I Hate Dialysis Message Board
Dialysis Discussion => Dialysis: General Discussion => Topic started by: fearless on February 27, 2012, 10:26:57 PM
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my clinic has begun to cut off the epo when Hg is above 11. Is this an implementation of a new medicare policy or just the tightwads at Fresenius?
policy is to be between 10-12, but they didn't used to cut you off til you went over 12 - so now my crappy-feeling weeks when i can't accomplish anything will be closer together :(
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It is new policy. 11 is fine. The maker of Epo was giving kickbacks to the clinics who would push Epo to 13. They were found out and everyone denied it. Using Epo is a delicate balance. If your blood gets too thick you have access problems and even heart attacks. In the old days before Epo they would wait until we got down to 8 before a blood transfusion. Talk about weak and tired.
11 is fine. :thumbup;
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forgive my ignorance - but what is epo ? Is Hg = haemoglobin ? Laurie's haemoglobin on last blood test is 7.8 . He has an injection once a month Mircera .
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My Hg is running 8.7 at last lab, and I take Epo once a week.
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Yep, the change took place last June 24th; here is the press release from Amgen:
http://www.amgen.com/media/media_pr_detail.jsp?releaseID=1579652
And here is the FDA press release:
http://www.fda.gov/Drugs/DrugSafety/ucm259639.htm
So no, it's not just Fresenius being cheap though I can understand why you'd think that!
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My Hg is 11.5, and I'm being firmly told to get it up to 12. I give myself Arenesp shots every three weeks.
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I think it is one big trial by the World Health Organization. In my clinic it is 12 (UK) But I have also had clots when over 11,5 so when I reach that I reduce my Epo (no I don't inform the ladies and gentlemen who get paid to 'look after my remaining health)
Good luck, and keep well, love Cas
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nope was told the same thing too. But now understand more of the heart attack cause. But im on PD without no arm or leg access. Will it still cause me to have a heart attack if my numbers were higher?
Lisa
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The range for Hgb to allow EPO treatment is now 9-10.5 at my clinic as of this month (once independent but now bought out by Fresenius). I do best at Hgb >12 at least and I think 13 would be better. I still work full-time and play a demanding competitive sport 3 times per week
Cheap bastards! :Kit n Stik;
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Well dont feel bad... even with transplant people my insurance want me to have my hemoglobin between 10 and 11...... since mine has been running in the 14 I get a letter each week reminding me of my goal..... which is between 10 and 11.......what am I suppose to do..... I dont want that low of level.......talk about being tired.....I feel bad for those of you that run low ....... when I was on dialysis and was in the 10's I was tired all the time...out of breath..... but when I was in the higher 11's I felt fine..... its all about the money.... I know there are some risk with epo....but there are risk with dialysis and transplant....what about quality of life.....
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I agree with Willis and tyefly--I do best with a Hgb over 12. Otherwise, I feel weak and breathless.
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Everybody's different. I don't know how anyone can make a blanket statement about what someone's Hg should be. Especially in that men are usually higher than women - so they are being more deprived by the low hemoglobin. I believe I've read that the "research" showing the danger of higher Hg in hemodialysis is rather controversial. If my iron is good, I'm good between 11-12 (I can do my laundry, buy groceries, take the trash out, wash dishes, get myself to dialysis, comfortably take off the fluid, don't feel exhausted before I get out of bed, able to speak coherently, enjoy some simple pleasures like going for a walk once in a while) below 11, I have to really budget my energy. I may accomplish one thing per day. And nothing on dialysis days (except dialysis) The problem is, I have no one to "pick up the slack". Things get depressing during the weeks after they stop giving me epogen and my Hg starts to drop. It takes a while for it to get back up there once the epo starts again. Also, long-term, anemia causes problems for the heart. Personally, I think some caution is warranted, but if I can't live my life because of anemia, then what's the point of preventing a heart attack? (also - anemia makes cardiovascular exercise difficult, and so is damaging to health in that way)
I believe Bill Peckham has written on this, and if I remember correctly, talked about leaving Hg to the discretion of the physician. Why not? Why should Medicare be making medical decisions? Let the doctors read the research and see what they think about it. And let informed patients decide what kind of risk they want to take (if there is one for that patient)
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fearless, it's not that high Hgb is the danger. It's the use of Epogen that's the danger. It wasn't a call made by Medicare but rather the FDA. Epogen is just plain dangerous. I, too, would love to have a higher Hgb level, but I'm not willing to risk a stroke to get it. There ARE worse things than dialysis... or anemia. To me, being a vegetable from a stroke is one of those things.
