Blood Test Results - Please Comment On My Condition

[yerrag]

I don't think this is quite right (please if you have evidence to the contrary, do share). As far as I know blood vessel injury due to for example oxidative stress leads to hypoxia since the vessel loses integrity and power to exchange gases and liquids. So the area fed by the vessel gets swollen, hypoxic, etc.
So it's not that the body is on purpose creating hypoxia as far I understand this. Therefore hypoxia is a result of injury, and the hypoxic area then in turn establishes a vicious cycle; hypoxia itself worsens redox stress. Uric acid, etc.., then are produced to mitigate some of this stress.

I couldn't locate the article I based my conclusions. I should have bookmarked it before. However, there is no question about uric acid being an an antioxidant (Uric Acid as an Antioxidant – Functional Performance Systems (FPS)), although it gets no respect in the same way cholesterol is maligned by medical media orthodoxy. Earlier, I referenced a study in which mercury chloride injected into the kidney of monkeys induced the production of uric acid, which served to protect the monkey from the mercury's toxic effects on the kidney.

As I understood it, hypoxia is needed in our tissues to produce uric acid (I have to add a reference later, as my Google searches turn into dead ends given time constraints, perhaps I should use Bing or some other search engine that isn't so mainstream; I've already accepted Wikipedia as biased towards big pharma - alternate views such as Ray Peat's are automatically edited and deleted by Wikipedia information control sentries). My reasoning is that my high uric acid level cannot just pop out of thin air. Hypoxia is needed, and a mechanism for restricting oxygenation is needed. I think the answer is in restricting oxygen transport to the cells. Any attempt to improve oxygen transport (Buteyko, baking soda - improving CO2 levels; salt - to expand volume of blood) in my body has no effect. In fact, the momentary improvement in oxygenation as a result of improving CO2 levels is simply met with increased vasoconstriction of my blood vessels, which would explain the higher blood pressure from Buteyko or baking soda.

I would need to submit a day's worth of urine and submit them to the lab to see the results of tests. That would give me an idea where I stand in terms of urine protein, and my kidney status. Since I have no access to reliable tests (hair, saliva, and blood) on heavy metals, I would assume that my previous toxic condition with mercury and lead still persists, and I would need to continue from where I left off 5 years ago with detox.

You are right that my earlier detox could have left heavy metals accumulated in my kidney, and clearing my kidney glomerules of this toxicity has to be part of my detox protocol.

However, if my urine test should show I have no residual heavy metal toxicity (indirectly), I will get the PTH and Vitamin D3 test done, to pursue further the possibility of a calcium: phosphate imbalance that is causing my hypertension.

A hypothesis on uric acid: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC349151/pdf/pnas00662-0320.pdf

 

[PakPik]

My reasoning is that my high uric acid level cannot just pop out of thin air. Hypoxia is needed, and a mechanism for restricting oxygenation is needed.

Thanks for the study. I did some searching on uric acid and nephrotoxins and nothing suggests at all that the body increases hypoxia on purpose. That would be self defeating -hypoxia is a consequence of injury and worsens the injury-.

All the information I read explained that nephrotoxins like mercury, lead, etc..., hurt kidney cells by multiple mechanisms. One of these mechanisms is by a direct damage to the cell physiology; damage to the mitochondria or the membrane lipids, for example, increases oxidative stress. The other mechanism of damage by the nephrotoxins is the hypoxia they cause by 1) direct action, and 2) and indirect action through the damage to the vascularity. This hypoxic condition also increases redox stress. The body responds to redox stress by increasing antioxidants. Hypoxia happens to be a powerful stimulus / signal to increase uric acid, so one may expect uric acid to rise within an area of hypoxic injury.

All of the above relationships may be more easily seen in this diagram:
(GFR: glomerular filtration rate; RBF: renal blood flow)

(taken from the Google Book "Clinical Nephrotoxins: Renal Injury from Drugs and Chemicals"
edited by Marc E. de Broe, 1998, page 72)

You may ask a doctor to do kidney hormone tests -renin, etc.-. Those hormones may have to do with the persistent high blood pressure.

 

[yerrag]

I'll ask around for a good nephrologist. Certainly getting their opinion would still be helpful, as far as needed tests go.

Pinning down cause and effect mechanisms in the biochemical relationships is indeed a challenge. A lot of associative relationships can't exactly be defined definitively as cause and effect relationships. In my case, I feel that the redox stress from heavy metals in the kidneys cries out for some antioxidants to relieve the stress. The body responds by producing the more than usual amount of uric acid. To do so, it has to create hypoxia thru ischemia. To do so, it has to send signals to my blood vessels to constrict, thereby limiting the rate of blood flowing thru the tissues. In so doing, it limits oxygen to the issues, to the point that allows for hypoxic conditions favorable to uric acid production.

