cardiac events and mortality compared with use of alternative antihypertensive medications in patients with chronic kidney disease (CKD), according to a recent population-based retrospective study published in the American Journal of Kidney Diseases.
I'd like to get OFF meds. Certainly in light of meds that increase your chances of entering dialysis whilst reducing your chances of dying of heart disease. I mean, what a choice!
My BP seems to be dropping over time as the diet beds in .. so it may be I can start trimming back on this ACE I'm on.
Then again, I've to keep an eye on the proteinuria but for sure, the aim is to reduce the meds.
I mean ACE is kinda described as innocuous enough compared to some meds. How long before we get a report splashed across the headlines that they infact cause cancer or some bloody thing.
Before this CKD I'd barely take an aspirin for a headache...
I feel ya…I guess my main point was another f@*#ing contradiction of guidance. Don’t take ACE if eGFR is what stage 3 or above but do take ACE in eGFR below 30…I’m so confused……
I got you alright. And it does get to be a head spin alright
I was reading a paper criticising pro statin advocates and the way the report the data. Was it something like relative risk ratio and absolute risk ratio? Using the one you would get a 45% difference in negative events, using the other you would get a 1% difference in negative events (medicated group vs control group). You get all these %'s thrun at you and your head starts spinning...
I'm getting a bottle of Guinness on the way home and watching the tellie for the evening and that's that!
Thought to bump this vascular calcification thread for the benefit of those newer to the site who might not appreciate this significant element of CKD.
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