Anemia in Chronic Kidney disease is a fascinating area of study both for the Basic scientist and Practising Nephrologist . In this talk , both areas are highlighted with emphasis on erythropoietin .
CSF - Cerebrospinal fluid examination - from tapping to pathological diagnosisAshish Jawarkar
This is a series of notes on clinical pathology, useful for undergraduate and postgraduate students, as well as practising pathologists. Prepared from standard text books with data in tabular and easily readable format
Autologous Blood Transfusion (ABT) means reinfusion of blood or blood products taken from the same patient
ABT is not a new concept, fear of transfusion- transmitted diseases stimulated the growth of autologous programme
Erythropoietins such as epoetin alfa are used to treat anemia associated with chronic kidney disease, chemotherapy, and HIV/AIDS. They work by stimulating red blood cell production in the bone marrow. Common side effects include hypertension, nausea, vomiting, and headache, so blood pressure and hemoglobin levels need to be monitored during treatment.
CSF:
Derived through ultrafilteration and secretion through choroid plexus, produced at the rate of 500 ml/day.
Provides physical support, collects wastes, circulates nutrients and lubricates the CNS.
Normal CSF volumes:
In Adults: 90 - 150 ml
In Neonates: 10 - 60 ml
Total CSF volume is replaced every 5-7 hours.
COLLECTION
Lumbar puncture, Cisternal puncture, Lateral cervical puncture, Shunts and cannulas
Opening pressure – 90-180 mm H2O
Approximately 15-20 cc fluid collected
LAB
REQUIRED
Opening CSF pressure
Total cell count
Differential cell count
Glucose
Total protein
OPTIONAL
Cultures, Gram stain, AFB, Fungal and bacterial
antigens, Enzymes, PCR, Cytology, Electrophoresis,
VDRL, D-Dimers
This document provides details on microscopic examination of urine sediment. Key points include:
- Urine sample collection and preparation for examination under microscope by centrifuging and examining the sediment.
- Classification of findings as organised or unorganised substances, and types of cells, casts, crystals and other formed elements that may be observed.
- Significance of various normal and abnormal findings in identifying renal and other diseases. Detailed morphology of different cell types, casts, crystals and other structures are described.
This document discusses the history and physiology of peritoneal dialysis. It describes how peritoneal dialysis evolved from early experiments in the 19th century to the development of continuous ambulatory peritoneal dialysis in the late 20th century. It also summarizes the anatomy of the peritoneum and various models that have been used to describe solute and fluid transport across the peritoneal membrane during dialysis.
CSF - Cerebrospinal fluid examination - from tapping to pathological diagnosisAshish Jawarkar
This is a series of notes on clinical pathology, useful for undergraduate and postgraduate students, as well as practising pathologists. Prepared from standard text books with data in tabular and easily readable format
Autologous Blood Transfusion (ABT) means reinfusion of blood or blood products taken from the same patient
ABT is not a new concept, fear of transfusion- transmitted diseases stimulated the growth of autologous programme
Erythropoietins such as epoetin alfa are used to treat anemia associated with chronic kidney disease, chemotherapy, and HIV/AIDS. They work by stimulating red blood cell production in the bone marrow. Common side effects include hypertension, nausea, vomiting, and headache, so blood pressure and hemoglobin levels need to be monitored during treatment.
CSF:
Derived through ultrafilteration and secretion through choroid plexus, produced at the rate of 500 ml/day.
Provides physical support, collects wastes, circulates nutrients and lubricates the CNS.
Normal CSF volumes:
In Adults: 90 - 150 ml
In Neonates: 10 - 60 ml
Total CSF volume is replaced every 5-7 hours.