Have you tried talking to your doc about administering the Epo subcutaneously? When you do it that way you do not have to use as much, and the effects last twice as long. I've found since I started doing it subcutaneously that I have to take Epo for about two weeks (twice a week) and then I'm off it for five or six months. I've probably had fewer than a dozen doses of Epo in the last 18 months, which makes me happy. Contrary to what you might have heard, it does not hurt at all if you're using a multi-dose vial.
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A side note just to indicate the "high end" of hemoglobin concentrations. For professional cyclist, the most notorious of performance enhancing drug users (as a former cyclist, I believe this to be true), the upper limits for hemoglobin are 18.5 g/dl for men and 16.5 g/dl for women. It's odd how "naturally" all of these cyclist have hemoglobin concentrations right at those limits... Of course, there have been many cases of these very tough athletes dying due to overly high hemoglobin concentrations - generally in their sleep because their heart rates drop so low (40 and 30s) and their blood clots. I know it doesn't apply to the legitimate use of EPO here but thought some of you might find it interesting in a relative sense.
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You can't leave it up to Doctors to decide how much Epo to use. That is what got us in trouble in the first place. Amgen, the maker of Epogen was giving kickbacks (aka money) to Doctors and Dialysis Centers to use more EPO and thus a higher Hgb for dialysis patients because Medicare would pay for it. GREED.... Can't trust them.
:stressed;
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Lillupie, the risks are the same for someone with no access other than that you do not have an access to clot off.
My take on this is that it is about balancing benefit against risk and I can understand the rationale for reducing it, if that is the real reason for doing so and it is not just a cost-cutting exercise. Nonetheless, I do feel that there should be a higher level for men fortherrason that healthy men have a higher level than women.
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Can someone please clarify, with references if possible, about epogen and anemia. I have heard conflicting theories. One is that you don't want to use too much because it causes heart attack/stroke when your hemoglobin gets too high. The other theory I'm reading is that it is actually the Epogen, as in the components of the Epogen, that are dangerous.
Which one is it?
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Can someone please clarify, with references if possible, about epogen and anemia. I have heard conflicting theories. One is that you don't want to use too much because it causes heart attack/stroke when your hemoglobin gets too high. The other theory I'm reading is that it is actually the Epogen, as in the components of the Epogen, that are dangerous.
Which one is it?
Go up the page just a little; I provided just the info you're looking for.
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I want to say my insurance wouldn't pay if I was over 9. I think. It's been over 3 years since I got the shots, but luckily my body recovered reallly quick from the shot and I don't think I ever got more than 2 shots in a row before they would have to stop. Now, this is all in the doctor's office and not at a dialysis clinic (never on dialysis), so maybe it's different there. I was on Humana at the time.
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Desert Dancer- do you know what it is about the epogen that is dangerous? what does the epogen do that makes it such a health risk? I'm sorry, but I am still trying to understand, and understand a little more completely.
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Desert Dancer- do you know what it is about the epogen that is dangerous? what does the epogen do that makes it such a health risk? I'm sorry, but I am still trying to understand, and understand a little more completely.
justme, quite frankly I don't believe the causal relationship is clearly understood by anyone. There have been numerous studies done and the only thing anyone can seem to say with any certainty is that it is the use of erythropoietin-stimulating agents - not high hemoglobin in and of itself - that are the problem. Here are a few articles:
http://www.nejm.org/doi/full/10.1056/NEJMp0912328
An excerpt:
The most obvious explanation is that higher hemoglobin concentrations increase cardiovascular risk, but several observations run counter to this premise. In both randomized trials, and within each of their treatment groups, higher hemoglobin values were associated with fewer cardiovascular events. Similar associations have been found in the trials that supported the approval of darbepoetin alfa,3 as well as in observational studies of patients with chronic kidney disease. These associations might be confounded, however, because patients in whom higher hemoglobin concentrations are achieved may be healthier and therefore more responsive to ESAs.
