Anemia due to Chronic Kidney Disease

Updated: August 12, 2024

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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. 

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. 

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. 

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. 

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%. 

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. 

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. 

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. 

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. 

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. 

Clinical History

Age Group 

  • Adults: CKD-related anemia is more prevalent in the adult population especially those who are above 50 years of age because the risk of developing CKD rises with age. 
  • Elderly: This is because older patients have reduced renal function due to aging and are generally more susceptible to the development of chronic kidney disease and its complications. 
  • Children: However, anemia related to CKD is not rare among children, especially those with congenital or hereditary renal diseases. 

Physical Examination

  • Pallor: It is noticed in the skin, conjunctiva, and nail beds. 
  • Tachycardia: Tachycardia as a compensation mechanism. 
  • Shortness of Breath: It usually happens inclusive of exertion or even in normal day to day activities as mentioned a while ago. 
  • Fatigue and Weakness: As a rule, generalized and can cause obvious changes in the child’s condition. 
  • Cold Extremities: This is due to poor circulation, which in turn leads to the formation of plaque on the walls of arteries. 
  • Peripheral Edema: Legs may swell occasionally, especially for those patients who have been diagnosed with congestive heart failure. 

Age group

Associated comorbidity

  • Diabetes mellitus 
  • Hypertension 
  • Cardiovascular diseases 
  • Autoimmune diseases 

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. 

Differential Diagnoses

  • Aplastic anemia 
  • Hypothyroidism 
  • Methemoglobinemia 
  • Systemic lupus erythematosus 
  • Alcohol misuse disorder 
  • Dialysis complications 
  • Hyperthyroidism 
  • Sickle cell anemia 
  • Hypoadrenalism 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

Manage CKD: 

Treat comorbidities that contribute to the injury (for example, diabetes or hypertension). 

It is also important to make some changes to diet to control the levels of electrolytes and nutrients. 

For advanced CKD, patients may need to undergo hemodialysis or peritoneal dialysis. 

Pharmacological Treatments: 

ESAs (e. g., Epoetin alfa, darbepoetin alfa): Regulate production of red blood cells. 

Iron Supplementation: Administer oral or intravenous iron; to avoid iron toxicity, measure the levels. 

Non-Pharmacological Approaches 

For the desired results some sort of changes are necessary, such as a considerable increase in intake of iron containing foods. 

It implied correction of the causes of anemia including bleeding. 

Monitoring and Follow-Up: 

Biometric assessments at least once a month involving a check-up on hemoglobin and iron levels. 

Monitor patient’s response to treatment and side effects to determine the necessity for change in the treatment plan. 

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: 

  • Iron-Rich Foods: Promote foods with high iron content, including lean meats, poultry, fish, beans, and iron-fortified cereals. 
  • Vitamin C: Encourage consumption of foods containing vitamin C (e.g., oranges, lemon, bell peppers) to improve the absorption of the non-heme iron present in plant-based diets. 
  • Vitamin B12 and Folate: Continue a diet high in B12 and folate or take a Vitamin B12 supplement if advised by a healthcare provider. 

Nutritional Supplements: 

  • Iron Supplements: Patients who are unable to take oral iron or who require a higher dose might have dietary iron augmented with supplements. Check for correct administration of dose an effective dose requires supervision. 
  • Vitamin B12 and Folate Supplements: Include supplements as part of the nutrition plan if the client cannot consume adequate amounts of vitamins and minerals or if they are deficient. 

Lifestyle Modifications: 

  • Exercise: Promote physical activity and exercise that will enhance general cardiovascular fitness and possibly red blood cell production and utilization. 
  • Education: Educate the patients regarding dietary practices in the treatment of anemia and how it augments pharmaceutical therapies. 
  • Support Groups: Appliance of psychological components of chronic disease and its treatment, such as enrollment of patients in support groups or counselling. 