COLLECTION
Lumbar puncture, Cisternal puncture, Lateral cervical puncture, Shunts and cannulas
Opening pressure – 90-180 mm H2O
Approximately 15-20 cc fluid collected
LAB
REQUIRED
Opening CSF pressure
Total cell count
Differential cell count
Glucose
Total protein
OPTIONAL
Cultures, Gram stain, AFB, Fungal and bacterial
antigens, Enzymes, PCR, Cytology, Electrophoresis,
VDRL, D-Dimers
This document provides details on microscopic examination of urine sediment. Key points include:
- Urine sample collection and preparation for examination under microscope by centrifuging and examining the sediment.
- Classification of findings as organised or unorganised substances, and types of cells, casts, crystals and other formed elements that may be observed.
- Significance of various normal and abnormal findings in identifying renal and other diseases. Detailed morphology of different cell types, casts, crystals and other structures are described.
This document discusses the history and physiology of peritoneal dialysis. It describes how peritoneal dialysis evolved from early experiments in the 19th century to the development of continuous ambulatory peritoneal dialysis in the late 20th century. It also summarizes the anatomy of the peritoneum and various models that have been used to describe solute and fluid transport across the peritoneal membrane during dialysis.
This document discusses artificial liver support systems for patients with liver failure. It begins by introducing the vital functions of the liver and describing acute and chronic liver failure. For patients awaiting transplantation or regeneration, extracorporeal devices have been developed to temporarily support liver function. Both non-cell based systems that provide detoxification and cell-based bioartificial systems that also support synthesis are described. While artificial systems have shown improvements biochemically, benefits to survival have not been clearly proven. Further development and clinical trials are still needed to establish efficacy and safety of bioartificial liver devices.
CSF examination is performed between the L4 and L5 vertebrae after injecting local anesthesia. The necessary apparatus includes various sized needles, a syringe, lidocaine, and sterile specimen pots. Removing too much fluid can cause herniation of the brain stem, so blood levels should be measured simultaneously for accurate interpretation. Before performing a lumbar puncture, the retina should be checked for signs of papilledema since its presence could indicate complications. The procedure involves performing a spinal tap to collect CSF in sterile pots. Normal CSF values provide a baseline.
AML is characterized by accumulation of abnormal blast cells in the bone marrow and impaired production of normal blood cells. It results from clonal expansion of myeloid precursor cells with reduced ability to differentiate. Treatment involves induction chemotherapy with anthracyclines and cytarabine to achieve complete remission, defined as less than 5% blasts in the bone marrow. Risk is then assessed based on genetics to determine if additional chemotherapy or stem cell transplant is needed.
This document discusses chronic kidney disease (CKD), anemia in CKD, and treatments for anemia in CKD. It defines CKD and its stages based on glomerular filtration rate and kidney damage. Anemia in CKD is defined based on hemoglobin levels. Causes of anemia in CKD include relative erythropoietin deficiency, iron deficiency, blood loss, shortened red blood cell lifespan, and the "uremic milieu." Iron therapy and erythropoiesis-stimulating agents (ESAs) are discussed as treatments for anemia in CKD, including criteria for starting therapy, drug options, dosing, monitoring, and dose adjustment.
This document describes the case of a 28-year-old man who presented with inability to speak and motor weakness after fever. He was diagnosed with left middle cerebral artery territory acute infarct and a small infarct in the right parietal region. Over several years, he developed hypertension, renal dysfunction, and was ultimately diagnosed with IgA nephropathy based on renal biopsy findings. The document then provides details on IgA nephropathy including pathogenesis, histological findings, risk factors for progression, and treatment options.
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
Transplantation in sensitized patients(seminar)Vishal Golay
This document discusses HLA typing, crossmatching, and transplantation in sensitized patients. It begins with a brief history of organ transplantation. It then covers topics such as the structure and function of MHC molecules, methods of HLA typing including serological and DNA-based techniques, interpreting HLA typing reports, detecting sensitization through antibody detection tests, defining and identifying sensitized patients, and challenges in transplanting sensitized patients. Advances in diagnostics and therapeutics have helped increase transplantation options for sensitized patients.