Another possibility, and one of long-standing concern to us at the FDA, is that the risk of cardiovascular events is related to the rapidity of the increase in hemoglobin concentration, as well as to oscillations in hemoglobin levels and overshoots of the target concentration; aggressive dosing can cause all these effects. Such instability in hemoglobin concentrations could exacerbate the cardiovascular risk through hemodynamic or rheologic mechanisms. The original label for epoetin alfa included a warning regarding the risk of exacerbation of hypertension with hematocrit increases exceeding 4 percentage points (corresponding to increases in the hemoglobin concentration of approximately 1.3 g per deciliter) within a 2-week period. During a review of the marketing application for darbepoetin alfa, an association was found between rates of increase in the hemoglobin level exceeding 1 g per deciliter per 2-week period and the risk of cardiovascular and thromboembolic events.3 This observation provided the basis for a warning on the label for darbepoetin alfa (and eventually a stronger warning on the label for epoetin alfa) regarding excessive rates of increase in hemoglobin concentrations. Subsequently, the FDA found a similar relationship between such excessive rates of increase and the risk of adverse cardiovascular events in analyses of data from the Normal Hematocrit Study and the CHOIR trial.4
A third possibility is that the adverse cardiovascular events are not related to hemoglobin concentrations at all but are instead due to some off-target effect of ESAs — for example, trophic effects on vascular endothelial or smooth-muscle cells, or conditions precipitated by higher exposure to ESAs (e.g., iron deficiency). We have already found one such effect — the ability of ESAs to enhance tumor progression and shorten survival in patients with some types of cancer.
Another: http://www.medscape.com/viewarticle/564202_5
And an excerpt:
A fourth hypothesis relates not to Hb level achieved, but to targeting higher Hb and how this is carried out. Two of the changes in treatment required to increase Hb include an increase in ESA dose and increased use of iron supplementation. The increased ESA dose raises the possibility that some aspect of ESA drug treatment other than Hb level could potentially increase risk. ESA treatment results in serum erythropoietin concentrations that differ greatly from the normal biology of erythropoietin.[47] In particular, serum kinetics are notably spiky, with rapid surges in concentration followed by a steady decline, often to very low levels.[47] The effects of the non-biologic stimulation of erythropoietin receptors, particularly in non-erythroid organs including the heart, are unknown. In the heart, erythropoietin has been demonstrated to stimulate and reset growth signals and pathways.[48] The possibility exists, and is worthy of exploration, that there may be detrimental cardiac effects of excessive and cyclical erythropoietin stimulation. A direct effect of ESA treatment on hypertension, mediated by ESA-stimulated effects on vascular smooth muscle cells including increases in cytoplasmic calcium concentration, resistance to the vasodilatory effects of nitric oxide, and increases in endothelin production, has also been proposed.
One more from Medscape:
http://www.medscape.com/viewarticle/745984
Excerpt:
The first issue is related to dose. The cardiovascular event rates for patients in TREAT who were responsive to darbepoetin alfa (those treated with the low dose of ESA) were similar to the placebo group, whereas an increased risk of events was seen in the subgroup who were less responsive to treatment (those receiving the high dose of ESA).[5] Further supporting a potential effect of dose, patients in the CHOIR trial receiving the highest doses of epoetin alfa had the greatest risk of cardiovascular outcomes.[6] Although dose has largely been felt to be a marker of increased comorbidity, resulting in hyporesponsiveness, results from these two studies indicate that a direct dose–risk relationship is a possibility.
