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Management of Anemia in CKD

Mar 22 | 2:30 PM

Anemia can occur early in kidney disease, but symptoms may not appear until the disease is advanced. The greater the kidney damage, the more severe the anemia is. Erythropoietin (EPO) and iron are the two most common therapies for anemia in kidney disease. Vitamin B12 or folic acid supplements, dietary adjustments, or blood transfusions are also possible treatments for anemia. Let's hear from Dr. Sonal Dalal, an eminent nephrologist, about new developments in the Mx of anemia in chronic kidney disease.

[Music] good evening everyone this is dr rishali from netflix and i welcome you all for this interesting session on management of anemia and ckd and as you all know for this month our hashtag has been hashtag women in medicine so today we have with us an amazing nephrologist from ahmedabad she is dr sonal dalal she is working as a consultant nephrologist and also as a transplant physician in the gujarat kidney foundation as well as sterling hospitals with almost two decades of experience i'm sure you all are going to learn a lot about the recent advances in managing the anemia she's done her mbbs then md in internal medicine and then dnb in nephrology so without any further delay i'll just hand it over to you ma'am thank you netflix for this wonderful opportunity uh this is a kind of a new thing for me and uh thanks for giving us some learning platform uh i'm sure uh this is going to be useful for all the medical facilities and today i am going to speak on recent advances in management of anime of ckd uh basically uh ckd uh is a rising uh like as the longevity of the person is increasing as chronic diseases are increases we also see the secretive scenario which is significantly increase the number of patients uh the prevalence of ckd has is almost five point uh it has gone up to nine point one percent so under the anemia is a one of the most significant key uh symptom or a key finding in the patients of ckd and as the ckd stages progress the incidence of anemia increases so as you can see the anemia in secret stage 1 or stage 2 is less common but as the secret stage progress the anemia incidence goes on increasing so in a general population if we see the anemia is around fifteen point uh seven point six percent as against the secret it is for fifteen point four percent and uh as the secretary uh uh since uh this is a stages progresses uh in stage one to stage two secretly the incidence is around eight point four percent whereas in secret stage uh four or five the incidence of anime is almost as high as 53 percent so it is one of the major problem of ckd patients which we need to treat well and why it is essential that we have to treat these patients uh anemia because if it increases the risk of mortality all cause mortality has increased it also increases the risk of fatigue depression reduced exercise tolerance stroke and there is also increased risk of hospitalization uh anemia is also associated with faster progression of lbh there is inflammation increase more myocardial infary peripheral oxygen demand which is also increased and there is increased risk of mi and heart failure so these are the adverse outcomes which patient will uh face when uh if anemia is untreated and that is why it is very important that we have to treat it uh what is the pathogenesis of anemia in patients of ckd it is a as you can see there are multiple uh things which are contributing to the anemia the most important uh in ckd is the reduction in the electroporting production erythropoietin is a hormone which is produced by the peripheral capillaries of the renal tables and in the as the anim security progresses the production of epo reduces and it is a very important hormone which is produced by the kidney and which is required for the synthesis of rbcs in the blood bone marrow other things which are responsible for the uh anemia of secret is uranic toxins which uh reduces the erythropoiesis uh so uh they inhibit there are multiple factors which are responsible for the any hemoglobin production so uranic toxins itself also are responsible for the anemia there is a shortened lifespan of the rbcs uh there is blood loss blood loss is majorly seen in patients who are on dialysis where they have multiple uh factors which can lead to blood loss like during dialysis multiple phlebotomies for the blood test so blood loss is one of the major factor uh then uh the other very important factor is the hypoxidine uh the hepatin is a enzyme which is uh responsible for the uh iron utilization so in secret the epsilon levels increases and this increased accident level prevents the iron utilization because of the reduced gi absorption of the iron and reduce the disintegration of iron and ferropointing so that's why uh hepatitis increase is one of the important factors of anemia contribution to the ckd and i availability of the iron also is one of the important factors for the pathogenesis of anemia of ckd the other factors which can cause anemia uh are there are three different factors one is the correctable factors then potentially correctable factors and not correctable factors the collectible factors are like iron deficiency which is either absolute or a functional ion deficiency then b12 are solid deficiency hypothyroidism incinerators and airways usually we don't use it after secretly stage three and four because of the hyperkalemia but sometimes