Dr. Manan B. Shah presented on biomarkers for acute kidney injury. The presentation discussed the need for biomarkers to detect AKI earlier than serum creatinine, as creatinine levels typically rise only after 50% kidney function is lost. Several promising urinary biomarkers were described, including NGAL, KIM-1, IL-18, and cystatin C, which can indicate kidney injury earlier. The presentation proposed that a panel of biomarkers may help guide whether renal replacement therapy is needed for patients with AKI. Early detection and treatment of AKI using biomarkers could potentially improve outcomes by preventing or minimizing kidney injury.
An illustrative presentation on Microscopic examination of Urine for Medical, Dental, Pharmacology and Biotechnology students to facilitate easy- learning and self-study..
This document provides guidelines for blood transfusion in clinical practice. It discusses the principles of transfusion medicine including avoiding unnecessary transfusions and using alternatives when possible. It provides triggers for transfusing red blood cells, fresh frozen plasma, cryoprecipitate and platelets based on hemoglobin, coagulation factor and platelet count levels. It also gives specific guidelines for transfusing patients with sickle cell disease, thalassemia, neonates and in emergency situations. The risks of transfusion are weighed against the benefits of maintaining adequate oxygen-carrying capacity and hemostasis.
Catheter related infections- DR Nadia MohsenFarragBahbah
This document discusses catheter-related bloodstream infections (CRBSIs) in patients undergoing hemodialysis. It defines CRBSIs and describes the types of dialysis catheters and associated infection risks. Common causative organisms are gram-positive cocci like Staphylococcus aureus. The diagnostic approach involves clinical evaluation and blood cultures, with treatment tailored based on culture results. Management typically requires systemic antibiotics and often catheter removal, with options for catheter exchange or salvage with antibiotic locks in some cases.
This document discusses erythropoietin (EPO) and anemia. It contains the following key points:
1. EPO is a glycoprotein hormone produced mainly by the kidneys that stimulates red blood cell production. Recombinant human EPO (rHuEPO) was developed with the same polypeptide backbone but differences in glycosylation compared to natural EPO.
2. Later generation ESAs like darbepoetin alfa have a longer half-life, allowing less frequent dosing. PEGylated ESAs like CERA have an even longer half-life of 130 hours, permitting monthly dosing.
3. Other experimental ESAs include those with fused
Frozen section is a pathology procedure that allows rapid microscopic examination of a specimen during surgery. Sir Louis B. Wilson pioneered the technique in 1905 at the Mayo Clinic to enable urgent intraoperative diagnosis. The procedure involves snap freezing tissue, sectioning it with a cryostat microtome, and staining for quick analysis. While fast, frozen sections can have artifacts from ice crystals and knife marks. Pathologists must communicate closely with surgeons to ensure the appropriate use of frozen sections for urgent diagnostic needs during operations.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Post-transplant lymphoproliferative disorder/disease (PTLD) is a B-cell proliferation disorder following infection with EpsteineBarr virus due to therapeutic immunosuppression after organ transplantation. The more intense the immunosuppression, the higher the incidence of PTLD and the earlier it occurs. The cornerstone of successful treatment of PTLD is reduction or withdrawal of immunosuppression.
1. The document discusses blood component therapy, including the components of blood, blood typing and compatibility, and the use of specific blood components for transfusion. It describes how whole blood can be separated into red blood cells, platelets, plasma, and other components.
2. Compatibility of blood type between donor and recipient is important to avoid agglutination or other adverse reactions. The ABO and Rh blood group systems are discussed.
3. Blood component transfusion involves using specific isolated components like red blood cells, platelets, or plasma rather than whole blood, allowing targeted therapy for different clinical needs. Risks of transfusion are also summarized.