A second recurring theme is related to subgroups of patients at particular risk. The risk of worse cardiovascular outcomes associated with treatment using an ESA or treatment to a high hemoglobin goal (that is, utilizing an increased dose of ESA) also seems to be more apparent in individuals without a history of the event or without risk factors for the event than in those who do have a history. In addition to the analysis presented here, the risk associated with the highest treatment target in the CHOIR study was strongest in patients without diabetes mellitus or congestive heart failure, with little risk seen among groups with either of these comorbidities.[7] On a population level, one could hypothesize that whatever the mechanism for the risk, it is simply easier to 'see' it statistically in a population at low risk (that is, increased statistical power because of a large sample size within these subgroups owing to lack of competing risk). In a population at high risk, the mechanism may be dwarfed in relation to the underlying comorbidity, thereby not generating an increased relative risk. This concept has now been suggested by investigators of TREAT and CHOIR, as well as by the authors of this current analysis.
Until we understand the mechanism for the risk observed with ESA use, we should seek to use the lowest ESA dose required to meet the clinical goals of the patient. However, the analysis by Seliger et al.[3] highlights the most important medical need: we must understand the mechanism. What is happening to the patient as ESA doses are increased? What is happening to platelets, endothelial cells, and their interaction? As we seek to responsibly mitigate the risk of ESA therapy so that we can harness its beneficial effects on quality of life and avoidance of transfusion, what other safety lessons are we missing? At this point, we need to stop asking whether a relationship exists and start answering how the risk is conferred.
I just love those last three sentences... um, aren't these questions that should have been explored BEFORE the drug was approved? You might think.
Bottom line... no one is sure yet just HOW the ESAs cause problems, though study is ongoing and several themes seem to be emerging that need to be chased down. In the meantime, the FDA has issued a 'Black Box' warning for ESAs - the last step before pulling a drug off the market. Personally, I'd rather deal with a lower Hgb level than take my chances with Epo and that's why I call all the shots when they want me to take it.
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hmmm, I see. that is what I was looking for. some studies on epogen and its risks. thanks!
not very comforting however, considering I take 50,000 units of procrit every week...:-(. and that keeps my Hgb in only the 7-8 range. :-( :-(
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hmmm, I see. that is what I was looking for. some studies on epogen and its risks. thanks!
not very comforting however, considering I take 50,000 units of procrit every week...:-(. and that keeps my Hgb in only the 7-8 range. :-( :-(
Ouch, that sucks. Have you ever considered administering the Procrit subcutaneously rather than intravenously (if you aren't already)? There have been studies showing that administering ESAs subcutaneously allows for a much lower dosage AND the effects last longer. The official guidelines actually recommend it. Here's one of them with an excerpt:
http://www.nejm.org/doi/full/10.1056/NEJM199808273390902#t=articleDiscussion
During the maintenance phase, the average weekly dose of epoetin was 32 percent lower in the subcutaneous-therapy group than in the intravenous-therapy group (Table 2Table 2Results during the Maintenance Phase of Subcutaneous and Intravenous Epoetin Therapy. and Figure 1Figure 1Average Epoetin Doses during the Maintenance Phase in the Subcutaneous-Therapy and Intravenous-Therapy Groups.). When the analysis was restricted to the 138 patients who completed the 26-week maintenance phase, the average dose in the subcutaneous-therapy group (104±60 U per kilogram per week; 75 patients) was 27 percent less (P<0.001) than that in the intravenous-therapy group (142±72 U per kilogram per week; 63 patients).
A concern with the subcutaneous administration of epoetin is the pain of injection.9,10,30,31 However, the acceptance of subcutaneous administration in our study was good. We attempted to minimize the pain of subcutaneous administration by using an epoetin concentration of 10,000 U per milliliter and using insulin syringes with small-gauge needles for injection. Since the initiation of our trial, epoetin with benzyl alcohol as a preservative has become available, and this formulation appears to decrease the pain of subcutaneous injection without reducing the efficacy of the drug16 and may thus further increase the acceptability of subcutaneous administration.
