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Гемодиализ форум. Жизнь вопреки ХПН. » Форум пациентов » Мы начали жизнь на диализе. » Фосфатбиндеры - новые и не очень (P - Ca - ПТГ, интервью с Жозе Арруда из Чи)
Фосфатбиндеры - новые и не очень
binnick
Дата: Четверг, 15.05.2008, 11:30 | Сообщение # 1
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новости с первой страницы этого сайта: Launch of Renvela for Patients With Chronic Kidney Disease in the United States - речь о преимуществах нового фосфат-биндера Renvela и всяких связанных с этим вопросов. Для тех, кто интересуется, но не может прочесть новость на английском, привожу версию машинного перевода на русский язык:
Запуск Renvela для пациентов с хроническим заболеванием почек, в Соединенных Штатах Америки
 
Igor76
Дата: Вторник, 03.06.2008, 22:49 | Сообщение # 2
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спасибо за статью.
повышение ПТГ- плата за нормальные уровни кальция и фосфора? можно ли утверждать, что приоритет- нормализация уровней кальция и фосфора (учитывая риск кальцификации сосудов и сердечно-сосудистую смертность в итоге) в ущерб росту ПТГ? севеламер и аналоги вит D- эта связка понятна. какое место у сансипара? он предпочтительнее аналогов вит D (при условии переносимости)?

статья конспективно:
1. Renvela сочетает преимущества ренагеля с отсутствием некоторых побочных эффектов последнего (не вызывает метаболический ацидоз из-за замены гидрохлорида на карбонат).
2. Суточная доля кальция для диализного пациента- 2г (1.5- препараты Са, 0.5- с пищей).
кальцификация может быть связана с более высоким уровнем смертности диализных больных. Севеламер- средство выбора в плане предотвращения кальцификации.
3. за поддержание нормальных уровней в сыворотке фосфатов и кальция придется заплатить гиперпаратиреозом. повышение PTH необходимо для поддержания нормального уровня кальция и фосфора.
4.сывороточный бикарбонат менее чем 22 мг-экв / л имеет отрицательное воздействие на пациентов. Метаболические ацидоз может вызвать заболевание костей и может вызвать катаболизм белка. sevelamer карбонат контролирует уровень фосфатов в сыворотке и препятствует метаболическому ацидозу.
5. Контроль сывороточного фосфата в одиночку не может быть достаточным для снижения PTH. Необходимо использовать аналоги витамина D, такие, как doxercalciferol или paricalcitol, вместо calcitriol, т.к. последний, как правило, вызывает гиперкальциемию.



суета сует, все суета, и нет ничего нового под солнцем


Сообщение отредактировал Igor76 - Вторник, 03.06.2008, 23:18
 
binnick
Дата: Суббота, 20.12.2008, 20:56 | Сообщение # 3
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Говорят, эта статья не у всех открывается. Для любопытных привожу ее целиком
[
b]Launch of Renvela for Patients With Chronic Kidney Disease in the United States: An Expert Interview With Jose Arruda, MD[/b]
Posted 05/14/2008

Jose Arruda, MD

On March 6, 2008, Genzyme announced the US launch of the phosphate binder Renvela (sevelamer carbonate) for dialysis patients. Genzyme also submitted a marketing authorization application to the European Medicines Agency seeking approval of Renvela for the control of serum phosphorus in patients with chronic kidney disease (CKD) with the first EU launch of Renvela anticipated in the third quarter of 2009. Renvela is a next-generation version of Renagel (sevelamer hydrochloride) and while both are calcium-free, metal-free, nonabsorbed phosphate binders proven effective in controlling serum phosphorus levels in patients with CKD, Renvela offers all of the advantages of Renagel with the benefit of a carbonate buffer. Elevated serum phosphorus levels are common in dialysis patients and have been shown to be associated with increased risk of cardiovascular morbidity and mortality so controlling serum phosphorus is critical. To help elucidate the impact and significance of the recent US launch of Renvela, Anne G. Le, PharmD, RPh, Editorial Director of Medscape Nephrology, conducted an interview with Jose Arruda, MD, Professor of Medicine and Chief of Nephrology at the University of Illinois College of Medicine in Chicago, Illinois.

Medscape: With the recent US launch -- and eventual global launch -- of Renvela for chronic kidney disease patients on dialysis, what impact will this new development have on the treatment of these patients?