PRCA post renal transplant-a case and reviewVishal Golay
Partha Choudhary, a 48-year-old male, developed progressive anemia after a liver transplant in 2011. His hemoglobin levels gradually decreased from 9.2 to 5.4 over a year despite EPO treatment. Testing found he was positive for Parvovirus B19 and negative for other potential causes. A bone marrow biopsy showed an absence of erythroblasts, consistent with a diagnosis of pure red cell aplasia caused by Parvovirus B19 infection. Treatment for this type of virus-induced PRCA typically involves intravenous immunoglobulin therapy.
Anavar is one of the most popular anabolic steroids and performance enhancing drugs to lose body fat and retain muscle mass and body strength. Classified as a Schedule III (non-narcotic) controlled substance under the Anabolic Steroids Control Act of 1990, this anabolic androgenic steroid is popular among male and female athletes as it is a mild steroid with extremely potent properties.
Erythropoietin (EPO) is a hormone produced by the kidneys that stimulates bone marrow to produce red blood cells which carry oxygen throughout the body. Chronic kidney disease can damage the kidneys and lower EPO production, resulting in anemia due to fewer red blood cells. Synthetic EPO has been developed to treat anemia in patients with chronic kidney disease.
This document discusses artificial liver support systems for patients with liver failure. It begins by introducing the vital functions of the liver and describing acute and chronic liver failure. For patients awaiting transplantation or regeneration, extracorporeal devices have been developed to temporarily support liver function. Both non-cell based systems that provide detoxification and cell-based bioartificial systems that also support synthesis are described. While artificial systems have shown improvements biochemically, benefits to survival have not been clearly proven. Further development and clinical trials are still needed to establish efficacy and safety of bioartificial liver devices.
CSF examination is performed between the L4 and L5 vertebrae after injecting local anesthesia. The necessary apparatus includes various sized needles, a syringe, lidocaine, and sterile specimen pots. Removing too much fluid can cause herniation of the brain stem, so blood levels should be measured simultaneously for accurate interpretation. Before performing a lumbar puncture, the retina should be checked for signs of papilledema since its presence could indicate complications. The procedure involves performing a spinal tap to collect CSF in sterile pots. Normal CSF values provide a baseline.
AML is characterized by accumulation of abnormal blast cells in the bone marrow and impaired production of normal blood cells. It results from clonal expansion of myeloid precursor cells with reduced ability to differentiate. Treatment involves induction chemotherapy with anthracyclines and cytarabine to achieve complete remission, defined as less than 5% blasts in the bone marrow. Risk is then assessed based on genetics to determine if additional chemotherapy or stem cell transplant is needed.
This document discusses chronic kidney disease (CKD), anemia in CKD, and treatments for anemia in CKD. It defines CKD and its stages based on glomerular filtration rate and kidney damage. Anemia in CKD is defined based on hemoglobin levels. Causes of anemia in CKD include relative erythropoietin deficiency, iron deficiency, blood loss, shortened red blood cell lifespan, and the "uremic milieu." Iron therapy and erythropoiesis-stimulating agents (ESAs) are discussed as treatments for anemia in CKD, including criteria for starting therapy, drug options, dosing, monitoring, and dose adjustment.
This document describes the case of a 28-year-old man who presented with inability to speak and motor weakness after fever. He was diagnosed with left middle cerebral artery territory acute infarct and a small infarct in the right parietal region. Over several years, he developed hypertension, renal dysfunction, and was ultimately diagnosed with IgA nephropathy based on renal biopsy findings. The document then provides details on IgA nephropathy including pathogenesis, histological findings, risk factors for progression, and treatment options.
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
Transplantation in sensitized patients(seminar)Vishal Golay
This document discusses HLA typing, crossmatching, and transplantation in sensitized patients. It begins with a brief history of organ transplantation. It then covers topics such as the structure and function of MHC molecules, methods of HLA typing including serological and DNA-based techniques, interpreting HLA typing reports, detecting sensitization through antibody detection tests, defining and identifying sensitized patients, and challenges in transplanting sensitized patients. Advances in diagnostics and therapeutics have helped increase transplantation options for sensitized patients.