In conclusion, in patients with end-stage renal disease treated by hemodialysis, hematocrit values of 30 to 33 percent can be maintained with about one-third less epoetin when the drug is given subcutaneously than when it is given intravenously.
Here's another link, to the KDOQI Guidelines (again, with an excerpt):
http://www.kidney.org/professionals/kdoqi/guidelines_updates/doqiupan_iv.html
IV. Administration of Epoetin
BACKGROUND
When Epoetin was administered during the initial clinical trials in the United States to patients with CKD, it was not known whether it would be effective and at what dose. Therefore, to assure that 100% of the dose would be available to stimulate erythropoiesis, Epoetin was administered intravenously. Subsequently, pharmacokinetic studies noted that subcutaneous (SC) administration provided elevated blood levels of Epoetin longer than the same dose given intravenously. In most countries outside of the United States, Epoetin is administered subcutaneously to most CKD patients. When the data from the many studies comparing IV to SC Epoetin are analyzed, the SC route of administration is as effective or more effective in the majority of patients than if Epoetin is given IV. Therefore, the Anemia Work Group recommends that SC Epoetin be the preferred route of administration.
I can tell you from my own experience that I decided to switch to SC administration probably, oh, about a year ago. When I am on Epogen (rarely) I take 2,000 IU twice a week and I inject it into my belly roll (the one everyone has when they sit down); there is absolutely no pain at all. I'd heard reports that it was painful but that has not been my experience at all. Generally I have to take Epogen for about two or three weeks - 4 to 6 doses - and then I don't have to take it again for another six months or so, so I end up taking about 8-12 doses per year total. I also get IV iron every month.
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yeah, I get mine subcutaneously in my arms. and it hurts, but it's not horrible. I actually see my hematologist tomorrow. we talked about the risks last time I saw her, and she said it was because procrit increases your blood pressure which puts you at higher cardiovascular risk. perhaps I should show her these excerpts of journal articles tomorrow. i don't know, i feel like she thinks I'm whining. I feel like she's thinking ' i'm treating patients that are dying of cancer and you're complaining about taking a procrit shot...'
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dear justme15 if you warm up the syringe (in your hand or on top of the machine) it doesn't hurt at all, and please show her those articles, cos a bit of schooling never goes a miss.
love Cas
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Desert Dancer,
I very much appreciate the links and your thorough replies.
It's apparent that your kidneys are still producing erythropoeitin. Mine are not and have not for a dozen years. When I get epo, I have blood. When i don't, I have no blood. My Hg goes up and down because of the parameters for administration. But it takes much longer for it to climb up than it does for it to fall down. So, for a brief time I am able to accomplish various tasks, and then for a much longer time I am not. So, although I don't like to risk having a stroke, at this point I'm willing to do it.
I don't like that my doctor, who has the information and can talk to me about what I want to do, is not allowed to give me a dosage that will allow me to continue to live a life worth living. When my hemoglobin gets down near 10, I have symptoms like irregular heartbeat and slight dizziness. Also, when my Hg is above 11, I am able to add exercise to my activities - this sort of activity wasn't factored into the studies. Also, in the studies, the upper levels that were studied were above "low normal" - and that's not what 11-12 even is. Two of the three studies were done on patients who were not on dialysis. It's very likely that those patients were still producing adequate erythropoeitin to force their Hg above the target when they were given higher doses of epo.
I think these studies are flawed. We've known for years that using epo to artificially raise Hg and hematocrit above the levels it would normally be in any given person can cause strokes and heart attacks. Increased hematocrit raises blood pressure (more red blood cells trying to fit in the vessels> higher pressure.
I'm angry that one more tool of normalcy has been taken away from me. And worse still, I feel overwhelmed at the prospect of trying to fight the bureaucracy to reclaim help. I feel too tired.
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My personal gut feeling on this is that they keep lowering the standard because it is cheaper and they want to cut cost every way possible. Lower hq bar= less epo= less money being spent on epo. I truely believe that. I may be wrong. I tend to not like studies because you dont know who is behind the study. The results can be played with to prove a point that they want to make up. If Im going to try to prove a point, Im going to focus more on the study results that will side with me.
