The Navigation Model of Therapy: Why Awareness Changes Everything
November 16, 2025
Background
Anemia is usually described as a condition where the hemoglobin levels in blood is less than 13.0 g/dL in males and below 12 in females. Anemia that develops in association with chronic kidney disease (CKD) is normocytic, normochromic, and hypo proliferative. This condition is one of the complications that are associated with CKD, and they show poor prognosis and higher mortality rates.Â
It is estimated that anemia typically starts manifesting when the Glomerular filtration rate is at 60 mL/min/1.73 m², but increases progressively as GFR deteriorates further, anemia is exceedingly uncommon if GFR is above 80 mL/min/1.73 m².Â
The association between anemia and CKD has been known for over 170 years since the discovery by Richard Bright. Anemia tends to develop more frequently as the person has kidney disease especially in the stage 5 CKD. This type of anemia results in decreased health-related quality of life, an increased risk of cardiovascular events, cognitive impairment, more frequent hospitalizations, as well as an increased mortality rate.Â
Epidemiology
Anemia is usually noticed when the GFR is below 60 mL/min/1.73m2 most often when more than 50% of kidney function is impaired. Anemia associated with CKD typically worsens with the progression of the CKD stage. However, there is a poor correlation between renal erythropoietin production and the degree of anemia with the severity of kidney disease. Chronic kidney disease anemia is common in almost all patients who are on dialysis.Â
Chronic kidney disease-related anemia has been found to be related to decreased quality of life, reduced renal survival, increased rate of morbidity and mortality, and increased health care cost. Evidence suggests that the prevalence of anemia in NDD CKD patients may be as high as 60%.Â
Thus, as the eGFR blood test value decreases, anemia is more frequent and more severe. National Health and Nutrition Examination Survey (NHANES) data from 2007-2008 and 2009-2010 showed that anemia was more common among CKD patients than non-CKD patients. Similar trends are evident in the present data retrieved from the CKD Prognosis Consortium’s work in the recent past.Â
Anatomy
Pathophysiology
The primary cause of anemia in patients with chronic kidney disease is absence of erythropoietin, but there are additional causes as well. These consist of factors that could be induced by uremia that may inhibit erythropoiesis although the actual inhibitors have not been well characterized. Further, mechanical and metabolic factors reduce the lifespan of red blood cells that also contribute to the disease.Â
On the other hand, disturbance of iron homeostasis has come to be appreciated as an important factor more and more. The CKD patients are at a higher risk of getting iron deficient as they experience increased iron losses due to chronic bleeding, blood retention in the dialysis equipment, and many blood draws. This deficiency coupled with a significantly reduced ability to absorb iron makes intravenous iron supplementation more preferential in hemodialysis patients. Another comorbidity found in CKD patients includes functional iron deficiency where though iron is in the body stores it cannot be used for use in red blood cell synthesis.Â
Etiology
The primary factor contributing to anemia in cases of chronic kidney disease (CKD) is the decreased synthesis of erythropoietin (EPO). This decline in EPO has been associated with the suppression of hypoxia-inducible factor (HIF), which is crucial for the expression of the EPO gene. Some of the other factors that may be contributory to anemia in CKD include uremia resulting in deviation in shape and destruction of RBCs, deficiencies of folic acid and vitamin B12, iron deficiency, functional platelet abnormalities that cause hemorrhage, and rarely, hemolysis due to hemodialysis.Â
Genetics
Prognostic Factors
Renal failure is characterized by a poor response to erythropoietin therapy and increased prevalence of cardiac events. These factors include the prevalence of inflammation associated with elevated C-reactive protein (CRP) and iron deficiency; for this reason, iron administration is generally suggested to enhance treatment outcomes. Chronic kidney disease associated anemia is aligned to cardiorenal anemia syndrome; studies have revealed that even a slight lowering of the extent of hemoglobin carries with it a proportionate propensity for heart issues. Cardiovascular diseases are the major cause of death in CKD patients, and anemia which is this case is manifested by low hemoglobin levels is known to increase the risk of hospitalization and mortality.Â