I'll keep on looking for references. Meanwhile, I'm dwelving on my own experiences that I think supports my thinking that my body is autonomically resisting higher oxygenation:

1. Higher CO2 levels in the blood leads to the hemoglobin being able to release oxygen more easily to the cells, as Ray Peat has mentioned. But this hasn't been my experience. Adding baking soda and practicing Buteyko breathing, or using paper bags to breathe thru - all these methods to increase CO2, are likely doing their job as far as increasing oxygenation. But because the improved oxygenation would relieve the hypoxic conditons needed to produce uric acid, the body would further restrict the blood flow, so that the higher oxygenation efficiency is negated by the lower flow rate. In constricting the blood vessels to restore hypoxa, a higher blood pressure would result. And a higher blood pressure is what I experience when I attempt to increase CO2 levels.

2. According to Ray Peat, high blood pressure is also a result of a lack of salt. By increasing the intake of salt, the volume of blood would expand as a result of osmolarity (the added salt would permit a higher blood volume with the same salinity as before). Because of the higher blood volume, the flow of blood can adjust to a lower rate. At a lower flow rate, the blood pressure will also become lower as a result. I tried increasing salt intake, and the result isn't as I would expect. My blood pressure would not back down. I believe it also went up, or at the very least stayed as before. It adds credence to my thinking that my body is resisting. More likely, the added salt is being urinated and my blood volume stays the same, and thus the level of oxygenation is kept where my body wants it - to maintain hypoxia for uric acid production.

3. Ray Peat also says that living in high elevations would also improve the oxygenation of the body, because of the higher CO2 content in the air. I haven't attempted to do so, but I would expect that I would experience higher blood pressure, instead of the contrary. If you search the web, like google "high elevation blood pressure" you would get results on higher elevation causing higher blood pressure. If I should extend Ray Peat's statement to imply that at higher elevations people would experience lower blood pressure as a result of better oxygenation, I would find the general experience, taking the google search as my basis, to be at odds with his thinking. Is it possible that the general population has similar issues as mine, arising from a need for hypoxia, due to unidentified and unaddressed defect in their own physiology? Why are some elite mountain climbers able to scale K2 every so easily without a tank? Perhaps their body is so efficiently metabolizing, with no impediments such as one caused by a need for hypoxia. Healthy individuals such as elite mountain climbers would be good examples of Ray Peat's thinking in this regard. I'm just not in that company.

For now, I will consider myself "handicapped" as far as oxygenation goes. I have to unlock the key to remove this handicap. I may still have the wrong key, but I hope differently.

 

[PakPik]

my case, I feel that the redox stress from heavy metals in the kidneys cries out for some antioxidants to relieve the stress. The body responds by producing the more than usual amount of uric acid. To do so, it has to create hypoxia thru ischemia.

I don't believe this is correct. If you analyse the chart the heavy metal generates the hypoxia as one of its toxic effects, both directly (through cell damage) and indirectly (through vascular damage). The body increases antioxidants to help counteract this damage.
In any tissue in the body, not only the kidney, hypoxia increases oxidative stress; hypoxia is an important both cause and consequence of oxidative stress damage.

1. Higher CO2 levels in the blood leads to the hemoglobin being able to release oxygen more easily to the cells, as Ray Peat has mentioned. But this hasn't been my experience. Adding baking soda and practicing Buteyko breathing, or using paper bags to breathe thru - all these methods to increase CO2, are likely doing their job as far as increasing oxygenation.

There could be many possible explanations. One important explanation that comes to mind is that when there's tissue water retention/swelling (as it may happens when a person has low blood albumin or when there's reduced kidney function), if the person increases CO2, the CO2 will pull excess water out of tissues, back into circulation, according to what Peat explains. So with all this water back into circulation, there's an increase in blood volume. Increased blood volume may further increase blood pressure in some people if the body doesn't adjust accordingly (for example,it may happen in certain renal disorders).

"For example, increased blood volume increases arterial pressure, renal perfusion, and glomerular filtration rate. This leads to an increase in renal excretion of water and sodium that is termed pressure natriuresis. In certain types of renal disease, the pressure natriuresis relationship is altered so that the kidneys retain more sodium and water at a given pressure, thereby increasing blood volume." CV Physiology: Blood Volume​

Interesting explanations here: A Study of the Renin-Angiotensin System and the Blood Volume in the Nephrotic Syndrome

the added salt would permit a higher blood volume with the same salinity as before). Because of the higher blood volume, the flow of blood can adjust to a lower rate. At a lower flow rate, the blood pressure will also become lower as a result.