Jose Arruda, MD: The launching of Renvela will help patients with chronic kidney disease on dialysis because it is an effective phosphate binder. It is as effective as Renagel, but in addition it appears to have fewer gastrointestinal (GI) side effects. A greater percentage of patients should tolerate the drug and not have GI problems. Renagel is an effective phosphate binder but some patients cannot tolerate it. Simply stated, it provides another option to control phosphate with fewer side effects than sevelamer hydrochloride and does not cause metabolic acidosis.

Medscape: What attributes of Renvela do you consider to be an improvement over currently available phosphate binders for dialysis patients?

Dr. Arruda: I believe that sevelamer hydrochloride and sevelamer carbonate are very good binders because they are non-metal-based binders. Use of aluminum and calcium as phosphate binders caused several problems. Aluminum caused dialysis dementia and bone disease. That was followed by a period of many years in which we used high-dose calcium. The high-dose calcium carbonate or calcium acetate was associated with hypercalcemia and calcification of vessels. I think Renagel has been shown not to cause calcification and or hypercalcemia because the polymer sevelamer binds phosphate but it is not absorbed. That's the first important point. Whereas the metal-based binders might be absorbed, the sevelamer hydrochloride and sevelamer carbonate are not absorbed.

The main difference between sevelamer carbonate and sevelamer hydrochloride is that the chloride in the sevelamer resin was replaced by bicarbonate. That's the only difference. With sevelamer hydrochloride some patients develop metabolic acidosis because in the intestine chloride is exchanged for bicarbonate. You gain chloride and you lose bicarbonate. Metabolic acidosis has been observed in some patients treated with sevelamer hydrochloride. When you compare sevelamer hydrochloride in a head-to-head crossover study, in that you give sevelamer carbonate followed by sevelamer hydrochloride, or alternatively you give sevelamer hydrochloride followed by sevelamer carbonate, the serum bicarbonate did not drop decrease with Renvela. Indeed, the serum bicarbonate went up by only 1.3 mEq/L. Metabolic acidosis is believed to contribute to bone disease and to protein malnutrition. Some patients who eat large amount of protein also ingest a high phosphate load and may develop more severe acidosis, which is then prevented by the sevelamer carbonate.

Phosphate binders are currently approved only for patients with chronic kidney disease [CKD] on dialysis. They are not approved for patients with CKD prior to dialysis. Many nephrologists believe that patients in stage 3, and certainly stage 4, should be treated with binders. If and when the [US Food and Drug Administration] FDA approves the use of binders, I think Renvela is going to have an additional benefit in preventing acidosis. This should be an additional benefit, especially for the predialysis patients.

Medscape: Do you think all phosphate binders are created equal or do sevelamer-based binders like Renvela provide an added advantage over calcium-based binders?

Dr. Arruda: I strongly believe that not all binders are created equal. They all certainly are able to bind phosphate effectively. Indeed, I believe that used at the right doses, all binders lower the serum phosphate to the same degree and that's a matter of dosing them right, but as far as the consequence of the binders, I think there are significant differences. For example, we talked about the problem of aluminum and the complications of aluminum, which are now completely abandoned except in short-term rescue therapy. The National Kidney Foundation, through the KDOQI guidelines, has issued very good recommendations regarding the amount of calcium to be used. The amount of calcium to be used is not to exceed 1.5 g of elemental calcium through medication, plus another 0.5 g from the diet. The total intake of elemental calcium should not exceed 2 g in most patients. If you really look at the amount of calcium that can be given to a patient as a calcium binder according to these guidelines, it's equivalent approximately to 4 tablets of calcium carbonate containing 1 g or 9 tablets of calcium acetate. The reason for this recommendation is the high incidence of hypercalcemia in patients taking calcium binders.

There are studies conducted with sevelamer hydrochloride compared with calcium carbonate or acetate that clearly show that the development of hypercalcemia is significantly higher with calcium binder than with Renagel, sevelamer hydrochloride, and therefore sevelamer hydrochloride, or now sevelamer carbonate, would be better choices. They would decrease incidence of hypercalcemia and decrease the amount of calcification. There are some new data to suggest that the development of calcification may be associated with higher mortality rate in dialysis patients.

Medscape: Based on your extensive experience with Renvela to date, what advice would you offer clinicians on how best to use this new tool to control serum phosphorus levels?