Clinical History
Age GroupÂ
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Chronic kidney disease anemia is a progressive process that occurs as the renal function deteriorates and may be asymptomatic in the first stage. The symptoms that manifest during the onset of the disease include fatigue, pallor, shortness of breath, dizziness, weakness and cold intolerance. As the severity of the condition increases, the symptoms would inevitably worsen – with exercise tolerance being decreased, increase in the heart rate, and increase in effects on the existing cardiovascular diseases.Â
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Manage CKD:Â
Treat comorbidities that contribute to the injury (for example, diabetes or hypertension).Â
It is also important to make some changes to diet to control the levels of electrolytes and nutrients.Â
For advanced CKD, patients may need to undergo hemodialysis or peritoneal dialysis.Â
Pharmacological Treatments:Â
ESAs (e. g., Epoetin alfa, darbepoetin alfa): Regulate production of red blood cells.Â
Iron Supplementation: Administer oral or intravenous iron; to avoid iron toxicity, measure the levels.Â
Non-Pharmacological ApproachesÂ
For the desired results some sort of changes are necessary, such as a considerable increase in intake of iron containing foods.Â
It implied correction of the causes of anemia including bleeding.Â
Monitoring and Follow-Up:Â
Biometric assessments at least once a month involving a check-up on hemoglobin and iron levels.Â
Monitor patient’s response to treatment and side effects to determine the necessity for change in the treatment plan.Â
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-a-non-pharmacological-approach-for-treating-anemia-due-to-chronic-kidney-disease
Dietary Modifications:Â
Nutritional Supplements:Â
Lifestyle Modifications:Â
Role of Erythropoiesis-Stimulating Agents
Role of Iron supplements
use-of-intervention-with-a-procedure-in-treating-anemia-due-to-chronic-kidney-disease
use-of-phases-in-managing-anemia-due-to-chronic-kidney-disease
Medication
Indicated for the treatment of persons who have CKD induced anaemia who have been receiving dialysis for less than four months:
Use the lowest effective dose for each patient to minimize the need for red blood cell (RBC) transfusions
Dosage for patients not using erythropoietin-stimulating medication (ESA):
The Hemoglobin (Hgb) level prior to treatment determines the starting
Hgb <9 g/dL: 4 mg orally daily as Starting Dose of Jesduvroq
Hgb 9-10 g/dL: 2 mg orally daily as Starting Dose of Jesduvroq
Hgb >10 g/dL: 1 mg orally daily as Starting Dose of Jesduvroq
Individuals Switching from an ESA:
In the case of adults switching from an ESA to Jesduvroq
Adults on Dialysis Who Are Switching from an Erythropoiesis-Stimulating Agent to Jesduvroq Starting Dose
Epoetin alfa IV (≤2,000 units/week), Darbepoetin alfa IV/SC (20-30 mcg/4 weeks), Methoxy polyethylene glycol (PEG)-epoetin beta SC/IV (30-40 mcg/month): 4 mg orally daily Dose of Jesduvroq
Epoetin alfa IV (>2,000 to <10,000 units/week), Darbepoetin alfa IV/SC (>30 to 150 mcg/4 weeks), Methoxy polyethylene glycol (PEG)-epoetin beta SC/IV (>40-180 mcg/month): 6 mg orally daily Dose of Jesduvroq
Epoetin alfa IV ( ≥10,000 to <20,000 units/week), Darbepoetin alfa IV/SC (>150 to 300 mcg/4 weeks), Methoxy polyethylene glycol (PEG)-epoetin beta SC/IV (>180-360 mcg/month): 8 mg orally daily Dose of Jesduvroq
Epoetin alfa IV (≥20,000 units/week), Darbepoetin alfa IV/SC (>300 mcg/4 weeks), Methoxy polyethylene glycol (PEG)-epoetin beta SC/IV (>360 mcg/month): 12 mg orally daily Dose of Jesduvroq
For females- 50-100 mg intramuscularly as a deep injection, once every week
For males- 100-200 mg intramuscularly as a deep injection, once every week
600 mg/day orally every day in 1-3 divided doses 
epoetin beta/methoxy polyethylene glycolÂ
For patients not on dialysis, utilize the lowest effective dose
Initially, 0.6 mcg/kg intravenously or subcutaneously once every 14 days
Maintenance dose- after the hemoglobin is stabilized, administer it once a month, utilizing it twice 14-day dose
Titrate as required
sodium ferric gluconate complexÂ
10
ml
Solutions
Intravenous (IV)
every hour
10 mL (125 mg) of undiluted slow IV can deliver up to 12.5 mg of elemental iron per minute.