Again, as above, the blood pressure adaptation would normally occur in a typical person, but in people with certain kidney disorders, for example, increased blood volume will only lead to increased blood pressure (failure to adapt).

If you search the web, like google "high elevation blood pressure" you would get results on higher elevation causing higher blood pressure. If I should extend Ray Peat's statement to imply that at higher elevations people would experience lower blood pressure as a result of better oxygenation, I would find the general experience, taking the google search as my basis, to be at odds with his thinking.

Same explanation as before; in some people with certain disorders this adaptation doesn't happen.
When Peat gives an explanation, he gives it in general terms. But for a particular person the context will determine exactly how the person reacts, and this can differ with what Peat says (for example, in the kidney disorders mentioned above the person probably will experience worsened hypertension at higher elevation.)
There's also the risk of worsened hypoxia with high altitude. Yes, Co2 is good at oxygenation and all, but there's a sharp drop in oxygen with high altitude. Both CO2 and O2 are needed for good oxygenation, not just a matter of high Co2. So yes, you are right in that some people won't be able to tolerate this sharp drop in oxygen -for example some people with lung problems or people with vascular diseases-. The people who do tolerate this drop would be the type of people who don't have these types of low oxygen disorders.

arising from a need for hypoxia

No, no need for hypoxia. Hypoxia is at the core of their problem.

Just as an anecdote, when I was severely hypoxic I couldn't tolerate a slight decrease in the oxygenation in my room. My vascular system was very bad, so the oxygen transport and use was terrible. Bag breathing would further decrease my oxygen and make me worse. Anything that would decrease my oxygen uptake -like bag breathing or not completely opening my windows- would worsen my condition. Yes Co2 is needed for oxygenation, but we need to have enough O2 already in the first place! Co2 without enough O2 will just make matters worse; both are needed in enough quantities.

Of course, I am not a nephrologist. I'm merely sharing what I would analyse for myself if I were in a similar situation to the one you present.

 

[tara]

PakPik's explanation looks likely to me - I too think hypoxia is more likely amongst the causes of the problem rather than the solution.
Increasing CO2 probably is safest done slowly for people who are sensitive to the effects to allow gradual adaptation.

While baking soda and bag breathing may both be able to raise CO2 levels, I think they have some different effects from each other too. In the short-term, IIUC, bag breathing would tend to lower system pH and baking soda would tend to increase it. The effects of such shifts in pH - and how useful each technique would be - probably very much depend on whether one is running too acidic or too alkaline to begin with.

 

[yerrag]

"For example, increased blood volume increases arterial pressure, renal perfusion, and glomerular filtration rate. This leads to an increase in renal excretion of water and sodium that is termed pressure natriuresis.

This statement, referring to a normal un-diseased context, seem to be at odds with what Ray Peat is saying. Ray Peat, IIUC, would have increased blood volume result in lower blood pressure.

"The old medical practice of restricting salt intake during pregnancy was an important factor in causing it, so it's interesting to look at the effects of salt restriction as a treatment for hypertension.The pregnant woman's blood volume expands, to permit the supply of energy to match the needs of the embryo. If the blood volume doesn't increase, or if it decreases, as in pregnancy toxemia, her blood pressure will increase. Typically, the decrease of blood volume is accompanied by an increase in the extracellular fluid, edema, resulting from leakage of fluid through the walls of the capillaries, and albumin appears in the urine as it leaks through the capillaries in the kidneys. The amount of blood pumped by the heart, however, is increased in toxemia (Hamilton, 1952), showing that the increased blood pressure is at least partially compensating for the smaller volume of blood. When energy fails: Edema, heart failure, hypertension, sarcopenia, etc.

Again, as above, the blood pressure adaptation would normally occur in a typical person, but in people with certain kidney disorders, for example, increased blood volume will only lead to increased blood pressure (failure to adapt).

That would happen if my body will allow an increase in blood volume. But as it is, the body isn't allowing an increase in blood volume. Any salt I take is not lowering my blood pressure, and I would deduce that the salt is being used to expand blood volume.