they are required in later stages of security in the potassium permits and they are one of the important factors for reduction in the hemoglobin and non-addurance to the therapy is another important factor which can be correctable for the anemia the potentially correctable factors are infections inflammations under dialysis then hemolysis because of certain uh dialysis of problems like patient uh having uh temperature values of temperature which is at a problem or because of the some heavy metals so hemolysis is one of the very very rare but responsible factor for the anemia then bleeding as i said during dialysis or gi bleed or because of the multiple flavor atoms which are required for the blood testing uh prca is a unique problem to the patients of anemia of ckd because when you use erythropoietin for long term patients can develop antirethropoid antibodies and which can lead to pure rate cell happens here so this is seen very rarely but it is a one of the problems which can be responsible for the erythropoietin non-sensitive a patient that is not responding to erythropoietin and which can contribute to the significant anemia because the modality of treatment is also not effective other correctable factors like some malignancies or malnutrition which can be treated and there are certain factors which are not treatable like patients who have a hemoglobinopathies like aplastic anemias or melodious plastic syndromes or something like that or bone marrow disorders wherein you will not be able to correct them and the patient will become transmission dependent but these are the major factors which can lead to anemia now what are the treatment options for the patients who are uh having anemia so there are four main treatment options one is transfusion then epithelium that is erythropoietin building agents which we called issa then iron and the newer ones are fifth phis these are the newer molecules uh hydrophilic factors which are this which are a very unique treatments which is now available so first we think about the transfusions uh as far as uh newer treatments like electroporting and iv iron and things are available we were dependent on transfusion in the earlier days when these newer modalities were not available every patients on dialysis would require blood transfusion every month or every three weeks and the major setback which these patients used to get because of the transfusion is they will get sensitized if they are planning for kidney transplant they will get hls sensitization and then they lose their chance to get a good donor match so transfusion is one of the main important uh problem is hla sensitization other side effects with al uh transfusion of course are viral infections like hiv h message and hcg and iron overload so it is not a good option unless it is very much necessary we should avoid transfusions in these patients uh other managements of ckd anemia the cadigo has given a lot of guidelines how to investigate these patients then what are the different uh definitions of hemoglobin and uh when to start iron when to start aeropod and so this is the guidelines which are been given by cadigo which i'll be discussing in details further so what are the target hemoglobin uh and iron diocese and patients of ckd so if patient is a of chronic kidney disease which is not on dialysis the target hemoglobin which we should aim is at about 10 grams and feratin should be above 100 and transfer and saturation should be about 20 this is what we should aim at and if patient is on dialysis already on secret stage 5d then the target of hemoglobin is between 10 to 11.5 the ferrari should not exceed 200 usually not 700 and transfer in saturation not more than 40 percent is what we should aim at the systemic ion absorption uh is required uh invention of the anemia with ckd when they have been given oral iron there is a lot of problem as far as iron metabolism is concerning patients of uh ckd uh basically uh how do we get iron in our routine uh hemophilosis the requirement of iron is supplemented by uh one of the few factors uh one important factor is the synesthetes so these are this is when they uh uh lives they will liberate some amount of iron so around 20 to 25 grams of iron of daily requirement is uh supplied by the cinesent rbcs and this ion gets recirculated and is uh available for the bone marrow uh there is another uh as i told you another enzyme which is very important for the ion utilization is a hepsidine it is a cell membrane iron exporter mainly expressed by the macrophages and on the basal lateral membrane of the intestinal cells and this hepatin production is stimulated by the iron concentration higher the iron concentration higher is the stimulation of the hepsidine and also by the pro inflammatory cytokines so if there is any inflammation the fat inflammatory cytokines will increase the production of accident which in itself will reduce the uh availability of the iron by reducing the uh making it unavailable because of the multiple enzymes which will inhibit by the activation of epsilon uh there are iv irons which are are now available uh which are of different uh areas we have got newer and newer ion molecules so to begin with we had iron sucrose and then now we have a uh carboxymaltose isometrics so we uh have uh evolved a lot uh as far as our iron availability and iron uh [Music] modulative treatment which is available has evolved a lot so to begin with we were dependent on oral iron