That may be so that epo increases your blood pressure then causes strokes and heart attacks. But does anyone on here really know of anyone who actually had a heart attack because they had high blood pressure straight from getting epo?? I have given myself epo over the last 4 years and it hasnt caused my blood pressure to be any higher then normal.
I guess Im wrong because I dont conduct my studies and Im also being paid to conduct studies to prove a point.
Its not fair and I feel sorry for guys because they need a higher HG themselves.
just my :twocents;
Lisa
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My personal gut feeling on this is that they keep lowering the standard because it is cheaper and they want to cut cost every way possible. Lower hq bar= less epo= less money being spent on epo. I truely believe that. I may be wrong. I tend to not like studies because you dont know who is behind the study. The results can be played with to prove a point that they want to make up. If Im going to try to prove a point, Im going to focus more on the study results that will side with me.
:2thumbsup;
If the BOTTOM range of normal for HgB is 13 (at least for adult males as printed out on my lab results) then what is different just because I'm a dialysis patient, especially so since I work full-time and exercise heavily 10-12 hours per week? Yes, I might concede that getting Epo during hemodialysis might be a greater concern (I'm on CCPD). And of course someone with coronary disease or other specific health issues might be at greater risk. Isn't that supposed to be the doctor's job to figure out instead of some bureaucrat at Medicare? It has to be about the money...
BTW, the range was just lowered to 9-10.5. Oh, jump for joy everyone...we are getting screwed again. I guess I should just be grateful I'm still alive even if the government thinks just being alive but not able to LIVE is the goal if it saves money. (I admit I'd be dead now without Medicare because I sure couldn't pay the $60,000 per month my clinic gets!)
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The blood gets thicker as the Hb gets higher, hence the increased risks of heart attack and stroke and also the risk to clotting off a fistula. If I rememer rightly these issues were first highlighted when it was given to cancer patients. Mind you, in the past I wasn't that great at remembering to take my epo, I kept getting told about how a low Hb is bad for my heart. Go figure.
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Two quick corrections here, if you please:
Isn't that supposed to be the doctor's job to figure out instead of some bureaucrat at Medicare?
Medicare has nothing to do with this. This was a recommendation from the FDA... AFTER Amgen voluntarily (!) lowered the range and terminated their studies early due to alarmingly high death rates.
BTW, the range was just lowered to 9-10.5.
Actually the officially recommended range is 10-11, though your clinic may have its own parameters (my clinic's is 10-11.5 and I disregard their upper limit).
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just a natural way to increase hemoglobin. i know it sounds crazy but a woman that I worked with told me that broccoli raises hemoglobin, i thought she was nuts, but ever since i have been eating more my hemoglobin runs 12 to 13, and i havnt had epo in so long the vials i had expired. i dnt know if there is any relevance but for me it works... now my iron thats another swtory... but dnt do it if your on potassim restriction, bad idea. I am on lasix so washes out my K so no worries... my on prob is that damn phosohorus... thts the only number that was out of range this month, and my calscium was low, but changed my sensipar... hope this helps... i hate takin epo, i hae shots
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hmm i might try that. Going to be hard because broccoli is one veggie i do not like. lol
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Two quick corrections here, if you please:
Isn't that supposed to be the doctor's job to figure out instead of some bureaucrat at Medicare?
Medicare has nothing to do with this. This was a recommendation from the FDA... AFTER Amgen voluntarily (!) lowered the range and terminated their studies early due to alarmingly high death rates.
BTW, the range was just lowered to 9-10.5.
Actually the officially recommended range is 10-11, though your clinic may have its own parameters (my clinic's is 10-11.5 and I disregard their upper limit).
Thank you for the correction. I did read somewhere after I posted it that is was the FDA and not Medicare.