Dr. Manan B. Shah presented on biomarkers for acute kidney injury. The presentation discussed the need for biomarkers to detect AKI earlier than serum creatinine, as creatinine levels typically rise only after 50% kidney function is lost. Several promising urinary biomarkers were described, including NGAL, KIM-1, IL-18, and cystatin C, which can indicate kidney injury earlier. The presentation proposed that a panel of biomarkers may help guide whether renal replacement therapy is needed for patients with AKI. Early detection and treatment of AKI using biomarkers could potentially improve outcomes by preventing or minimizing kidney injury.
An illustrative presentation on Microscopic examination of Urine for Medical, Dental, Pharmacology and Biotechnology students to facilitate easy- learning and self-study..
This document provides guidelines for blood transfusion in clinical practice. It discusses the principles of transfusion medicine including avoiding unnecessary transfusions and using alternatives when possible. It provides triggers for transfusing red blood cells, fresh frozen plasma, cryoprecipitate and platelets based on hemoglobin, coagulation factor and platelet count levels. It also gives specific guidelines for transfusing patients with sickle cell disease, thalassemia, neonates and in emergency situations. The risks of transfusion are weighed against the benefits of maintaining adequate oxygen-carrying capacity and hemostasis.
Catheter related infections- DR Nadia MohsenFarragBahbah
This document discusses catheter-related bloodstream infections (CRBSIs) in patients undergoing hemodialysis. It defines CRBSIs and describes the types of dialysis catheters and associated infection risks. Common causative organisms are gram-positive cocci like Staphylococcus aureus. The diagnostic approach involves clinical evaluation and blood cultures, with treatment tailored based on culture results. Management typically requires systemic antibiotics and often catheter removal, with options for catheter exchange or salvage with antibiotic locks in some cases.
This document discusses erythropoietin (EPO) and anemia. It contains the following key points:
1. EPO is a glycoprotein hormone produced mainly by the kidneys that stimulates red blood cell production. Recombinant human EPO (rHuEPO) was developed with the same polypeptide backbone but differences in glycosylation compared to natural EPO.
2. Later generation ESAs like darbepoetin alfa have a longer half-life, allowing less frequent dosing. PEGylated ESAs like CERA have an even longer half-life of 130 hours, permitting monthly dosing.
3. Other experimental ESAs include those with fused
Frozen section is a pathology procedure that allows rapid microscopic examination of a specimen during surgery. Sir Louis B. Wilson pioneered the technique in 1905 at the Mayo Clinic to enable urgent intraoperative diagnosis. The procedure involves snap freezing tissue, sectioning it with a cryostat microtome, and staining for quick analysis. While fast, frozen sections can have artifacts from ice crystals and knife marks. Pathologists must communicate closely with surgeons to ensure the appropriate use of frozen sections for urgent diagnostic needs during operations.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Post-transplant lymphoproliferative disorder/disease (PTLD) is a B-cell proliferation disorder following infection with EpsteineBarr virus due to therapeutic immunosuppression after organ transplantation. The more intense the immunosuppression, the higher the incidence of PTLD and the earlier it occurs. The cornerstone of successful treatment of PTLD is reduction or withdrawal of immunosuppression.
1. The document discusses blood component therapy, including the components of blood, blood typing and compatibility, and the use of specific blood components for transfusion. It describes how whole blood can be separated into red blood cells, platelets, plasma, and other components.
2. Compatibility of blood type between donor and recipient is important to avoid agglutination or other adverse reactions. The ABO and Rh blood group systems are discussed.
3. Blood component transfusion involves using specific isolated components like red blood cells, platelets, or plasma rather than whole blood, allowing targeted therapy for different clinical needs. Risks of transfusion are also summarized.