Same explanation as before; in some people with certain disorders this adaptation doesn't happen.
When Peat gives an explanation, he gives it in general terms. But for a particular person the context will determine exactly how the person reacts, and this can differ with what Peat says (for example, in the kidney disorders mentioned above the person probably will experience worsened hypertension at higher elevation.)
There's also the risk of worsened hypoxia with high altitude. Yes, Co2 is good at oxygenation and all, but there's a sharp drop in oxygen with high altitude. Both CO2 and O2 are needed for good oxygenation, not just a matter of high Co2. So yes, you are right in that some people won't be able to tolerate this sharp drop in oxygen -for example some people with lung problems or people with vascular diseases-. The people who do tolerate this drop would be the type of people who don't have these types of low oxygen disorders.

Yes, context is everything. And I share the same kind of context with a lot of people who don't feel the salutary effect of having a better CO2 content in air at high elevations. Where a person with good health is blessed to experience the good effects of better oxygen:carbon air content, people with defects in their physiology would find it hard to adapt, and would experience their blood pressure rising, instead of dropping. I see that I have to correct this "defect," even as I grasp for answers, while most people would find no defect and move on.

Just as an anecdote, when I was severely hypoxic I couldn't tolerate a slight decrease in the oxygenation in my room. My vascular system was very bad, so the oxygen transport and use was terrible. Bag breathing would further decrease my oxygen and make me worse. Anything that would decrease my oxygen uptake -like bag breathing or not completely opening my windows- would worsen my condition. Yes Co2 is needed for oxygenation, but we need to have enough O2 already in the first place! Co2 without enough O2 will just make matters worse; both are needed in enough quantities.

Why were you hypoxic, if you don't mind?

PakPik's explanation looks likely to me - I too think hypoxia is more likely amongst the causes of the problem rather than the solution.
Increasing CO2 probably is safest done slowly for people who are sensitive to the effects to allow gradual adaptation.

You and PakPik are probably right!

I've just been doing some digging. I looked at my neutrophil results, and they're above range. It may be significant in that 50% of neutrophils "adhere to the vascular endothelium (Difference Between Neutrophils and Macrophages) and considering that about a significant amount of blood flows through the kidney (22%) and if my kidney has some problems (due to heavy metal toxicity), it may be that the high neutrophil count is because of my putative kidney condition. My low albumin could also be due to my albumin leaking out to urine, and I would know after I get results from my 24hr urine collection, which I will submit tomorrow (I'm looking at my 24 hr urine protein, as well as creatinine, creatinine clearance, as well as uric acid). My low WBC may be from a heavy use of neutrophils to deal with the chronic kidney vascular endothelial tissues. I looked at my urinalysis results, and I also see "occasional" epithelial cells. I don't know what that means for now, it could be normal and nothing to fear, or it could be a warning sign, although as I look at my previous urinalysis test dating from seven years back, it was already there. But then, I was already hypertensive further back than that.

FYI, I'm also going to take the PTH (ECLIA) test and the vitamin D total [25(OH)D]. I hope to show you the results soon.

I saw this nice link The Vascular Endothelium and Human Diseases . It is rather hard to read because of the way the web page is laid out (It helps to have the Readability browser extension or app). And it's a long read but very interesting and worth sharing. I still have to read once or twice more before I can internalize it. I had to vet many articles for being very mainstream and have nothing enlightening really to share, but this one is rather recent, of 2013 vintage, and seem more open-minded and less institutionalized in its bearing and tone.

 

[yerrag]

I have the following results from my latest blood tests and 24hr urine collection:

PTH - 40.06 pg/mL (reference 15.00 -65.00)

Vitamin D Total 25(OH)D - 47.32 ng/mL (>30)

C-Reactive Protein - Negative

Serum Creatinine - 1.16 mg/dL (0.67 - 1.18)

24H Hr Urine Collection:

Urine Creatinine - 1.80 g/24h (1.02 - 2.37)

Creatinine Clearance - 107.40 ml/min (106.80 - 139.20)

Urine Protein - 210.45 mg/24h (22.00 - 120.00)

Urine Uric Acid - 644.50 mg/24h (204.00 - 1,003.00)

Urine Calcium - 134.40 mg/24h (100.00 - 300.00)

Urine Phosphorus - 0.97 g/24h (0.40 - 1.30)

In an earlier blood test from a month ago, here are some results that can be helpful to use in context:

WBC - 4.5 (5-10x10^12)

Neutrophils - 74 (50 - 66%)
Lymphocytes - 23 (20 - 40%)
Monocytes - 2 (2-6%)
Eosonophils - 1 (1 -3%)
Basophils- insignificant
Stabs - insignificant
Platelet Count - 194 (150 - 400x10^3/cum)

Serum Calcium - 9.40 mg/dL (8.4 - 10.6)
Ionized Calcium - 1.14 mmol/L (1.12 - 1.32)
Serum Phosphorus - 3.11 mg/dL (2.5 - 4.6)

Serum Uric Acid - 7.49 mg/dL (less than 7.10 mg/dL)
Blood Urea Nitrogen - 15.54 mg/dL (4.76 - 23.25)

Albumin = 3.74 g/dL (3.5 - 5.0)

Carbon Dioxide - 24 mmol/L (22 - 31)

Note: There was no test available for the active form of vitamin D 1,25(OH)D, so there was no way I could tell whether my kidneys were able to do a good job converting 25(OH)D to 1.25(OH)D calcitriol.

