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C) There is no P in protein. Any difference is [P] between plants and animals (I'll take your word for it that there is) must be from some other component (most bio-P is in nucleic acids & activated carbs). You might find this interesting about dietary P & CRF. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318242/ Less P from plant sources excreted than from animal sources, ie-- in terms of P retention, you're better off with flesh. The problem there is that protein usually needs to be limited in CRF.
You're right of course. The P is not in the protein but in the meat. P is known to cause a lot of problems in CKD. Renal osteodystrophy is one. That is why many CKD patients are taking P blockers or inhibitors or must limit the P intake. Again P is less in plants than meat.
Well I tell you I can find pub med studies to contradict just about anything and a lot of the research is tainted by corruption. My personal experience has been that patient reviews such as those on drugs dot com are often a better indication of which drugs are really any good and which aren't.
Your idea that meat is better for P goes against all the literature that advises patients to limit their consumption of animal protein, and for one reason to limit P intake, thus curtailing CKD bone disease.
That's why they have phosphate binders for CKD patients to avoid the side-effects of phosphorous in the diet. From the study you cite: " As expected, a smaller proportion of phosphorus from plant foods was excreted in urine compared to animal foods" Don't have time to delve into how they are allegedly measuring this, but the idea that you phosphorous levels from plants is greater than meat is bogus and goes against all now accepted medical advice
Your idea that statin prescriptions are under control of attorneys is pretty ridiculous imo. Even if it were true the fact is that most experts in CKD advise to limit your consumption of facts and keep your lipid profiles healthy.
But I thank you for the links and I will take a look at those.
Well I tell you I can find pub med studies to contradict just about anything and a lot of the research is tainted by corruption. ]
Amen.
I rarely quote isolated research reports, but do reference reviews & meta- analyses (for what they're worth.)
Your anecdotal report of a cough caused by an ARB and resolved with an ACE is a "Man Bites Dog" bit of news. Interesting, but decidedly a rarity. As I said, If I had a pt who started to cough after taking an ARB, I'd stop the med, but look hard for other causes of cough.
P/Ca metaboism is disrupted in CRF. Secondary hyperparathyroidism https://www.kidney.org/atoz/content/...rathyroidism-- one way to manage it is to limit P intake...Diets to limit protein is mainy to alleviate the uremia (excess N). It's benefit on P is secondary, but welcome just the same.
Yes and that is why protein derived from plant sources is preferable to that from animal sources. Metabolic acidosis from CKD also contributes to CKD bone disease.
If you do not mind I have another question. Can blood in urine be easily noticed by observation and does amber colored urine not caused by dehydration a sign of blood.
Also the thing that would worry me about ARBs is that one of the effects is lowering of GFR. If you're trying to reduce uremia, what good does that do?
Also if the unmedicated BP is below 120 taking ARBs might lower it too much and cause other problems, no? You mentioned something earlier about this being a false indicator.
I rarely quote isolated research reports, but do reference reviews & meta- analyses (for what they're worth.)
Your anecdotal report of a cough caused by an ARB and resolved with an ACE is a "Man Bites Dog" bit of news. Interesting, but decidedly a rarity. As I said, If I had a pt who started to cough after taking an ARB, I'd stop the med, but look hard for other causes of cough.
P/Ca metaboism is disrupted in CRF. Secondary hyperparathyroidism https://www.kidney.org/atoz/content/...rathyroidism-- one way to manage it is to limit P intake...Diets to limit protein is mainy to alleviate the uremia (excess N). It's benefit on P is secondary, but welcome just the same.
You seem to suggest you are a doctor. Like many doctors your field of reference is too small.
Two more sources identifying ARBs as having "cough" as a side-effect. One from Merckmanuals
and the other from a monograph losartan from drugs.com (highly respected sight on medications;one of the most popular ARBs) listing cough as a side-effect.So if you are, in fact, a doctor (and not just posing as one), your clinical experience doesn't seem to match the official data on ARBs.
I rarely quote isolated research reports, but do reference reviews & meta- analyses (for what they're worth.)
Your anecdotal report of a cough caused by an ARB and resolved with an ACE is a "Man Bites Dog" bit of news. Interesting, but decidedly a rarity. As I said, If I had a pt who started to cough after taking an ARB, I'd stop the med, but look hard for other causes of cough.