Dr. Arruda: Well, I should first clarify that I have extensive experience with sevelamer hydrochloride. Our experience with Renvela is just beginning since it was just approved by our formulary committee and by the agencies that pay for the medications. Since we are now approved, we have begun to use Renvela. I think the experience is going to be very similar to that of sevelamer hydrochloride. My initial approach to these patients is to start every new dialysis patient that needs a phosphate binder on Renvela and gradually switch patients that are on sevelamer hydrochloride to sevelamer carbonate. I will start first with the patients that, for one reason or the other, are intolerant or have GI side effects with sevelamer hydrochloride, or lanthanum carbonate.

Medscape: How would you characterize the existing body of evidence for sevelamer and how will additional clinical trials already under way contribute to that knowledge?

Dr. Arruda: There are 3 important trials that have been conducted with sevelamer hydrochloride. The first trial is the Treat-to-Goal trial, whose aim was to look at the development of vascular calcification in patients on dialysis which is prevalent in dialysis patients.[1] Patients had been on dialysis for varying periods of time and were evaluated by electron beam computerized tomography [EBCT] to assess the degree of vascular calcification. They were then randomized either to sevelamer hydrochloride or calcium. They followed the degree of calcification for 1 year and both agents were equally effective in controlling serum phosphate. This study showed a significant increase in vascular calcification in patients treated with calcium. In patients treated with sevelamer hydrochloride, though, the calcification changed very little. There was a statistically significant greater degree of calcification in patients receiving calcium, as compared to patients receiving sevelamer hydrochloride. That was the first study to show that you can prevent the progression of calcification in patients on dialysis. Remember that the patients, when they start dialysis already had a significant degree of calcification, which tends to increase and this increase is prevented by sevelamer hydrochloride.

Another very important study is called RIND, which stands for Renagel in New Dialysis patients and instead of taking patients that were already on dialysis for a varying period of time, the investigators only studied patients who were new to dialysis.[2,3] They were randomized to receive either calcium or Renagel. The EBCT was obtained prior to and at the end of the study. There were 2 parts of the study: the first part included the degree, the prevalence and progression of calcification in patients treated with calcium as compared with Renagel. The second part of the study was to evaluate the mortality rate. After 18 months the patients were continued on their respective binders and the mortality was assessed. There are 2 striking features of the study. One feature was the fact that calcification was greater in patients that received calcium as compared to sevelamer. This was first study to show a correlation between the degree of calcification and mortality rate. The greater the degree of calcification, the more likely the patients were to die. Of interest is the fact that this is the first study to show that 15% of the patients do not develop vascular calcification, however, the reasons why these patients do not develop calcification remain unclear. The patients were followed after for a total of 60 months. There was a significant difference between the patients taking calcium vs the patients taking sevelamer hydrochloride. The mortality rate was significantly higher in the patients treated with calcium as compared to the patients treated with sevelamer hydrochloride. The limitations of this study were that the number of patients in each group studied was relatively small (approximately 60 patients) and they were relatively young.

The third study that I think is of great importance is the DCOR trial, which stands for Dialysis Clinical Outcomes Revisited. This was a multicenter, open-label, randomized study.[4] It included patients who had been on dialysis for different durations of time. They were randomized on a 1:1 ratio either to calcium or to sevelamer. The patients were followed for a period of approximately 4 years. A thousand patients, approximately, were recruited in each arm of the study. The primary endpoint of the study was all-cause mortality and the secondary endpoints were cause-specific mortality, such as cardiovascular, infection, and other causes of mortality, and all-cause hospitalization. There was no statistical difference between the sevelamer hydrochloride and the calcium regarding overall mortality. In other words, the study failed its primary endpoint. However, if you look at the group of patients, there are potentially 2 reasons as to why it failed. They enrolled approximately 1050 patients on the calcium and 1053 patients on the sevelamer. By the end of the first year, more than 300 patients in each arm had dropped out from the study. By year 2, they were down to 430 and 439 patients in each arm, respectively. For patients on treatment for 2 years or more, years there was a difference that appeared to emerge that favored sevelamer hydrochloride over calcium, but statistically was not valid to analyze that because the number of patients by year 3 was down to 161 in the calcium group and 196 in the sevelamer group. The trial was stopped after approximately 36-42 months and the number of patients that could be analyzed in between year 3 and year 4 was significantly decreased as compared to the beginning. The other problem is that the mortality rate was lower than originally predicted and that changed the number of patients that would be required to see a difference. The study did show a significant difference in overall mortality, all-cause mortality, in patients over the age of 65 at a significant level: P < .02. That difference was not seen in patients that were younger than 65 years old. This analysis has been criticized because the contention is that if a trial fails the primary endpoint, then it is not valid to analyze other endpoints. However, in this study design, prior to the beginning of the study, the authors had clearly prespecified that they would look for treatment interactions with certain variables which included race, age (which was specified at less than 65 and age greater than 65), gender, diabetes, primary cause of the end-stage renal disease, and how many years they had been on dialysis, in other words, dialysis vintage. This, I think, is a valid analysis because the pre-specified treatment interaction was clearly defined in the methods and therefore I think it was valid to analyze the group greater than 65.