It looks like these are solid numbers that could help explain the most likely cause of my hypertension.

Do you think it would help to take the 24hr urine potassium, sodium, and magnesium? I now regret overlooking including these tests, as they don't cost much and I don't know why I left them out.

 

[yerrag]

Watching the video posted by j. in this thread Vitamin D and PTH , I realize that 25(OH)D activation to calcitriol 1,25(OH)D3 isn't only done by the kidneys, other body tissues as well as macrophages do that function as well. So, maybe I shouldn't be too concerned about calcitriol deficiency on account of a putative ailing kidney. My PTH isn't too high, my Vitamin D Total is sufficient, and my blood calcium levels are fine as well.

I think I can focus now on the other values that may help explain my hypertensive condition. Low WBC (outside range) , high neutrophil percentage (outside range), high uric acid (outside range), low CO2, high urine protein (outside range), and low creatinine clearance.

Also notable is that my C-Reactive Protein test is Negative, and indicates an absence of inflammation.

From the high urine protein and low creatinine clearance, I can deduce that there is a problem with my kidney.

From the high neutrophil percentage, I can guess that the endothelial vascular system in the kidney is recruiting neutrophils to combat stress. The Vascular Endothelium and Human Diseases Is it possible my WBC is low because of the continual use of neutrophils to combat stress is slowly using up my white blood cells?

The endothelial cells are activating the RAAS (Renin-Angiotensin System) leading to hypertension. The hypertensive condition creates hypoxic conditions that contribute to uric acid production, causing my uric acid levels to be high.

I can't explain the low CO2 levels, but I think that low CO2 levels are needed to decrease the efficiency of the transport of oxygen by red blood cells, in order to sustain a level of ischemia that is needed for hypoxic conditions to occur, for uric acid production.

Since the problem is mainly with my kidneys, and since my kidneys have been holding out for so long, I may face kidney failure if I don't fix my kidneys.

Is the high uric acid level helping me manage through this condition, since uric acid is an antioxidant? Or should I heed the advice of conventional doctors to take prescription drugs to lower the blood pressure? They've warned for a while that if I don't take such drugs to lower my blood pressure, I would face kidney failure. But if I take their drugs, won't I lose the protective influence of uric acid?

 

[yerrag]

After watching Dr. Horlick from the youtube video shown on Vitamin D And PTH , I realized that my Vitamin D is still below 75 ng/ml, above it being where he considers as where PTH levels are in healthy territory. I could take steps to increase my vitamin D levels, and lower my PTH, but would it have any significant impact in lower my blood pressure levels?

 

[dbh25]

At 25:44, the slide has Preferred 30-60 ng/ml, not 75. (He says 75 nm/L) The slide also has > 60 ng/ml is excess range. I always try for around 50 ng/ml, which for me is about 12,000 IU Vitamin D per week.

 

[yerrag]

At 25:44, the slide has Preferred 30-60 ng/ml, not 75. (He says 75 nm/L) The slide also has > 60 ng/ml is excess range. I always try for around 50 ng/ml, which for me is about 12,000 IU Vitamin D per week.

Thanks for correcting me. My Vitamin D levels are fine then.

That sharpens my focus on the cause of my hypertension to my kidney.

 

[yerrag]

Thanks Pakpik, Mittir, Tara, dbh25, Emstar1892, Such_Saturation, and Giraffe for your helpful comments and observations. I should look for a kidney forum to continue with treating my kidney issue, now that I can count out other causes for my chronic hypertensive situation.

 

[Giraffe]

@yerrag, I had issues (low level pains) with my kidneys for a while. When I noticed that I did not have them any longer, my best guess as to what might have helped was calcium: I had started to add eggshell powder to phosphate rich meals to balance the phosphate.

Peat mentioned that calcium can help with hypertension.
Need Help with Stubborn Hypertension

 

[PakPik]

That would happen if my body will allow an increase in blood volume. But as it is, the body isn't allowing an increase in blood volume. Any salt I take is not lowering my blood pressure, and I would deduce that the salt is being used to expand blood volume.