which is very much uh unpredictable as far as absorption is concerned and also there is a intolerance to the oral iron in majority of the patient because of the gi intolerance they are not able to take it so widespread use of ib iron has now been accepted high molecular weight dextran form of iron used to cause anaphylaxis and so now it has not been used but other iv preparations consisting of iron poly nuclear so basically the iron is coated by the uh polynuclear core is surrounded by a carbohydrate shell that acts as a stabilizer and it prevents the uncontrolled release of the toxic free irons and this will prevent the reaction uh so what is the difference in various compounds in the in in nutshell is a difference in the carbohydrate moiety which is uh attached to this free iron and this stabilizes the iron and depending upon the this carbohydrate moiety we can decide which ion can be given at one dose so the one which are available uh is uh iron sucrose which we can give up to 200 milligram in one single dose then comes the carboxymaltox which we can give up to 1000 milligram in one single dose and then isomaltos which is also very safe we can give up to 200 milligram per kg and so all these newer ions are very safe and can be given in a single dose and even in a single push instead of giving an infusion even you can give over 10 minutes very slowly you can immediately without dilution also you can give the newer ones the other compound which is now available which makes ion utilization is a lactoferrin ectopherine and a disodium guanosine and f5 monophosphate it is lactoferrin is a non hemain binding protein with high affinity at ph lower than four it reduces the hexagon level and inflammation it stabilizes the iron ferro part in excess and it increases the iron flux from the macrophages into the circulation so when patients who are having on optimal essa's and optimum iron therapy but still they are not responding sometimes giving lactoferrin helps so according to the results obtained in a clinical trial oral lactoferrin was better tolerated and more acceptable with higher increase in main hemoglobin when compared to the oral ion therapy alone so oral lactoferrin can be used as a good substitute in patients who are having iron deficiencies who are not responding only to the iron therapy then came the era of essa's that is erythropoietin stimulating agents which was uh initially discovered in 1977 uh in the patients who were having a plastic anemia from the urine of these patients it was isolated and the it was then recombined electrocutions were available in 1990 and it was one of the wonder drug which was available for the patients of ckd for anemia and as you can see uh the increase in hemoglobin from baseline was almost 5 grams in period of 12 months so a very good rapid rise of hemoglobin could be achieved with the these agents but over the period of time we also link learned a lot about this molecule and as you can see in this study it was a double blind randomized placebo control study wherein 118 patients of hemoglobin hemodialysis they were randomized and what was observed is that the hemoglobin was significantly improved the quality of life and exercise tolerance also improved significantly but there was increase in uh diastolic blood pressure and there is also increase in vascular excess clotting so increase thrombotic tendency so this was the thing which was then studied by multiple other trials in patients who are on uh dialysis like there are so many trials which were done to evaluate the safety of these molecules mainly the normal hematocrit trial coil trial create trial and pre-trial these are the landmark trials which were done to see the efficacy of these molecules and safety of these molecules and what we came to know is that when we give the hemoglobin this is us to improve the hemoglobin if we overshoot and if we increase the hemoglobin concentration above 12 or 13 there is increased risk of cardiac evidence there is increased risk of vascular excess thrombosis and there is also increased risk of uh all kind of cardiac events like mace score increased in all of this patient and so there came a black box box warning on isage that it should not be given if the hemoglobin concentration rises above 12.5 or maximum 13 because of the associated side effects so management uh is a when it comes to the management we have to do a balance between the iron and esa's and uh what are the different modalities of treatment like if you have a anemia due to blood loss we have to give a blood transfusion there is no uh substitute for it but along with that we have to uh after correction of initial this we have to start uh giving the iron and ether which is given at the later date if patient has a nutritional deficiency we have to give b12 and other things and if it is due to the ckd first we have to replenish the patient with the iron which is then followed by the erythropoietin don't start electro14 immediately without replenishing the ions so we have to assess the ion status make the iron transfer in saturation about 20 and then start with ess and target your ess to not to exceed the hemoglobin concentration about 12.5 so uh at present what is the unmet need with the current therapy after using this erythrocotin agent for so many years we have learned that it is wonderful molecule and it has changed a lot of quality of life in patients who are on dialysis but those patients who have a progressive