Role of Erythropoiesis-Stimulating Agents

  • Epoetin alfa: Erythropoietin is a cytokine which stimulates the production of red blood cells; this is a recombinant form of it. It is given through an intravenous (IV) or subcutaneous (SC) route of transmission. Usually given at intervals of 2 to 3 days, but the dosing schedule can be adjusted depending on the clinical outcome and the patient’s hemoglobin status. 
  • Darbepoetin alfa: A more sustained form of erythropoietin thus implying that it can be administered with less frequency than epoetin alfa. It can also be administered Intravenously or Subcutaneously. Typically given once in one to four weeks based on the dose and the body response of the patient. 
  • Methoxy polyethylene glycol-epoetin beta (Mircera): A running EPO stimulator with a tethered half-life of the agent, perhaps requiring administration only once a week. It is administered SC. Administered every 2 to 4 weeks. 

Role of Iron supplements

  • Ferrous Sulfate: It is one of the most widely used types of iron supplements, usually containing 65 mg of iron in the form of ferrous salt per tablet. 
  • Ferrous Fumarate: Provides approximately 33 mg of elemental iron per 100 mg, which is about one-third of the total weight of the supplement as iron. 
  • Ferrous Gluconate: It is composed of approximately 12% elemental iron; 300 mg of ferrous sulphate yields about 36 mg of elemental iron. 

use-of-intervention-with-a-procedure-in-treating-anemia-due-to-chronic-kidney-disease

  • Iron Supplementation: When it comes to patients with iron deficiency, IV iron is administered more often than oral iron because oral iron is not well absorbed in CKD patients. Procedures may involve: 
  • Intravenous Iron Infusions: Given in outpatient care settings like the infusion center. Typical preparations are iron sucrose, ferric gluconate or ferric carboxymaltose. 
  • Erythropoiesis-Stimulating Agents (ESAs): ESAs are used to encourage the production of red blood cells. The procedure involves: 
  • Subcutaneous or Intravenous Administration: Given in a hospital or any other health care facility. Some ESAs are epoetin alfa and darbepoetin alfa some of the agents that it contains. 
  • Blood Transfusions: Those with severe anemia or where there’s no improvement, Blood transfusion may be required. The procedure involves: 
  • Transfusion Therapy: These are given in a hospital or an outpatient facility that is an infusion center. 
  • Dialysis-related Procedures: For patients who are on dialysis, that management of anemia can also include: 
  • Dialysis Modifications: Supplementing the patient’s diet, because low nutrient intake may result to inadequate dialysis that worsens anemia. 

use-of-phases-in-managing-anemia-due-to-chronic-kidney-disease

  • Assessment and Diagnosis: Assess severity of anemia and its potential causes (e.g., level of hemoglobin, iron stocks, vitamin B12, and folate). Decide on the kind of CKD a patient has to start the appropriate management. 
  • Treatment of Underlying Causes: Correct scientific or vitamin and mineral deficiencies through dietary supplements. Optimise management of patients with the condition to reduce progression and effects on anemia. 
  • Erythropoiesis-Stimulating Agents (ESAs): Prescribe ESAs such as erythropoietin or darbepoetin alpha with the aim of increasing red blood cell mass. Supervise ESA dosing to maintain target hemoglobin concentrations in the patient’s body. 
  • Supportive Therapy: Educate that blood transfusion should be given when necessary and be aware of risks. Dosage of medications that may cause anemia or interfere with chosen treatments should be modified accordingly. 
  • Long-term Management and Monitoring: It is important to periodically check levels of haemoglobin, iron stores and kidney function. Monitor the patient response and update ESA and iron therapy based on the observational data collected 

Medication

 

daprodustat 

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



nandrolone 

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



ferrous fumarate 

600 mg/day orally every day in 1-3 divided doses 



epoetin beta/methoxy polyethylene glycol 

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 complex 

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 beta 

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

roxadustat 

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



ferrous sulfate anhydrous 

Initial dosage of 1000 mg per day orally in 1 to 3 times a day



iron sucrose 

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 



 

nandrolone 

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 glycol 

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 complex 

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 beta 

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



iron sucrose 

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 



 

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Anemia due to Chronic Kidney Disease

Updated : August 12, 2024

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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. 