Hi yerrag,
As I mentioned in my latest post there are certain kidney disorders where the decrease in low blood pressure that *should* happen from higher blood volume doesn't happen. So in those people with kidney disorders: higher blood volume-> higher blood pressure (their kidneys fail to adapt). That's why I suggest digging deeper to see if you have one of those disorders.

I have to correct this "defect," even as I grasp for answers, while most people would find no defect and move on.

Where a person with good health is blessed to experience the good effects of better oxygen:carbon air content, people with defects in their physiology would find it hard to adapt, and would experience their blood pressure rising, instead of dropping. I see that I have to correct this "defect," even as I grasp for answers, while most people would find no defect and move on.

In high altitude there is way less oxygen than lower altitudes. There is NO better oxygenation when a person with poor oxygen uptake and/or poor oxygen tension in tissues goes to high altitude;they in fact more than often get worse with high altitude. As I said, for oxygenation both oxygen and CO2 are needed. These people don't have enough oxygen to begin with so there's nothing magical that CO2 will do for them. They are starving from oxygen and no amount of CO2 will correct that: they need to "get in" enough oxygen into the body and the tissues.

Peat's descriptions on the good effects of high altitude are therefore are only suitable for people without overt problems with oxygen uptake/tension. High-altitude/Oxygen-restriction is likely detrimental to those who have serious problems with that. (that's why all of Peat's explanations need to be taken as generalizations that may not apply to people with certain specific disorders)

Another thing to consider is , as I've said before, according to Peat CO2 draws water from swollen tissue back into circulation; this represents and increase in blood volume, but in a kidney disorder situation/Cardiovascular disease situation it may happen that the blood pressure isn't adjusted for this increase.

My low WBC may be from a heavy use of neutrophils to deal with the chronic kidney vascular endothelial tissues.

I think this can be a possibility. Another possibility that comes to mind is that white blood cells are being lost through kidney leakiness into the urine. Have you gotten some sort of test measure of white blood cells lost in urine?

Serum Creatinine - 1.16 mg/dL (0.67 - 1.18)

Urine Creatinine - 1.80 g/24h (1.02 - 2.37)

Urine Protein - 210.45 mg/24h (22.00 - 120.00)

With those urine and creatinine results I personally would definitely consider there may be a kidney issue.

My PTH isn't too high, my Vitamin D Total is sufficient, and my blood calcium levels are fine as well.

I think I can focus now on the other values that may help explain my hypertensive condition.

I would think the same way.

Also notable is that my C-Reactive Protein test is Negative, and indicates an absence of inflammation.

Mmm... C reactive protein can be very low in very diseased body, so a low result doesn't exclude the possibility of bad problems. Personally, it's not a test I would use to exclude anything other than an acute phase reaction. A person can be experiencing lots of tissue damage that may not be revealed by those popular markers (some people are immunosuppressed and can't even mount an effective classic inflammatory response).

The hypertensive condition creates hypoxic conditions that contribute to uric acid production, causing my uric acid levels to be high.

I'm starting to sound like a broken record but this is not true. It is the reverse: the hipoxic/irritating condition leads to hypertension, at least with regards to nephrotoxin-induced kidney injury according to the papers/books I've shared before. Nephrotoxin->Hypoxia->Vascular damage->More hypoxia , and a vicious circle is established that is ultimately injuring more and more the kidney tissue. Ultimately the kidney gets so injured that it starts failing to regulate blood pressure, leaking albumin which is important for blood pressure, etc... (this is from the papers on the kidney I read and also from my research on antioxidant/vascular system -please keep in mind I am not a nephrologist diagnosing you; merely sharing information-).

For further evidence, a 2016 paper that explain how hypoxia is at the core of chronic kidney disease (hypoxia is a strong driver and consequence of it, not a solution to it). See this quote:

" A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. " Hypoxia: The Force that Drives Chronic Kidney Disease
In that paper there's a section called "Causes of Kidney Hypoxia". I found it very illuminating and suggest to read it.

Nephrotoxicity also acts thorugh mithocondrial damage (as per the references I've shared before). This indeed happens in any tissue when facing Mitochondrial damage leads to oxygen wasting (Peat has explained this before), therefore mitochondrial damage can be a source of low oxygen due to the increased oxygen demands it imposes. It really is a multifactorial problem, that's why I like to look at it as a system of many factors.

in order to sustain a level of ischemia that is needed for hypoxic conditions to occur, for uric acid production.

No, the body isn't generating ischemia on purpose. The ischemia is a product of the damage which then intensifies the damage even more.