reduction in the response to erythropoietin that is there is a hypo responsiveness to the other part and in spite of giving a very high dose of erythropoietin there is a class of patients who will have a hypo responsiveness they will not respond to the erythropoietin and if we over bored and if we over target we are also getting the risk of adverse cardiovascular events there is also risk of hypertension re stroke thrombotic events micro infection heart failure related hospitalization and all cause modality so these are the side effects which we can face if we if we don't use erythropoietin judiciously very very rarely there are certain incidences where in it has been said that it can increase the risk of cancer progression it can increase the possibility of diabetic retinopathy of course pure red cell apresia is one of the rare complication which can be seen patients who are on the electrocution stimulating agent and anaphylactic reaction which is very very rare but it can be so these are the side effects which we can face in some of the patients who are on research and if we don't use it then properly and the side effects which we can see with the iv iron therapy or oral iron therapy which is one of the thing which has been observed if we use overuse iron or if patient has a setting of infection there is increased chances of bacterial growth uh other side effects like gi intolerance hypersensitivity reaction uh risk of infection increased risk of mortality and severe related risk if there is an increase in the hemoglobin above the target so these are the side effects which we see in patients who have been given iv iron uh and the most important thing is uh increase epsilon production so if there is increase or absolute production because of inflammation though the iron is available it is uh not functionally available for the erythropoiesis and so we keep moving more iron and it's a vicious cycle and in that situation again we are left with the no response to retroparting or no response to iron because of the unavailability of iron which is because of the increased hepsidine so in such scenario when patient is also having no responsiveness to esr we have used optimumly iron and still the patient is not responding and now we have a newer class of agents which are called hip stabilizers uh that is hypoxia inhibitor factor stabilizers which is uh an enzyme which is uh responsible for increasing the hip level is a proline hydroxylase domain inhibitors so uh it is one of the major recovery of this decade uh basically the 2019 nobel prize was also given for the discovery of this particular molecule which is a new era of treatment for patients of ckd and anemia and i would like to focus little bit on this because iron and issa we know much and we have used it a lot but this is a new molecule which is available now it has been recently available and so i thought i would give more time to this particular molecule so in 2019 the nobel prize in physiology and medicine was awarded to professor william ken uh junior sir peter uh cliff and uh dr jeff mirza for the contribution to the delineating the molecular mechanism underlying the heat oxygen sensation the phd oxygen sensing pathway plays a central load in cellular adaptation of hypoxia and regulating biological process essential for the cell survival so this includes glycolysis mitochond mitochondrial metabolism angiogenesis immune response and erythropoiesis so one of the major pathway which has been covered by the phd oxidant sensitive pathway is the endothermicist so in normal scenario when there is a hypoxia how how basically if x is a if is a constitutively produced it is produced in our body continuously and it is rapidly degraded because if the hemoglobin concentration is normal and if there is no requirement of there is no hypoxia whatever heat is produced it is continuously been degraded under normal oxygen condition if the oxygen condition in the body is normal the heat produce which is degraded and this degradation of heat is mediated by a proline hydroxylase domain phd1 phd2 and phd3 enzymes so these enzymes will degrade the hip and then it will be not not uh not available for the uh erthoposis so hydroxylated heat alpha is a lubricatedly be uh by the bonnie pale endopathy which leads to degradation of the hip uh this phd utilizes oxygen and two oxygen uh oxo regulate as a substrate and so this enzyme uses these two particular molecules for the degradation when there is a hypoxia if you are at a high altitude or because of anemia of any reason or there is a hypoxia because of uh as a seen with the anemia of any reason mainly patients of ckd or there is a if phd inhibitors which will mimic like hypoxia because it will block this enzyme it reduces the phd catalytical activity and which leads to the cellular accumulation of the hip alpha which is then it is transported to the nucleus it is a nuclear translocation heterodymerization with the peta so it it joins with hip beta and then increases the transcription of multiple genes which will regulate the formation of many genes like erythropoietin gene then ldh then phosphoglycerate kinase gene and vascular endothelial growth factors genes so these are the genes which are been activated by the translocation and dimerization of the hip gene so as you can see in normal oxygen condition the hip which is produced by the proline hydroxylase is deactivated or degraded but in condition of hypoxia or when this enzyme