Note
The majority of patients need an overall dose of 1000 mg of elemental iron spread out over 8 dialysis sessions
Administer during the actual dialysis session
Adverse effects may occur more frequently or with greater severity with doses of elemental iron exceeding 125 mg
methoxypolyethylene glycol-epoetin betaÂ
Recommended for the treatment of anemia brought on by chronic kidney disease (CKD) in people receiving dialysis or not
Use the lowest dose necessary to minimize the need for RBC transfusions and customize the dosage
Give IV or SC treatment
Every adult suffering with CKD:
Do not raise the dosage regularly not more than 4 weeks; dosage reductions are possible more regularly; Steer clear of making frequent dose modifications
Lower the dosage by at least 25% if hemoglobin goes up quickly (for example, more than 1 gram/dL in any of the 2 week-interval) in order to slow down quick reactions
Four weeks later: For non responsive individuals (that is, whose hemoglobin [Hgb] has not raised by more than 1 gram/dL), up the increase of dose with 25%
After a 12-week-interval increase in dosage: Increasing the dosage in the event of a poor response will lead to increase in risks with an unsatisfied response
Utilize the lowest dosage necessary to keep your Hgb level high enough to minimize the need for RBC transfusions
Examine additional sources of anemia
If responsiveness does not improve, stop
Dialysis patients in their adult years:
When Hgb is below 10 gram/dL, start
Reduce or stop the dose if Hgb is greater than 11 gram/dL
Dose in the absence of ongoing ESA therapy via IV/SC is 0.6 mcg/kg every two weeks at first
After hemoglobin has stabilized, administer a dose once a month at a dose twice as high as the dose every two weeks, and then titrate as needed
Adult non-dialysis patients:
Only think about starting when Hgb is below 10 g/dL and the factors following are true
One of the goals is to reduce the alloimmunization risk and/or other dangers connected to receiving red blood cells transfusions, as shown by the rate of Hgb drop
If Hgb is more than 10 g/dL, use the lowest dose necessary to minimize requirement of the RBC transfusions and reduce or stop the medication
Dose in the absence of ongoing ESA therapy: First, 1.2 mcg/kg IV/SC every month; subsequently, 0.6 mcg/kg IV/SC every two weeks
After Hgb has stabilized, give a dose once a month at a dose twice as high as the dose every two weeks, and then titrate as needed
Switching Patients Who Are Now on Different ESA:
Getting darbepoetin <40 mcg/week or epoetin <8,000 units every week: 120 mcg/qMonth or 60 mcg/q2Week IV/SC
Getting 40–80 mcg/week of darbepoetin or 8,000–16,000 units of epoetin: 200 mcg/qMonth or 100 mcg/q2Week IV/SC
Darbepoetin >80 mcg/week or epoetin >16,000 units per week will be administered as follows: 360 mcg/qMonth or 180 mcg/q2Week IV/SC
Dose Adjustments
Dose Modifications
Age (6-89 years), gender, race, severe hepatic impairment (Child-Pugh Class C), site of subcutaneous injection (abdomen, arm, or thigh), or dialysis use did not affect the pharmacokinetics of methoxy polyethylene glycol-epoetin beta
Required dose to be taken orally three times a week but not on consecutive days
Note: the target of the dose is to achieve 10 to 12g/dl of Hb levels
Patients who are not on treatment with ESA (erythropoiesis- stimulating agent)
For patients weighing <100kg
70mg orally thrice a week
For patients weighing >100kg
100mg orally thrice a week
the drug is administered orally, as advised by the doctor
Initial dosage of 1000 mg per day orally in 1 to 3 times a day
Non dialysis dependent CKD: 200 mg IV 5 doses in 14 days 
Hemodialysis dependent CKD: 100 mg elemental Fe IV per dialysis session  
Do not exceed 1000 mg divided in 3 times/week 
Peritoneal dialysis dependent CKD: 300 mg IV 2 doses 14 days apart, following 400 mg IV infusion 14 days later 
For 2-13 years- 25-50 mg intramuscularly as a deep injection, every 3-4 weeks
For >13 years
Males-100-200 mg intramuscularly as a deep injection once a week
Females- 50-100 mg intramuscularly as a deep injection once a week
epoetin beta/methoxy polyethylene glycolÂ
For 5-17 years, patients receiving ESA-
Epoetin alfa- 4 times weekly epoetin alfa previous dose as (Units)/125 intravenously
Darbepoetin alfa- 4 times weekly darbepoetin alfa as previous dose (mcg)/0.55 intravenously
sodium ferric gluconate complexÂ
Maximum dosage: one dose of 125 mg of elemental iron:
0.12
ml/kg
Solution
Intravenous (IV)
every hour
for 6years and above