Is the high uric acid level helping me manage through this condition, since uric acid is an antioxidant?

As I've commented before, the body normally increases antioxidant production when it faces an oxidative stress situation. Of course this is a way to help mitigate the damage. Uric acid happens to increase for example when the body is facing hypoxic-induced kind of oxidative stress. There are other antioxidants that may increase due to that, as well. Therefore when there is a situation like hypoxia-induced oxidative stress, uric acid plus other antioxidants are produced by the body to help manage, as you say. But this is due to the negative consequences of hypoxia; hypoxia participates in the damage process.

I hope this helps

 

[tara]

I can't explain the low CO2 levels, but I think that low CO2 levels are needed to decrease the efficiency of the transport of oxygen by red blood cells, in order to sustain a level of ischemia that is needed for hypoxic conditions to occur, for uric acid production.

Peat's descriptions on the good effects of high altitude are therefore are only suitable for people without overt problems with oxygen uptake/tension. High-altitude/Oxygen-restriction is likely detrimental to those who have serious problems with that. (that's why all of Peat's explanations need to be taken as generalities that may not apply to people with certain specific disorders)

+1
IIRC, Peat's referred to people who are adapted to higher altitudes having some potential advantages. Getting adapted can be stressful and is risky for people in some states - occasionally terminally so.

 

[dbh25]

Thanks Pakpik, Mittir, Tara, dbh25, Emstar1892, Such_Saturation, and Giraffe for your helpful comments and observations. I should look for a kidney forum to continue with treating my kidney issue, now that I can count out other causes for my chronic hypertensive situation.

Good luck yerrag.

 

[yerrag]

I'm in agreement that hypoxia isn't induced by the body specifically to create uric acid. But I'm wondering if I should take blood pressure lowering meds that will artificially lower my blood pressure. Wouldn't doing so eliminate hypoxia, leading to the loss of much needed uric acid production to protect me from the oxidative stresses my kidney us experiencing?

I'll have to look more into the urine wbc. Last month's urinalysis shows 0-2 /hpf for both WBC and RBC. Would need to see if there are more definitive test for WBC leakage through urine.

Are there more definitive markers other than CRP that you can recommend? Even without any, it may be just moot to look further as the tests have narrowed my issue to the kidney.

 

[PakPik]

But I'm wondering if I should take blood pressure lowering meds that will artificially lower my blood pressure. Wouldn't doing so eliminate hypoxia, leading to the loss of much needed uric acid production to protect me from the oxidative stresses my kidney us experiencing?

According to the last paper I mentioned lowering hypertension may lower oxygen consumption, so it seems you are right: hypoxia may be lessened to some extent if the blood pressure is lowered. It is also bad for blood vessels to have chronic hypertension (that would be one legitimate reason for taking something to lower blood pressure in my opinion):

"hypertension leads the kidney to consume approximately twice as much oxygen as normal to transport a given amount of sodium.16 Consequently, the combination of reduced oxygen delivery caused by vasoconstriction and increased oxygen demand caused by aberrant metabolism results in lower renal oxygenation."​

(this information is new to me; so now I understand hypertension as an indirect cause of hypoxia -through the increase in oxygen consumption-, as well as a consequence in certain kidney diseases. It's good to learn new things! However, I still understand there are deeper and direct causes of the hypoxia, as the studies I've referenced before show)

So, a blood pressure med wouldn't eliminate all of the causes of hypoxia that 2016 paper describes (for example, they mention atherosclerosis, cigarette smoking , air pollution, sleep-apnea [so oxidative stress], etc... as causes of kidney hypoxia. Thus, if atherosclerosis or sleep apnea is one cause, it would be necessary to target that; or if a nephrotoxin like mercury is a driving force for hypoxia in your situation, my guess would be that the mercury induced damage would need to be somehow be ameliorated or mercury removed (I don't have knowledge on how to remove the mercury). )

Are there more definitive markers other than CRP that you can recommend? Even without any, it may be just moot to look further as the tests have narrowed my issue to the kidney.

Unfortunately I still haven't come across an all around test for everything. However, from all I've studied until now, there a two very important tests I'd certainly try to get to see where I'm at since they can be quite reliable for pointing to tissue damage, either acute or chronic damage to basically any tissue in the body (at least these are better tests than CRP, etc, in that regard). These are the Lactate Dehydrogenase test and the Prostaglandin-E2, especially the lactate dehydrogenase:

Lactate dehydrogenase (LDH) (taken from LD: The Test | Lactate Dehydrogenase; LD Test: Lactate Dehydrogenase; LDH | Lab Tests Online)

"A lactate dehydrogenase (LD or LDH) test is a non-specific test that may be used in the evaluation of a number of diseases and conditions. LD is an enzyme that is found in almost all of the body's cells (as well as in bacteria) and is released from cells into the fluid portion of blood (serum or plasma) when cells are damaged or destroyed. Thus, the blood level of LD is a general indicator of tissue and cellular damage. The level of LD may also rise in other types of body fluids (e.g.,cerebrospinal fluid, pleural fluid, etc.) in the presence of certain diseases.