And it's interesting that the "official" range is 10-11. My "independent" clinic was just bought out by Fresenius (though they PROMISE, just PROMISE that we'll still be using Baxter equipment and supplies as long as we want). Now all of a sudden I'm told that the range is 9-10.5 and there's nothing they (my clinic) can do about it. I could use that extra 0.5! My last HgB count was 10.8--so no EPO for me.
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Thank you for the correction. I did read somewhere after I posted it that is was the FDA and not Medicare.
The confusion is understandable. The FDA recommendations refer to the upper limit of Hgb but I do believe there is an ongoing discussion about Medicare eliminating the lower limit. To me the latter just reeks of cost savings and nothing more and I strongly disagree with it.
And it's interesting that the "official" range is 10-11. My "independent" clinic was just bought out by Fresenius (though they PROMISE, just PROMISE that we'll still be using Baxter equipment and supplies as long as we want). Now all of a sudden I'm told that the range is 9-10.5 and there's nothing they (my clinic) can do about it. I could use that extra 0.5! My last HgB count was 10.8--so no EPO for me.
Perhaps print out the recommendations from Amgen and the FDA and show them the official range?
Last month my Hgb was 10.9 and my nurse told me to continue with the Epo. Uh, NO. I stopped taking it. Three weeks later my Hgb was 12.2 and she told me to hold the Epo. I informed her that I had stopped it when my Hgb reached 10.9 (it was noted on all my flowsheets, guess she doesn't look at them). Can you imagine if I'd followed her instructions? My Hgb probably would have been north of 13, 14 or more!
She didn't say anything but I could tell she was pissed. I just love how these clinics think their 'policy' should override science. Luckily I don't want a transplant so they don't have the 'non-compliance' threat to hold over my head.
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Amgen placed new prescription recommendations on it's labels, and the FDA followed suit. But it IS Medicare that's limiting the reimbursement for patients whose Hg's are over 11.
So: welcome to the brave new world: Your doctor wants to keep your Hg at 11.5? Sorry, medicare won't pay for it. So, it's official, the GOVERNMENT is deciding what's good for the patient, NOT the doctor. YES IT'S ABOUT MONEY! Have you noticed the brand new surge of lawyers advertising to sue for patients who've been "injured" by epogen? I'm highly suspect of the way the results of this research have been used to re-write government reimbursement policy. It reeks of big corporate greed and lobbyists.
No one is really examining the validity of these studies for various kinds of renal patients. And there is no accounting for those of us who become disabled by anemia, even though there are many people who seem to "adjust".
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So: welcome to the brave new world: Your doctor wants to keep your Hg at 11.5? Sorry, medicare won't pay for it.
My clinic's official range is 10 -11.5; somehow I don't think they're giving away Epo for free.
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Desert Dancer,
What clinic are you at? (if you don't mind) I may join you!
But I believe the CMS payment has just been limited to maintenance at or below 11 and above 10. I would REALLY be happy to find out that it's 11.5, because then all I'll have to do is put the screws to my doc instead of the federal government! :)
(thanks DD)
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Desert Dancer,
What clinic are you at? (if you don't mind) I may join you!
But I believe the CMS payment has just been limited to maintenance at or below 11 and above 10. I would REALLY be happy to find out that it's 11.5, because then all I'll have to do is put the screws to my doc instead of the federal government! :)
(thanks DD)
It's a DaVita clinic and they get very pissed when I refuse to go above 11. I have to think it's a corporate-wide policy, though I could be wrong. My clinic is very big on parroting 'corporate policy' at me.
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"Until we understand the mechanism for the risk observed with ESA use, we should seek to use the lowest ESA dose required to meet the clinical goals of the patient."
Like Fearless, i suffer from palpitations, exhaustion and the inability to,function normally when my Hb falls. My clinical goas are to overcome these so that I can attempt to live as normal a life as possible.
I was on EPO way before it was available for use in the US and even before it was marketed in the UK. I was
Prescribed it when it was only available on a named-patient basis as part of its pre-marketing research.
I was also on heavy doses during pregnancy, without which,,I suspect, I would not have had a successful outcome.