administer during the actual dialysis session
Adverse effects may occur more frequently or with greater severity with doses of elemental iron exceeding 125 mg
methoxypolyethylene glycol-epoetin betaÂ
Recommended for the treatment of anemia linked to chronic kidney disease (CKD) in young patients receiving hemodialysis (5–17 years old) who are switching from one ESA to another after the ESA stabilized their hemoglobin level
Give IV only
<5 years: No proven efficacy or safety
5–17 years old:
Those whose hemoglobin level has been stabilized by treatment with an ESA should have an IV once every four weeks
beginning dosages for individuals who are already on an ESA
Epoetin alfa: 4 Ă— prior weekly epoetin alfa dose (Units)/125 (for example, 4 x weekly epoetin alfa dosage of 1500 Units/125 = 48 mcg of Mircera IV once every four weeks)
Darbepoetin alfa: 4 x prior weekly darbepoetin alfa dose (mcg)/0.55 (per week) = 145.5 mcg of Mircera IV once every four weeks, or 4 Ă— 20 mcg of darbepoetin alfa each week/0.55
Hemodialysis-dependent: 0.5 mg/kg IV 6 times for 12 weeks 
Do not exceed 100 mg/dose 
Non-dialysis dependent or peritoneal-dependent: 0.5 mg/kg IV 3 times for 12 weeks 
Future Trends
Anemia is usually described as a condition where the hemoglobin levels in blood is less than 13.0 g/dL in males and below 12 in females. Anemia that develops in association with chronic kidney disease (CKD) is normocytic, normochromic, and hypo proliferative. This condition is one of the complications that are associated with CKD, and they show poor prognosis and higher mortality rates.Â
It is estimated that anemia typically starts manifesting when the Glomerular filtration rate is at 60 mL/min/1.73 m², but increases progressively as GFR deteriorates further, anemia is exceedingly uncommon if GFR is above 80 mL/min/1.73 m².Â
The association between anemia and CKD has been known for over 170 years since the discovery by Richard Bright. Anemia tends to develop more frequently as the person has kidney disease especially in the stage 5 CKD. This type of anemia results in decreased health-related quality of life, an increased risk of cardiovascular events, cognitive impairment, more frequent hospitalizations, as well as an increased mortality rate.Â
Anemia is usually noticed when the GFR is below 60 mL/min/1.73m2 most often when more than 50% of kidney function is impaired. Anemia associated with CKD typically worsens with the progression of the CKD stage. However, there is a poor correlation between renal erythropoietin production and the degree of anemia with the severity of kidney disease. Chronic kidney disease anemia is common in almost all patients who are on dialysis.Â
Chronic kidney disease-related anemia has been found to be related to decreased quality of life, reduced renal survival, increased rate of morbidity and mortality, and increased health care cost. Evidence suggests that the prevalence of anemia in NDD CKD patients may be as high as 60%.Â
Thus, as the eGFR blood test value decreases, anemia is more frequent and more severe. National Health and Nutrition Examination Survey (NHANES) data from 2007-2008 and 2009-2010 showed that anemia was more common among CKD patients than non-CKD patients. Similar trends are evident in the present data retrieved from the CKD Prognosis Consortium’s work in the recent past.Â
The primary cause of anemia in patients with chronic kidney disease is absence of erythropoietin, but there are additional causes as well. These consist of factors that could be induced by uremia that may inhibit erythropoiesis although the actual inhibitors have not been well characterized. Further, mechanical and metabolic factors reduce the lifespan of red blood cells that also contribute to the disease.Â
On the other hand, disturbance of iron homeostasis has come to be appreciated as an important factor more and more. The CKD patients are at a higher risk of getting iron deficient as they experience increased iron losses due to chronic bleeding, blood retention in the dialysis equipment, and many blood draws. This deficiency coupled with a significantly reduced ability to absorb iron makes intravenous iron supplementation more preferential in hemodialysis patients. Another comorbidity found in CKD patients includes functional iron deficiency where though iron is in the body stores it cannot be used for use in red blood cell synthesis.Â