PRCA post renal transplant-a case and reviewVishal Golay
Partha Choudhary, a 48-year-old male, developed progressive anemia after a liver transplant in 2011. His hemoglobin levels gradually decreased from 9.2 to 5.4 over a year despite EPO treatment. Testing found he was positive for Parvovirus B19 and negative for other potential causes. A bone marrow biopsy showed an absence of erythroblasts, consistent with a diagnosis of pure red cell aplasia caused by Parvovirus B19 infection. Treatment for this type of virus-induced PRCA typically involves intravenous immunoglobulin therapy.
Anavar is one of the most popular anabolic steroids and performance enhancing drugs to lose body fat and retain muscle mass and body strength. Classified as a Schedule III (non-narcotic) controlled substance under the Anabolic Steroids Control Act of 1990, this anabolic androgenic steroid is popular among male and female athletes as it is a mild steroid with extremely potent properties.
Erythropoietin (EPO) is a hormone produced by the kidneys that stimulates bone marrow to produce red blood cells which carry oxygen throughout the body. Chronic kidney disease can damage the kidneys and lower EPO production, resulting in anemia due to fewer red blood cells. Synthetic EPO has been developed to treat anemia in patients with chronic kidney disease.
The document provides information about searching patents in the European Patent Office (EPO) database called espacenet. It discusses:
- A brief history of the EPO being established in 1977 by the European Patent Convention to create a centralized patent application and grant system.
- Basic search tips for espacenet including quick search, advanced search, classification search, and number search. It describes search fields, Boolean operators, truncation, and nested queries.
- Examples of different search types like quick search, advanced search, classification search, numbers search, and searching for legal status, event history and citations.
- Limitations of searching in espacenet including limitations on search terms, fields, number of results
This document provides guidelines for managing anemia in chronic kidney disease patients at General University Teaching Hospital of Slemani. It outlines the historical background of understanding renal anemia and effects of anemia like increased mortality and cardiovascular disease. The guidelines recommend targets for hemoglobin concentration, iron status markers, and schedules for parenteral iron and erythropoiesis-stimulating agent administration and monitoring based on hemoglobin levels and dialysis status. Potential complications and contraindications of treatments are also discussed.
This document discusses the management of anemia in chronic kidney disease (CKD). It begins by defining anemia and its causes in CKD, which include reduced erythropoietin production and decreased red blood cell survival due to kidney failure. Left untreated, anemia in CKD can lead to deterioration in cardiac function, impaired cognition, and increased fatigue and mortality risk. The main therapeutic options for treating anemia in CKD are red blood cell transfusions, androgens, and erythropoiesis-stimulating agents (ESAs). ESAs such as epoetin alfa and darbepoetin alfa are now the standard treatment as they reduce transfusion needs and risks while helping to mobilize
This document summarizes the regulation and production of erythropoietin (EPO) and factors involved in erythropoiesis. EPO is produced mainly in the kidney and promotes red blood cell formation in the bone marrow. Its production is stimulated by hypoxia and regulated by oxygen sensors in the kidney and liver. EPO increases red blood cell production by promoting progenitor cell production, shortening maturation time, and promoting early reticulocyte release. Other general and maturation factors involved in erythropoiesis include growth inducers, vitamins B12 and folic acid, iron, copper, and proteins for hemoglobin and heme synthesis.
EPO is a performance-enhancing drug that stimulates red blood cell creation, increasing oxygen levels in the body. It allows athletes in endurance sports like cycling and running to maintain steady breathing and not slow down or stop during long distance events. While originally developed to treat medical conditions causing anemia, athletes use EPO to enhance performance and chances of winning. However, EPO is dangerous as it raises hematocrit levels, thickening the blood and risking strokes, heart attacks, and clogged capillaries.