P/Ca metaboism is disrupted in CRF. Secondary hyperparathyroidism https://www.kidney.org/atoz/content/...rathyroidism-- one way to manage it is to limit P intake...Diets to limit protein is mainy to alleviate the uremia (excess N). It's benefit on P is secondary, but welcome just the same.
In further research on ARBs which are now almost universally accepted for CKD with protein leakage,
I find the side effects can be quite serious and are actually what the drug is intented to PREVENT:
acute kidney failure, lowering of GFR and other serious side effects that the drug is supposed to treat, not cause. Like many drugs on the market the drug companys go with what is expedient and profitable not neccessarily good. And doctors are quick to hop on the bandwagon with pressure from drug reps. I seriously question if CKD patients should even be taking these drugs.
.... your clinical experience doesn't seem to match the official data on ARBs.
Get a PDR and page thru it. You will see that diarrhea AND constipation are listed as a side effect for virtually every drug in there, when in fact, most drugs don't cause either. The FDA rules say that ANY symptom reported by a test subject during the trial must be listed as a side effect-- and over a test period of many weeks to months, it would be very likely that at least some pts in test or control group would experience those symptoms .... The real questiuon is "does that symptom occur at an increased rate in the test subjects compared to the control subjects?"...As I said-- if a pt started a new, dry cough soon after newly starting an ARB, we'd have to suspect the ARB, but it's highly unlikely that it would turn out ot be the drug....A "wet" cough surely would NOT be from the ARB.... ARBs have been around for 20 yrs or so and I prescribed them to 100s of pts-- never saw anyone who developed a cough.
It is not my experience that is too limited-- it's yours. You have no basis to apply a weight to anything you read. "Possible" and "probable" are two different things.
Blood in urine-- usually microscopic and not enough to see by looking at a urine sample. If the urine looks bloody, look for an additional problem like UTI.
Effects & side effects of drugs-- always a need to balance-- over all, the benefits of taking ACES or ARBs in diabetic nephropathy outweigh any theoretical deficits. Most importantly, they seem to slow down the inevitable deterioration of the conditon over time.....Risks are evaluated based on statistics- which NEVER apply to an individual. Eg- the risk a side effect A may be 25% for a group of 100 pts, but for any single pt, it's either 0% or 100%.
Get a PDR and page thru it. You will see that diarrhea AND constipation are listed as a side effect for virtually every drug in there, when in fact, most drugs don't cause either. The FDA rules say that ANY symptom reported by a test subject during the trial must be listed as a side effect-- and over a test period of many weeks to months, it would be very likely that at least some pts in test or control group would experience those symptoms .... The real questiuon is "does that symptom occur at an increased rate in the test subjects compared to the control subjects?"...As I said-- if a pt started a new, dry cough soon after newly starting an ARB, we'd have to suspect the ARB, but it's highly unlikely that it would turn out ot be the drug....A "wet" cough surely would NOT be from the ARB.... ARBs have been around for 20 yrs or so and I prescribed them to 100s of pts-- never saw anyone who developed a cough.
It is not my experience that is too limited-- it's yours. You have no basis to apply a weight to anything you read. "Possible" and "probable" are two different things.
Blood in urine-- usually microscopic and not enough to see by looking at a urine sample. If the urine looks bloody, look for an additional problem like UTI.
Effects & side effects of drugs-- always a need to balance-- over all, the benefits of taking ACES or ARBs in diabetic nephropathy outweigh any theoretical deficits. Most importantly, they seem to slow down the inevitable deterioration of the conditon over time.....Risks are evaluated based on statistics- which NEVER apply to an individual. Eg- the risk a side effect A may be 25% for a group of 100 pts, but for any single pt, it's either 0% or 100%.
I give a lot of weight to Merckmanuals and drugs.com. If they list a side effect it usually occurs, maybe much less frequency than with ACE inhibitors. Good point that the risks are based on statistics. But that doesn't do much good for the pt who has acute kidney failure from taking a drug that supposedly protects the kidneys. There are just way too many drugs out there sometimes on the market for years before the downsides become evident-cox inhibtors as just one of many examples. A pharmacist once told me there are very few drugs on the market that are good. Doctors prescibe with abandon and patients accept without knowing the possible downsides. ARBs main indication is for lowering BP. So why would a CKD patient with leaky protein take that drug with potential serious harm when his/her BP is 115/70?
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So you are a physician?