The primary factor contributing to anemia in cases of chronic kidney disease (CKD) is the decreased synthesis of erythropoietin (EPO). This decline in EPO has been associated with the suppression of hypoxia-inducible factor (HIF), which is crucial for the expression of the EPO gene. Some of the other factors that may be contributory to anemia in CKD include uremia resulting in deviation in shape and destruction of RBCs, deficiencies of folic acid and vitamin B12, iron deficiency, functional platelet abnormalities that cause hemorrhage, and rarely, hemolysis due to hemodialysis.Â
Renal failure is characterized by a poor response to erythropoietin therapy and increased prevalence of cardiac events. These factors include the prevalence of inflammation associated with elevated C-reactive protein (CRP) and iron deficiency; for this reason, iron administration is generally suggested to enhance treatment outcomes. Chronic kidney disease associated anemia is aligned to cardiorenal anemia syndrome; studies have revealed that even a slight lowering of the extent of hemoglobin carries with it a proportionate propensity for heart issues. Cardiovascular diseases are the major cause of death in CKD patients, and anemia which is this case is manifested by low hemoglobin levels is known to increase the risk of hospitalization and mortality.Â
Age GroupÂ
Chronic kidney disease anemia is a progressive process that occurs as the renal function deteriorates and may be asymptomatic in the first stage. The symptoms that manifest during the onset of the disease include fatigue, pallor, shortness of breath, dizziness, weakness and cold intolerance. As the severity of the condition increases, the symptoms would inevitably worsen – with exercise tolerance being decreased, increase in the heart rate, and increase in effects on the existing cardiovascular diseases.Â
Manage CKD:Â
Treat comorbidities that contribute to the injury (for example, diabetes or hypertension).Â
It is also important to make some changes to diet to control the levels of electrolytes and nutrients.Â
For advanced CKD, patients may need to undergo hemodialysis or peritoneal dialysis.Â
Pharmacological Treatments:Â
ESAs (e. g., Epoetin alfa, darbepoetin alfa): Regulate production of red blood cells.Â
Iron Supplementation: Administer oral or intravenous iron; to avoid iron toxicity, measure the levels.Â
Non-Pharmacological ApproachesÂ
For the desired results some sort of changes are necessary, such as a considerable increase in intake of iron containing foods.Â
It implied correction of the causes of anemia including bleeding.Â
Monitoring and Follow-Up:Â
Biometric assessments at least once a month involving a check-up on hemoglobin and iron levels.Â
Monitor patient’s response to treatment and side effects to determine the necessity for change in the treatment plan.Â
Dietary Modifications:Â
Nutritional Supplements:Â
Lifestyle Modifications:Â
Hematology
Hematology
Hematology
Hematology
Anemia is usually described as a condition where the hemoglobin levels in blood is less than 13.0 g/dL in males and below 12 in females. Anemia that develops in association with chronic kidney disease (CKD) is normocytic, normochromic, and hypo proliferative. This condition is one of the complications that are associated with CKD, and they show poor prognosis and higher mortality rates.Â
It is estimated that anemia typically starts manifesting when the Glomerular filtration rate is at 60 mL/min/1.73 m², but increases progressively as GFR deteriorates further, anemia is exceedingly uncommon if GFR is above 80 mL/min/1.73 m².Â
The association between anemia and CKD has been known for over 170 years since the discovery by Richard Bright. Anemia tends to develop more frequently as the person has kidney disease especially in the stage 5 CKD. This type of anemia results in decreased health-related quality of life, an increased risk of cardiovascular events, cognitive impairment, more frequent hospitalizations, as well as an increased mortality rate.Â
Anemia is usually noticed when the GFR is below 60 mL/min/1.73m2 most often when more than 50% of kidney function is impaired. Anemia associated with CKD typically worsens with the progression of the CKD stage. However, there is a poor correlation between renal erythropoietin production and the degree of anemia with the severity of kidney disease. Chronic kidney disease anemia is common in almost all patients who are on dialysis.Â
Chronic kidney disease-related anemia has been found to be related to decreased quality of life, reduced renal survival, increased rate of morbidity and mortality, and increased health care cost. Evidence suggests that the prevalence of anemia in NDD CKD patients may be as high as 60%.Â