Management of anemia in chronic kidney disease -Boushra Alsaoor
This document provides an overview of the management of anemia in chronic kidney disease. It defines anemia according to WHO criteria and notes that nearly 90% of CKD patients with a GFR below 30 mL/min have anemia. The main causes of anemia in CKD are decreased erythropoietin production and a shorter red blood cell lifespan. Treatment with erythropoiesis-stimulating agents or ESAs like epoetin and darbepoetin can help increase hemoglobin levels and improve outcomes. The goals of ESA therapy are to raise hemoglobin by 1-2 g/dL per month until it reaches 10-11.5 g/dL without exceeding 13 g/dL. Iron supplementation is
Recent clinical trials have raised safety concerns about erythropoiesis-stimulating agents (ESAs) used to treat anemia in cancer patients. Updated guidelines recommend more restrictive use of ESAs due to increased risks of thromboembolic events and decreased survival shown in trials. ESAs are now only recommended when hemoglobin levels are low due to chemotherapy and potential risks should be considered, with close monitoring of hemoglobin levels and iron status. Ongoing research continues to evaluate the effectiveness and safety of ESAs in different cancer patient populations and treatment settings.
Anemia is a common complication of chronic kidney disease that can cause fatigue. While the kidneys normally produce erythropoietin to stimulate red blood cell production, CKD patients have relative erythropoietin deficiency. This leads to anemia which, if left untreated, can negatively impact quality of life and cardiovascular health. Erythropoiesis-stimulating agents and iron supplementation are used to treat anemia in CKD, though the appropriate hemoglobin target level remains an area of ongoing research and debate given risks identified with higher targets in some studies.
This document provides an overview of chronic kidney disease (CKD)-related anemia, including its definition, causes, effects, evaluation, and management. It defines the stages of CKD based on glomerular filtration rate and describes how anemia is defined for CKD patients based on hemoglobin levels. The main causes of anemia in CKD are identified as relative erythropoietin deficiency, iron deficiency, blood loss, shortened red blood cell lifespan, and inflammation. Evaluation involves testing hemoglobin, reticulocyte count, ferritin, transferrin saturation, and vitamins. Iron therapy is indicated based on ferritin and transferrin saturation levels, and intravenous iron is generally preferred for patients on dialysis
Mata kuliah Biokimia pangan tentang Metabolisme Vitamin E. Cari lebih banyak materi kuliah semester 3 di: http://muhammadhabibielecture.blogspot.com/2014/12/kuliah-semester-3.html
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE 2013Ayman Seddik
1) Anaemia is common in chronic kidney disease (CKD) due to reduced kidney function and erythropoietin production. It can cause lower quality of life and increased risk of cardiovascular complications.
2) Guidelines recommend diagnosing anaemia of CKD in adults with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73m2 and hemoglobin ≤11 g/dL.
3) Treatment involves iron supplementation and erythropoiesis-stimulating agents (ESAs) to increase hemoglobin levels, with a target range of 11-12 g/dL according to recent guidelines. Higher targets may increase risk without clear benefits.
Resistencia a la Eritropoyetina @DokRenalIgor Romaniuk
La anemia es una complicación común en la enfermedad renal crónica y requiere tratamiento con eritropoyetina. La causa principal es la producción inadecuada de eritropoyetina por el riñón. Se han aprobado biosimilares de epoetina para tratar la anemia. Algunos pacientes son resistentes a altas dosis de eritropoyetina, lo que puede estar relacionado con un aumento de la mortalidad. Las posibles causas de la resistencia incluyen deficiencia de hierro, inflamación, enfermedades y tratamientos
Erythropoiesis is the formation of red blood cells in the bone marrow. It involves 6 stages: 1) pronormoblast, the first identifiable erythroid cell; 2) basophilic normoblast; 3) polychromatic normoblast where hemoglobin formation takes place; 4) orthrochromatic normoblast; 5) reticlulocyte, the immature red blood cell containing ribosomal remnants; 6) red blood cell, the final mature form lacking a nucleus with a biconcave disk shape. Each stage involves a decrease in cell and nuclear size along with increasing hemoglobinization until the nucleus is lost in the final red blood cell.