An LD blood test may be used:

• As a general indicator of the existence and severity of acute or chronic tissue damage
• To detect and monitor progressive conditions such as anemia, including hemolytic anemia and megaoloblastic anemia, or severe infections
• To help stage, determine prognosis, and/or monitor treatment (i.e., chemotherapy) of cancers, such as germ cell tumors (e.g., some types of testicular cancer and ovarian cancer), lymphoma, leukemia, melanoma, and neuroblastoma

An LD test is performed on body fluids for a few different reasons:

• To help evaluate cerebrospinal fluid and distinguish between bacterial or viral meningitis
• To evaluate other body fluids such as pleural, peritoneal or pericardial fluid and help determine whether the accumulation of fluid is due to injury and inflammation (exudate) or due to an imbalance of pressure within blood vessels and the amount of protein in the blood (transudate). This information is helpful in guiding treatment."

They also explain: "With some chronic and progressive conditions, moderately elevated LD blood levels may persist. Low and normal levels of LD do not usually indicate a problem. Low levels are sometimes seen when someone ingests large amounts of ascorbic acid (vitamin C)."

​

The Prostaglandin-E2 test (specially the urine 24 hrs), is less popular than the LDH but is still a marker that can get chronically high in many chronic injury states. However, if I had to choose only one test, I'd prefer the LDH.

If kidney toxicity due to mercury is a concern, in this paper they say mercury can cause adrenaline and noradrenaline to increase, which then increase blood pressure. So those may be good tests to take (I suspect the 24-urine tests for catecholamines are more revealing, although I can't say for sure): "Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity." Role of mercury toxicity in hypertension, cardiovascular disease, and stroke. - PubMed - NCBI

Finally, I read they recommend stopping taking aspirin and other specific meds/supplements if a person is going to perform certain tests like prostaglandins, etc. I think I also read that about the LDH test -not sure-. So I suggest checking out the details for the tests that interest you. NSAIDs may have to be careful considered in kidney injuries as well since some people may not do well with these meds (it probably varies according to the type, extent, etc., .. of kidney problem, so I suggest finding out what applies for you.)

All the best :)

 

[yerrag]

@yerrag, I had issues (low level pains) with my kidneys for a while. When I noticed that I did not have them any longer, my best guess as to what might have helped was calcium: I had started to add eggshell powder to phosphate rich meals to balance the phosphate.

Peat mentioned that calcium can help with hypertension.
Need Help with Stubborn Hypertension

That's great news. I made 2 kgs. of eggshell powder from the eggshells I had saved for the garden. I've started to use them. 4 grams of eggshells/day to get 1500 mg of calcium. At a minimum, I'm taking 1500 mg (eggshell powder) for breakfast, mixed with my sunny-side up egg. I keep forgetting to add them in to my coffee. When I put in the milk froth, the eggshell powder can be sprinkled on top and makes my coffee crunchy.:)

 

[yerrag]

IIRC, Peat's referred to people who are adapted to higher altitudes having some potential advantages. Getting adapted can be stressful and is risky for people in some states - occasionally terminally so.

I didn't mean very high altitudes like K2 and Everest. More like places such as Mexico City (height 7,000+ feet) or Baguio, Philippines (height 5,000+ ft), where oxygen isn't so scarce but the CO2 concentration in the air would be higher in the lowlands.

I thought that with what Ray Peat is saying, it would benefit people to live there because the CO2 concentration would enable better oxygen release from the blood cells to the cells. That healthy (but not super people) people should be able to go there and experience the benefits, such as have lower blood pressure. But it seems to not be the case with most people. And the point I was making was that maybe most people are not really healthy, and that is why they do not benefit from the high altitude as much as a healthy person would. My hypertensive condition and the way by body is currently disposed, I would likely not benefit from the high altitude just as well.

It doesn't take one to be superhuman, but to be healthy, to experience the benefits of high altitude, but because most of the population is unhealthy, the healthy person becomes the exception, and a person benefiting from the high altitude becomes an anomalous case. Perhaps deemed superhuman. Whereas the truth is, he isn't. It's just that he's human, and the rest are - subhuman.