The reason I mentioned these 3 trials is because sevelamer hydrochloride is the only binder that has outcome data regarding mortality rate and calcification and the possible relationship of calcification to mortality. The other binders have data to show that lower serum phosphate and lowering of the serum phosphate decreases secondary hyperparathyroidism and bone disease but there are no other outcome data.

Medscape: Considering the global burden of chronic kidney disease and the heavy toll it takes on patients across multiple organ systems, does sevelamer have other so-called pleiotropic effects that beneficially impact the heart, bones, and other areas of the body?

Dr. Arruda: That's a very difficult question to answer, but if I would say, yes, many people believe that sevelamer has pleiotropic effects on other organs. I believe this has been suggested in animal studies but clinical evidence is still lacking.

Medscape: Genzyme is currently in discussions with the FDA regarding the potential expansion of Renvela's label to treat hyperphosphatemic chronic kidney disease patients who are not yet on dialysis. What potential impact do you see this anticipated label expansion having on the overall care of patients with chronic kidney disease?

Dr. Arruda: I believe that it is extremely important to treat secondary hyperparathyroidism prior to the beginning of dialysis. The development of secondary hyperparathyroidism begins very early in dialysis. Most patients in stage 3 already have elevated parathyroid hormone (PTH) even though the serum phosphate and the serum calcium are normal. This is the so-called trade-off hypothesis, that's a term that they coined.[5] You maintain normal serum phosphate and normal serum calcium, but the price that you have to pay for that is secondary hyperparathyroidism. In other words, the serum PTH is elevated to maintain a normal serum phosphate and calcium. I believe that it is important to prevent the secondary hyperparathyroidism. It's important to prevent secondary hyperparathyroidism and bone disease, but now the evidence shows us that if you do not lower the serum phosphate, the serum phosphate starts to rise leading to vascular calcification.

A study recently published in Kidney International by Russo and colleagues studied patients with CKD stage 3-5 before dialysis.[6] They studied approximately 90 Italian patients that were randomized to 3 groups: a low-phosphate diet, a low-phosphate diet plus calcium carbonate, and a low-phosphate diet plus sevelamer hydrochloride. They did an EBCT at the beginning of the study and at the end of the study which averaged 2 years. At the end of the study there was progression of calcification in both the patients receiving the low-phosphate diet, as well as in the patients receiving calcium but in the sevelamer hydrochloride group the degree of calcification did not increase. The data was further analyzed by looking at the net increase in calcification at the end of the study. The net increase in calcification was significantly higher in the groups receiving the low-phosphate diet and in the group receiving calcium, as compared to the group receiving sevelamer hydrochloride. Not to be simplistic and say that calcium is the only culprit in the vascular calcification -- we now know that there are several factors that modulate calcification: calcium, phosphate, and PTH favor calcification while other factors inhibit calcification, such as fetuin and pyrophosphates as well as others. To make a long story short, there is no evidence that calcium, PTH, and phosphate play a role in vascular calcification. The vascular muscle cells transform to osteoclasts and these cells then promote vascular calcification. And as we said earlier, a large percentage of the patients who come to dialysis already have vascular calcification with EBCT scores varying from 200 to 400. Recall that the RIND study showed that the higher the vascular calcification at the beginning of dialysis, the greater the mortality.

The FDA has invited all 3 companies to present data on the potential beneficial effect of controlling phosphate in predialysis patients. The main advantage that Renvela will have for these patients is that most patients in stage 3 and 4 CKD have low serum bicarbonates, especially in stage 5. The KDOQI guideline has acknowledged that a serum bicarbonate less than 22 mEq/L has a detrimental effect on patients. Metabolic acidosis by itself can cause bone disease and can induce protein catabolism. Therefore, treating these patients with sevelamer carbonate would control serum phosphate and would prevent metabolic acidosis.