is blocked the degradation is uh not taking place and there is accumulation of the reason which will increase the formation of all the genes which are responsible for the electrophoresis so this hypoxia mediated gene expression by the uh if inducible factors and this increase if causes increase in epo uh to within two near or physiological range so it will produce endogenous electroprotein rather than what we see erythropoietin injections which we gave from outside it is increased endogenous epo production and so it will give a physiological range of hemoglobin there will be increased iron absorption there will be decreased episode level and there is increased iron transport to the bone marrow and ultimately all this will lead to increased red cell production uh it also regulates the erythropoiesis by the in its effect on iron metabolism so what heat does is it it coordinates erythropoiesis with iron metabolism as it regulates gene involved in the iron optic iron release and from the uh these internal stores and reticular endothelial system all this will release iron with the help of these genes the absorbed and stored iron is released into the circulation via ferro poetin and it is com complex with the transferrin for transport to the liver bone marrow and reticular endothelial system with the help of these transport factors which have been activated by the hip so basically a ferro pattern uh is a surface expressed in regulated by the hypside whereas if to participate into the transcription regulation of the ferro parties uh similarly which mediates the separation of epsilon production in the liver under the condition of the accelerated electrophoresis there is another protein which is activated is the celluloplasmin which is an heat regulated copper carrying peroxidase that also catalyzes the oxidation of the ferrous to the ferric form so uh there is increase in the iron availability iron utilization and erythropoietin production this all three together will increase the production of hemoglobin there are multiple trials which have been conducted on this molecule uh which is uh shown in this uh trial which has been published uh where you can see there is a dose dependent increase in hemoglobin and there is a reduction in the hepatin as you increase the dose the production of hemoglobin also increases and with similarly you can see the uh on the left hand side that the hexadine has significantly reduced as you give uh thief inhibitors so there is increase in hemoglobin production and reduction in hepatin which is dose dependent one very interesting thing which we have observed in this particular molecule is whether you give iv iron or oral iron because of the good utilization of the iron and because of the availability of epsilon there is a because of the blockage of the epsilon the iron absorption from the intestine from the deodorant has also improved so if uh this study you can see that along with the hip inhibitors uh as compared to placebo whether you give iv iron or oral iron the rise of hemoglobin is similar so you don't require iv iron in patients who are on different emitters another good thing about this molecule is that it can reduce the inflammation so in patients who are having inflammation if you can see the crp is high patients who are having high crp erythropoietin will not give good response whereas patients who have a high crp and if you give uh give benefit pih the response is still seen so in patients who are having inflammation uh this molecule works better as compared to the issues there are multiple clinical trials which have been uh done on these molecules and as i showed you the effectiveness there are certain adverse effects also uh have been monitored in clinical trials and as you can see the a's and essays are not very significant the statistical significance is as compared to the placebo is same so no major serious adverse events or major modalities has been observed with this molecule this is a study of meta-analysis of nine different studies wherein they have seen whether there is any major significant adverse side effect or not and it was not statistically significant and they are well tolerated and there is no major safety concern so major potential benefits of fuel stabilizers are they increase or maintain hemoglobin levels effectively they increase the endogenous epo production in a physiological range uh they regulate hepatin they increase the iron absorption and they are not influenced by the inflammation so in patients who are having high crp they are not influenced uh one of the most important thing is they can be given orally so most of the uh erythropoietin or iron we need to give iv or substitute whereas these are the molecules which can be given orally they are in tablet forms and they inhibit uh phd enzymes so this mechanism is reversible and transient so as soon as you stop the tablet the effect is reversible so within three or four days there is no long term side effects of any of these molecules uh there is no risk of hypertension uh there is one important thing uh or one of the observational factor which has come in these molecules uh is the they have shown some effect on lowering of cholesterol levels uh how does it work uh it's still not been clear but there is a significant lowering of cholesterol as being seen in few of the molecules and there is avoidance of high epo level so we don't see other side effects of high epo levels like thrombotic cardiovascular