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. 

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. 

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. 

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%. 

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. 

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. 

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. 

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. 

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. 

Age Group 

  • Adults: CKD-related anemia is more prevalent in the adult population especially those who are above 50 years of age because the risk of developing CKD rises with age. 
  • Elderly: This is because older patients have reduced renal function due to aging and are generally more susceptible to the development of chronic kidney disease and its complications. 
  • Children: However, anemia related to CKD is not rare among children, especially those with congenital or hereditary renal diseases. 
  • Pallor: It is noticed in the skin, conjunctiva, and nail beds. 
  • Tachycardia: Tachycardia as a compensation mechanism. 
  • Shortness of Breath: It usually happens inclusive of exertion or even in normal day to day activities as mentioned a while ago. 
  • Fatigue and Weakness: As a rule, generalized and can cause obvious changes in the child’s condition. 
  • Cold Extremities: This is due to poor circulation, which in turn leads to the formation of plaque on the walls of arteries. 
  • Peripheral Edema: Legs may swell occasionally, especially for those patients who have been diagnosed with congestive heart failure. 
  • Diabetes mellitus 
  • Hypertension 
  • Cardiovascular diseases 
  • Autoimmune diseases 

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. 

  • Aplastic anemia 
  • Hypothyroidism 
  • Methemoglobinemia 
  • Systemic lupus erythematosus 
  • Alcohol misuse disorder 
  • Dialysis complications 
  • Hyperthyroidism 
  • Sickle cell anemia 
  • Hypoadrenalism 

Manage CKD: 

Treat comorbidities that contribute to the injury (for example, diabetes or hypertension). 

It is also important to make some changes to diet to control the levels of electrolytes and nutrients. 

For advanced CKD, patients may need to undergo hemodialysis or peritoneal dialysis. 

Pharmacological Treatments: 

ESAs (e. g., Epoetin alfa, darbepoetin alfa): Regulate production of red blood cells. 

Iron Supplementation: Administer oral or intravenous iron; to avoid iron toxicity, measure the levels. 

Non-Pharmacological Approaches 

For the desired results some sort of changes are necessary, such as a considerable increase in intake of iron containing foods. 

It implied correction of the causes of anemia including bleeding. 

Monitoring and Follow-Up: 

Biometric assessments at least once a month involving a check-up on hemoglobin and iron levels. 

Monitor patient’s response to treatment and side effects to determine the necessity for change in the treatment plan. 

Dietary Modifications: 

  • Iron-Rich Foods: Promote foods with high iron content, including lean meats, poultry, fish, beans, and iron-fortified cereals. 
  • Vitamin C: Encourage consumption of foods containing vitamin C (e.g., oranges, lemon, bell peppers) to improve the absorption of the non-heme iron present in plant-based diets. 
  • Vitamin B12 and Folate: Continue a diet high in B12 and folate or take a Vitamin B12 supplement if advised by a healthcare provider. 

Nutritional Supplements: 

  • Iron Supplements: Patients who are unable to take oral iron or who require a higher dose might have dietary iron augmented with supplements. Check for correct administration of dose an effective dose requires supervision. 
  • Vitamin B12 and Folate Supplements: Include supplements as part of the nutrition plan if the client cannot consume adequate amounts of vitamins and minerals or if they are deficient. 

Lifestyle Modifications: 

  • Exercise: Promote physical activity and exercise that will enhance general cardiovascular fitness and possibly red blood cell production and utilization. 
  • Education: Educate the patients regarding dietary practices in the treatment of anemia and how it augments pharmaceutical therapies. 
  • Support Groups: Appliance of psychological components of chronic disease and its treatment, such as enrollment of patients in support groups or counselling. 