I think the nephrologists who are currently caring for CKD patients in late stage 3 and stage 4 will have a new drug to control serum phosphate and at the same time will prevent acidosis. I think the market for phosphate binders will expand significantly with the potential of preventing vascular calcification. I believe that there are studies now ongoing to evaluate the effectiveness of phosphate binders in CKD stage 4.

Medscape: How do you see Renvela ultimately working together with doxercalciferol, a current treatment for patients with chronic kidney disease?

Dr. Arruda: This is a very important question because I believe that the treatment of secondary hyperparathyroidism involves the control of serum phosphate. The control of serum phosphate alone may not be sufficient to lower PTH to the desired goal. You need to use analogs of vitamin D, such as doxercalciferol or paricalcitol, whatever your experience is, instead of calcitriol, because calcitriol tends to cause hypercalcemia. Hypercalcemia develops in a significant percentage of patients taking calcitriol. The prevalence of hypercalcemia with doxercalciferol or paricalcitol is around 2% as compared with 30% in patients taking calcitriol. In addition to preventing hypercalcemia, these new analogs of vitamin D prevent secondary hyperparathyroidism by 2 mechanisms. One is by enhancing absorption of calcium, increasing calcium to become elevated and thereby suppressing PTH. An additional mechanism is that they bind to the parathyroid receptor decreasing the synthesis of the messenger RNA for PTH. They are more effective in controlling PTH because they have a greater affinity for the parathyroid receptor as compared to the intestinal receptor, hence a lesser incidence of hypercalcemia.

There are 2 retrospective studies looking at the mortality rate of patients taking paricalcitol or doxercalciferol.[7,8] These 2 studies, albeit both retrospective, have clearly shown a 25% decease in the mortality rate with the analogs doxercalciferol and paricalcitol as compared to calcitriol. I think the tendency now is not to use calcitriol unless the patient has severe hypocalcemia, and instead use the analogs because the analogs decrease the mortality rate in dialysis patients. These studies have been criticized for being retrospective but I doubt that there will be a prospective study because the intuitional review boards for the protection of human subjects would likely not approve such a study. The effectiveness of these analogs in controlling secondary hyperparathyroidism and the decreased mortality will lead to the use of the combination of Renvela and doxercalciferol or paricalcitol to treat secondary hyperparathyroidism and to prevent cardiovascular mortality. This has already been done in stage 5 CKD patients on dialysis. It probably will extend to patients in stage 4 CKD, in which doxercalciferol is already approved for treatment of secondary hyperparathyroidism. And as we discussed earlier, Renvela and other phosphate binders are now being considered by the FDA but currently are not approved for treatment of high serum phosphate in predialysis patients.

 
suzdalka
Дата: Среда, 28.11.2012, 12:26 | Сообщение # 4
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У меня какой вопросик по новому фосфат-биндеру (Не по РЕНВЕЛЕ - судя по дате собщений это уже далеко не новый препарат)
Называется он ФОСРЕНОЛ (FOSRENOL) . Это ясное дело, иностранное лекарство.
Мужу прописала врач, так как у него не снижается фосфор, он сидит на Нефродине, но тот помогает только чуть.

Кто-нибудь слышал о Фосреноле? Насколько эффективен, есть ли принимающие его или информация от врачей по его эффективности?
 
Алексей_Денисов
Дата: Среда, 28.11.2012, 13:00 | Сообщение # 5
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ФОСРЕНОЛ - это карбонат лантана.. говорят что он эффективен.. а почему не используете дешевый и очень эффективный альмагель?
 
suzdalka
Дата: Среда, 28.11.2012, 14:30 | Сообщение # 6
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Хм, врач про Алмагель ничего не говорила. Изначально он пил Ренагель, потом его отменили из-за неэффективности (мы даже подарили новую упаковку таблеток нуждающемуся больному) и назначили Нефродин.
А насколько эффективен Алмагель по сравнению с Осварен'ом например?
 
Алексей_Денисов
Дата: Среда, 28.11.2012, 14:53 | Сообщение # 7
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Альмагель в хорошей дозе - один из самых эффективных фосфатбиндеров. Несколько десятилетий назад его активное применение было в ряде стран приостановлено в связи с возможной нефротоксичностью препаратов алюминия, однако в последующем алюминиевая токсичность этого препарата была признана многими специалистами ничтожной, скорее всего плохая очистка воды в то время давала эффект алюминиевой интоксикации. В настоящее время во многих странах гидроокись алюминия с успехом применяется. Назначаем альмагель и мы. Но все должно происходить под контролем врача.
 