things and there is a avoidance of side effects associated with the high ib iron so you don't have to give very high iv iron overload is not since uh there are potential concerns with the hip phis uh which still need to be addressed which are there's studies which are ongoing we have to have a very long term experience of these molecules and then only we will be able to answer certain questions a few of these concerns are whether there is any concern regarding the malignancy or not uh which needs to be answered then there is a concern about retinopathy which has still not been seen in any of the trials uh liver dysfunction hypertension hyperkalemia so these are the concerns still uh having no significance still evidence anywhere yes there is some evidence about the thrombotic events and vascular calcifications uh so which has been uh seen uh in some trials uh the hazard ratio is around one point four percent so uh that uh was also again dose dependent so uh that is one concern which has been a little more prominent than any other if we compare the hip phis versus esi yes yes uh the esa's are short acting and long acting the pros of the esa's is it reduces the need of rbc transmission it may reduce the overall quality of life is improved because of the good immunoglobulin response and it can be given iv during the dialysis uh the cons about is it it has a higher dose is required in patients who have a hyper responsiveness uh or there can if there is a higher shoot up of hemoglobin we can get a cardiovascular cardiovascular system related side effects like increase thrombosis or increase cardiac events similarly and long-acting ecs yes is where the side effects are similar uh you have higher chances of cardiac events or thrombotic tendencies to the fishula as against this hip phi inhibitors uh have been shown to be uh non-inferior to yes's they have as good as effect as the essays and they increase the hemoglobin uh comparable to the property and it can be given orally so that is a convenient to the patient and it may reduce the need for iron supplementation because it also improves the iron utilization so that way also it is useful as it is it increases the iron utilization thus supplemented supplementation of iron requirement is less uh the research is required additional research is required to know the long-term side effects on tumor growth on cardiac events is because we don't still have a long term experience about these molecules and more studies would be required as far as the cons of this particular molecules are concerned these molecules still have not been approved by the fda and because of concern again because there was a dose dependent increase in the hemoglobin and when the higher dose was increased there was higher hb and the cardiac incidences were seen and so the fda had given the advisory uh to the panel uh advisory panel had given that they would submit one more trial with the low lower doses and uh uh with the hemoglobins in the target range and after that only the approval can be considered so so far it has not been approved by the fda but in india yes they are available so to conclude the it is a dose-dependent increase in hemoglobin in known dialysis and dialysis patients of ckd maintenance of hemoglobin level when patient is switched from electrocuting is seen uh there is reduction in the hepatin and increase in ion utilization it improves the response uh and as against the ess in patients with inflammation so in inflamed patient also it is very effective there is a reduction in cholesterol which needs further studies to know the mechanism there is reduction in the blood pressure and there are no major safety issues so far so to take a message despite the initial promise promises the erythropoietin simulating agents must be used with caution and in low doses to avoid the harm and may be unsuitable for some patients uh higher versus lower iv dosing reduces epo requirement and it leads to the improved cardiovascular outcome in incidences hemodialysis patients in the pivotal studies uh pivotal study is one of the very landmark study wherein it showed that the high dose iv iron with seraton target up to 700 reduces reduces the epo requirement and it is safer so this was one of the landmark studies and ibran has been recommended little on the higher side now as compared to the initial conservative approach the hip stabilizers show promise in improving the oral and oral elimination to ess with reduced need for ib iron however as with all agents that raise hb care is needed particularly in patients with esrd particularly in respect to the cardiovascular outcomes thank you thank you ma'am thank you so much it was indeed a very informative session about the treatment of anemia like you said that the erythropoiesis stimulating factor must be used in low doses and with great caution as well as how the hip stabilizers may now provide a good oral alternative instead of the iv im so i am sure our audience has learned a lot we do have a raise and i'll just accept that quickly yeah good evening ma'am um i would like to know in a non dielectric ckd what is the initial choice whether it is oral iron or iv iron uh non dialysis ckd patients oral iron depends uh if patient is tolerating oral iron if patient is tolerating oral and we can do oral and uh in spite of that if there is a no significant improvement we can add electrophile to the oral iron which also improves the iron utilization and if there