Hematology

  • Epoetin alfa: Erythropoietin is a cytokine which stimulates the production of red blood cells; this is a recombinant form of it. It is given through an intravenous (IV) or subcutaneous (SC) route of transmission. Usually given at intervals of 2 to 3 days, but the dosing schedule can be adjusted depending on the clinical outcome and the patient’s hemoglobin status. 
  • Darbepoetin alfa: A more sustained form of erythropoietin thus implying that it can be administered with less frequency than epoetin alfa. It can also be administered Intravenously or Subcutaneously. Typically given once in one to four weeks based on the dose and the body response of the patient. 
  • Methoxy polyethylene glycol-epoetin beta (Mircera): A running EPO stimulator with a tethered half-life of the agent, perhaps requiring administration only once a week. It is administered SC. Administered every 2 to 4 weeks. 

Hematology

  • Ferrous Sulfate: It is one of the most widely used types of iron supplements, usually containing 65 mg of iron in the form of ferrous salt per tablet. 
  • Ferrous Fumarate: Provides approximately 33 mg of elemental iron per 100 mg, which is about one-third of the total weight of the supplement as iron. 
  • Ferrous Gluconate: It is composed of approximately 12% elemental iron; 300 mg of ferrous sulphate yields about 36 mg of elemental iron. 

Hematology

  • Iron Supplementation: When it comes to patients with iron deficiency, IV iron is administered more often than oral iron because oral iron is not well absorbed in CKD patients. Procedures may involve: 
  • Intravenous Iron Infusions: Given in outpatient care settings like the infusion center. Typical preparations are iron sucrose, ferric gluconate or ferric carboxymaltose. 
  • Erythropoiesis-Stimulating Agents (ESAs): ESAs are used to encourage the production of red blood cells. The procedure involves: 
  • Subcutaneous or Intravenous Administration: Given in a hospital or any other health care facility. Some ESAs are epoetin alfa and darbepoetin alfa some of the agents that it contains. 
  • Blood Transfusions: Those with severe anemia or where there’s no improvement, Blood transfusion may be required. The procedure involves: 
  • Transfusion Therapy: These are given in a hospital or an outpatient facility that is an infusion center. 
  • Dialysis-related Procedures: For patients who are on dialysis, that management of anemia can also include: 
  • Dialysis Modifications: Supplementing the patient’s diet, because low nutrient intake may result to inadequate dialysis that worsens anemia. 

Hematology

  • Assessment and Diagnosis: Assess severity of anemia and its potential causes (e.g., level of hemoglobin, iron stocks, vitamin B12, and folate). Decide on the kind of CKD a patient has to start the appropriate management. 
  • Treatment of Underlying Causes: Correct scientific or vitamin and mineral deficiencies through dietary supplements. Optimise management of patients with the condition to reduce progression and effects on anemia. 
  • Erythropoiesis-Stimulating Agents (ESAs): Prescribe ESAs such as erythropoietin or darbepoetin alpha with the aim of increasing red blood cell mass. Supervise ESA dosing to maintain target hemoglobin concentrations in the patient’s body. 
  • Supportive Therapy: Educate that blood transfusion should be given when necessary and be aware of risks. Dosage of medications that may cause anemia or interfere with chosen treatments should be modified accordingly. 
  • Long-term Management and Monitoring: It is important to periodically check levels of haemoglobin, iron stores and kidney function. Monitor the patient response and update ESA and iron therapy based on the observational data collected 

Free CME credits

Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.

Digital Certificate PDF

On course completion, you will receive a full-sized presentation quality digital certificate.

medtigo Simulation

A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.

medtigo Points

medtigo points is our unique point redemption system created to award users for interacting on our site. These points can be redeemed for special discounts on the medtigo marketplace as well as towards the membership cost itself.
 
  • Registration with medtigo = 10 points
  • 1 visit to medtigo’s website = 1 point
  • Interacting with medtigo posts (through comments/clinical cases etc.) = 5 points
  • Attempting a game = 1 point
  • Community Forum post/reply = 5 points

    *Redemption of points can occur only through the medtigo marketplace, courses, or simulation system. Money will not be credited to your bank account. 10 points = $1.

All Your Certificates in One Place

When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.

Our Certificate Courses