Николай
Дата: Среда, 28.11.2012, 18:21 | Сообщение # 8
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Quote (Алексей_Денисов)
ФОСРЕНОЛ - это карбонат лантана.. говорят что он эффективен..

Ну вообще-то ГИДРОкарбонат, но для простого обывателя это ничего не скажет smile
Quote (suzdalka)
Кто-нибудь слышал о Фосреноле? Насколько эффективен, есть ли принимающие его

Я принимаю Фосренол уже 2 года, что позволяет совершенно спокойно употреблять все продукты питания без оглядки на содержание фосфора (конечно же при адекватном диализе). Из всех Фосфат биндеров, которые я пробовал - это самый эффективный, на уровне с Ренвеллой, но ту надо разводить, выпивать суспензию, что в не домашних условиях не сильно удобно, а Фосренол выпускается в форме жевательных таблеток которые по размеру и консистенции похожи на нашу аскорбиновую кислоту. Он не имеет побочных реакций и не накапливается в организме.
Quote (Алексей_Денисов)
Альмагель в хорошей дозе - один из самых эффективных фосфатбиндеров.

А почему Вы не говорите, что это разовая мера? Ведь речь идет о постоянном применении фосфат-биндера.
 
Алексей_Денисов
Дата: Среда, 28.11.2012, 20:33 | Сообщение # 9
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Ну вообще-то ГИДРОкарбонат
да, спасибо за поправку.
Quote (Николай)
А почему Вы не говорите, что это разовая мера?
потому что это не разовая мера.. длительный прием альмагеля возможен. Я бы не стал рекомендовать постоянный прием, но врач вполне может назначить прием в течении нескольких месяцев.
 
Николай
Дата: Среда, 28.11.2012, 20:54 | Сообщение # 10
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врач вполне может назначить прием в течении нескольких месяцев

А потом?
Quote (Николай)
Ведь речь идет о постоянном применении

Quote (Алексей_Денисов)
Я бы не стал рекомендовать постоянный прием

Quote (Алексей_Денисов)
это не разовая мера

wacko wacko wacko
 
Ludmila
Дата: Среда, 28.11.2012, 21:09 | Сообщение # 11
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и назначили Нефродин.

Он не шибко эффективен. В процессе применения выявились побочные: подъём кальция в крови до опасных для диализного пациента величин, и появление сильных болей в суставах, природа которых пока не ясна, т.к. препарат применяют недавно и у малого количества пациентов. Связь определённая-после отмены препарат боли исчезли.
Для тех, кто в курсе моих проблем с ревматоидным артритом, чтобы не возникло ложного восприятия информации: ЭТО НЕ ОБО МНЕ. О женщине с совершенно здоровыми суставами.


Бегущая по граблям
 
Алексей_Денисов
Дата: Среда, 28.11.2012, 21:10 | Сообщение # 12
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а потом после хорошего снижения уровня фосфора, если это будет нужно, можно перейти на другой фосфатбиндер
 
Igor76
Дата: Среда, 28.11.2012, 22:15 | Сообщение # 13
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Ну вообще-то ГИДРОкарбонат

лантана гидрокарбонат- это La(HCO3)3
вот китайский мешок такого порошка в 25 кг- http://en.yyre.com/product....03.html
Фосренол- это гидрат карбоната лантана La2(CO3)3xH2O http://dailymed.nlm.nih.gov/dailyme....id=3334
Quote (Николай)
но для простого обывателя это ничего не скажет smile


наверное, из такого порошка и делают таблетки, жаль цены на мешок в 25 кг китайцы не привели smile


суета сует, все суета, и нет ничего нового под солнцем


Сообщение отредактировал Igor76 - Среда, 28.11.2012, 22:19
 
Алексей_Денисов
Дата: Среда, 28.11.2012, 22:45 | Сообщение # 14
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Фосренол- это гидрат карбоната лантана
точно
 
Vasiliy
Дата: Среда, 28.11.2012, 22:55 | Сообщение # 15
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и появление сильных болей в суставах, природа которых пока не ясна, т.к. препарат применяют недавно и у малого количества пациентов.

Это ацетат-то кальция применяют недавно???
И природа болей в суставах из-за него не ясна?
biggrin biggrin biggrin
На сайт этого нефродина зашел - там ну такая развесистая клюква!!!


Десять лет я озвучивал фильм, но это было немое кино. (С)
 
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