is a significant uh low hemoglobin and iv iron will increase the endogenous very fast or if we want to start insert and the transferring is very low then ibrm should be given but otherwise good okay thank you thank you so much dr sawmaker [Music] there is a question by dr sonam asrd with severe anemia that is hb around 6 grams and pulmonary edema should patient be given blood transfusion or iron transfusion patient was a symptomatic having a pulmonary edema antihemoglobin of 6 so that is already dilutional factor so it is always better to give a blood transmission to pesticide this patient first this iron iv iron can be followed up afterwards once the patients have levels thank you um i hope dr sonam that answered your question uh we have another question by dr deviga can we give essa in cad ckd anemia and cva ckd essa can cause thrombotic events so is it advisable to given cad slash cva yes it can be given provided you don't overshoot the target so you should see to that that you don't cross the limit of 11.5 or 12 in those patients who are having increased thrombotic tendency or who have a cardiovascular or severe risk never to cross the target of 11.5 or 12. okay dr mancha shaikh is asking whether you can guide regarding uh which one would be better if pih or sr in hepatic failure or hepatic disorders essa's have no major hepatic side effects uh hip phis are still very new so far whatever studies are uh available there are no major hepatic side effects or any major concerns about liver dysfunction so both can be used there is no concern in like you can choose either of it both are safe so both is asking any comments on diabetes in alpha that operating is a good longitude uh if we uh compared to the uh protein uh there are three types short acting long acting and pegulated so derbyviotin is a longer thing we can give once a weekly more effective and uh in fact it turns out more cost effective than it also okay dr devi guy is asking what is the dose of essa and how long to give in severe anemia in ckd uh dose of erythropoietin to begin with we can start with 75 microgram per kg but most of the time if we are patient on hemodialysis then it is given with the dialysis and if we are giving 4000 units we can give twice a weekly or ten thousand it once a weekly which can be then reduced as you uh reach the target and then you can reduce the maintenance rules depending upon hemoglobin target of 10.5 so it will not be dependent upon the body weight or anything it is it will depend on the hemoglobin levels hemoglobin yeah so i think uh the next question is somewhat that that dr sonam is asking how is the optimal dosage and frequency of epo calculated doses and frequency like most important thing first is you have to see to that your iron is been properly depleted so you should uh because uh uh if you start with an iron deficient condition it will be a problem so c2 that your ferratins are more than uh 200 at least and your transferring saturation is about 30 after that you can start with the isa and then insert those is to be monitored as for the immunoglobulin concentration it is not uh as i told you yeah dr nishmita is saying that the bell zuti fan is a commercially fda approved uh hiff papi so if ph ph fda i don't think still has approved because uh it is available it has been approved in other countries mainly in japan china some of the european countries are now going to approve in india it has been approved by the decision so if phi's cost wise in india they are much cheaper as compared to issues okay so that would be a better option than their points they are much cheaper okay yeah right um the next question is uh by dr mohammad uh first choice iv in essa or hif in ckd with hb around eight first is to uh correct the iv ir uh give the iv iron and replicate the best if the iron is already been replicated then uh we can go for the issue or if either of it is like okay mainly patients who are on conservative treatment of ckd or patients who are on peritoneal dialysis who will not be going to the dialysis on it it is always better to give phi because they are to be given orally whereas the other who would require injectable forms which is the safe essa i mean is sr safe in pregnancy in case of severe anemia it is safe but it is not recommended so these are patients of pregnancy patients will have a good erythropoietin productions and as the anemia is there if they have a normal kidneys the electrocuting level if you major in this fascia in this people uh the electrocution is not deficient so i don't see any point of giving extrapolating patients in a pregnancy doctor rhythm is asking what is the dosage of deciduous stat it is 50 milligram residue stat is the 50 milligram tablet is available and it is given two tablets that is hundred milligram twice a weekly okay thank you so much i hope uh dr rhythm that answered your question and we are done with the questions as well so i would like to thank you ma'am a very nice informative amazing session thank you for taking out time from your opd schedule for netflix we are truly honored to have you and also thank you to our audience

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dr. Sonal Dalal

Dr. Sonal Dalal

Consultant Nephrologist | Gujarat Kidney Foundation, Ahmedabad

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dr. Sonal Dalal

Dr. Sonal Dalal

Consultant Nephrologist | Gujarat Kidney Foun...

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