Thus, as the eGFR blood test value decreases, anemia is more frequent and more severe. National Health and Nutrition Examination Survey (NHANES) data from 2007-2008 and 2009-2010 showed that anemia was more common among CKD patients than non-CKD patients. Similar trends are evident in the present data retrieved from the CKD Prognosis Consortium’s work in the recent past.Â
The primary cause of anemia in patients with chronic kidney disease is absence of erythropoietin, but there are additional causes as well. These consist of factors that could be induced by uremia that may inhibit erythropoiesis although the actual inhibitors have not been well characterized. Further, mechanical and metabolic factors reduce the lifespan of red blood cells that also contribute to the disease.Â
On the other hand, disturbance of iron homeostasis has come to be appreciated as an important factor more and more. The CKD patients are at a higher risk of getting iron deficient as they experience increased iron losses due to chronic bleeding, blood retention in the dialysis equipment, and many blood draws. This deficiency coupled with a significantly reduced ability to absorb iron makes intravenous iron supplementation more preferential in hemodialysis patients. Another comorbidity found in CKD patients includes functional iron deficiency where though iron is in the body stores it cannot be used for use in red blood cell synthesis.Â
The primary factor contributing to anemia in cases of chronic kidney disease (CKD) is the decreased synthesis of erythropoietin (EPO). This decline in EPO has been associated with the suppression of hypoxia-inducible factor (HIF), which is crucial for the expression of the EPO gene. Some of the other factors that may be contributory to anemia in CKD include uremia resulting in deviation in shape and destruction of RBCs, deficiencies of folic acid and vitamin B12, iron deficiency, functional platelet abnormalities that cause hemorrhage, and rarely, hemolysis due to hemodialysis.Â
Renal failure is characterized by a poor response to erythropoietin therapy and increased prevalence of cardiac events. These factors include the prevalence of inflammation associated with elevated C-reactive protein (CRP) and iron deficiency; for this reason, iron administration is generally suggested to enhance treatment outcomes. Chronic kidney disease associated anemia is aligned to cardiorenal anemia syndrome; studies have revealed that even a slight lowering of the extent of hemoglobin carries with it a proportionate propensity for heart issues. Cardiovascular diseases are the major cause of death in CKD patients, and anemia which is this case is manifested by low hemoglobin levels is known to increase the risk of hospitalization and mortality.Â
Age GroupÂ
Chronic kidney disease anemia is a progressive process that occurs as the renal function deteriorates and may be asymptomatic in the first stage. The symptoms that manifest during the onset of the disease include fatigue, pallor, shortness of breath, dizziness, weakness and cold intolerance. As the severity of the condition increases, the symptoms would inevitably worsen – with exercise tolerance being decreased, increase in the heart rate, and increase in effects on the existing cardiovascular diseases.Â
Manage CKD:Â
Treat comorbidities that contribute to the injury (for example, diabetes or hypertension).Â
It is also important to make some changes to diet to control the levels of electrolytes and nutrients.Â
For advanced CKD, patients may need to undergo hemodialysis or peritoneal dialysis.Â
Pharmacological Treatments:Â
ESAs (e. g., Epoetin alfa, darbepoetin alfa): Regulate production of red blood cells.Â
Iron Supplementation: Administer oral or intravenous iron; to avoid iron toxicity, measure the levels.Â
Non-Pharmacological ApproachesÂ
For the desired results some sort of changes are necessary, such as a considerable increase in intake of iron containing foods.Â
It implied correction of the causes of anemia including bleeding.Â
Monitoring and Follow-Up:Â
Biometric assessments at least once a month involving a check-up on hemoglobin and iron levels.Â
Monitor patient’s response to treatment and side effects to determine the necessity for change in the treatment plan.Â
Dietary Modifications:Â
Nutritional Supplements:Â
Lifestyle Modifications:Â
Hematology
Hematology
Hematology
Hematology

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