To me, the benefits outweigh the risks. If the problem is due to dosing methods, then that issue certainly needs to be addressed. I find it extremely irritating that clinics chase the guideline figures, overshoot it and then cold-turkey me from EPO completely until it plummets below the guideline minimum, just to repeat this over and over again. I can chug along quite happily on a low level, but when my Hb is allowed to drop suddenly, as it does when administered in this manner, then I get symptomatic. In my view the lowest dose possbile should be given that mitigates the symptoms of anaemia, tailoring it to suit the individual but, most importantly avoiding swings that the article that you have quoted, Desert Dancer, may be one of the issues associated with adverse outcomes.
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Amanda,
once again, my experience mirrors yours exactly.
I'm encouraged that DD's DaVita clinic has a range up to 11.5. Perhaps Fresenius is simply placing their upper limit at 11 to avoid having people go over 11.5, because it seems the reimbursement is based on staying within the range. For me they will have a hard time meeting the lower end, since my HG also plummets below that when my epo is held. Perhaps with others reacting the same way, that is why providers might seek to drop the lower limit. That way it would be very easy to ALWAYS be reimbursed for every drop of epo that's dispensed. Perhaps still further, there may be a grand unrealized experiment: we know people have strokes and heart attacks when their Hg is kept artificially high. Let's see how many heart attacks they have when we keep them just above transfusion level. (but as you say, isn't that already known?)
This has effected me so profoundly the last couple weeks (with my Hg dropping quickly from 11 to 9.5) - heart pounding, skipping beats, etc. - as you mentioned the dangers of the fluctuations) that right now it's simply about keeping my peace of mind, as I have absolutely no control over the short-term future, and I have no idea if or when I, or anyone else will be able to bring about a change.
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Hi, im not currently on dialysis but my gfr is 8.8%, they're holding off as im having a live donor transplant in 8wks from my dad. They said id have to have epo but havent bothered as im so close to transplant. They said anything under 8 and id have transfusion during op. Funny thing is my iron was 9.5 and then 7 weeks later is now 10.3! I never feel ill with low hg anyway, think my bodys just adapted cos it was permanently low when i was pregnant (my daughters 8 mths). So anyway i didn't want my iron to drop so started taking spatone (hope u have it in the states?), midwives recommended it to me, its a liquid iron u can take 1-2x daily and is better for absorption. I took it along with true food easy iron capsules hoping to keep iron level steady and am amazed its gone up so maybe if u hate the epo try spatone? Children can have it so its not bad for system or anything, and obviously pregnant women too. Docs were surprised it had gone up , is apparently quite unheard of at this stage without epo so give it a try!
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dear Iainiepop Maybe you it is an idea to ask for a bloodtransfusion from your dad, so you won't increase antibodies. I had that with my TX from my dad in the 80's, cos operating on you with a low Hg is no good.
Just a suggestion
good luck already, love Cas
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Hi Cassandra, i actually suggested to the transplant team what u just said 2 mths ago when my hg was down at 9. They refuted this and said its not something they do, and if i desperately needed a transfusion after the op it wouldn't matter once the kidney was in, wouldn't affect the antibodies or rejection as this is what i was worried about. However she said they do not tranfuse you at all unless hg goes below 8, they'd rather just give a few iron infusions after the surgery. But now its gone up to over 10, i don't think they're thinking bout infusions at all as when i get dads kidney they say hg will go up over 11 anyway. I think this is standard in the UK as when i had my daughter 9mths ago i had a c-section where i lost a litre of blood, iron was 9, no transfusion until under 8, the midwives wouldnt even give me an iron infusion as i wasn't showing any symptoms of anemia and was coping fine! The kidney specialists got one organised for me later which put it up to 11.7. Funnily enough i asked the nephs about a blood tranfusion during the section and they said they didn't want me to have a transufusion unless hg dropped to 4!!! This was because obviously transfusions raise antibodies and they knew id need a transplant soonish, they said id just have to have a shed load of iron infusions, luckily this didn't happen! So i don't know really....i totally get what you're saying cos its what i thought myself! Guess different hospitals have different policies too! x
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