This document discusses anaemia and its causes in chronic kidney disease (CKD). It defines anaemia and outlines how it is diagnosed based on haemoglobin levels. The main causes of anaemia in CKD are decreased erythropoietin production and iron deficiency. Iron supplementation using oral or intravenous iron is recommended to treat iron deficiency anaemia in CKD, along with erythropoiesis-stimulating agents (ESAs) like epoetin and darbepoetin to treat all anaemia. Guidelines on monitoring haemoglobin levels and initiating/maintaining ESA therapy are provided. Red blood cell transfusion is indicated when rapid correction of anaemia is needed or ESA therapy is ineffective.
This document provides the official journal of the International Society of Nephrology, which includes the KDIGO Clinical Practice Guideline for Anemia in Chronic Kidney Disease. The guideline was developed by an international work group to provide evidence-based recommendations on the diagnosis, evaluation, and treatment of anemia for patients with chronic kidney disease. It includes recommendations on the use of iron, erythropoiesis-stimulating agents, and red blood cell transfusions to treat anemia in kidney disease. Tables, figures, and references are provided to support the recommendations and guidelines.
ERYTHROCYTES
- Major function - carry O2 , CO2, buffer
- Contain Haemoglobin (Fe atoms)
- 14 gms/100ml
- Biconcave disc
- High surface to volume ratio
Plasma membrane contain special polysaccharide & proteins - spectrin
- Differ from person to person - blood type/group
Normal count 4.5 - 5 million/cumm
This document summarizes various causes of rickets, including calcium deficiency, phosphorus deficiency, rickets of prematurity, and several genetic disorders. Calcium deficiency can result from low dietary intake or malabsorption and presents with signs of rickets in infancy. Phosphorus deficiency is usually due to inadequate intake or antacid use. Rickets of prematurity occurs in very low birth weight infants and is prevented by mineral supplementation. The document also describes several genetic causes of rickets, including X-linked hypophosphatemic rickets, autosomal dominant hypophosphatemic rickets, and Fanconi syndrome. Treatment involves calcium, vitamin D, and phosphorus supplementation tailored to the specific deficiency.
Anemia develops during the early stages of CKD and is common in patients with End Stage Renal Disease, ESRD. Anemia is an important cause of left ventricular hypertrophy and congestive heart failure. Early detection and treatment of anemia associated with CKD has proven to provide positive cognitive and physical effects.
This document discusses anemia management in chronic kidney disease (CKD). It covers the mechanisms of anemia in CKD, including erythropoietin deficiency and iron deficiency. It reviews guidelines for hemoglobin targets and the use of erythropoiesis-stimulating agents (ESAs) to treat anemia. Larger studies on hemoglobin targets in both dialysis and non-dialysis CKD patients, such as the CHOIR and CREATE trials, found higher risks with higher hemoglobin targets and no benefits to quality of life. Iron deficiency is a major cause of ESA treatment failure in CKD patients.
This document discusses anemia of chronic kidney disease (CKD), including its causes, prevalence, benefits of treatment, evaluation, and treatment with iron and erythropoietic stimulating agents (ESAs). It notes that anemia is common in CKD due to reduced kidney function and erythropoietin production. While untreated anemia can cause many symptoms, managing it with iron and ESAs can improve quality of life and reduce risks. The document provides guidelines on testing, supplementing iron, dosing ESAs, monitoring treatment response, and managing side effects in patients with CKD.
This document summarizes key information about anemia in chronic kidney disease (CKD). It defines CKD as kidney damage or decreased glomerular filtration rate (GFR) below 60 mL/min/1.73m2 for at least 3 months. Patients with CKD are more likely to die from cardiovascular causes than progress to end-stage renal disease. Anemia is common in CKD due to erythropoietin deficiency and has negative consequences if left untreated. The K/DOQI guidelines recommend evaluating hemoglobin levels when GFR is below 60 and treating anemia according to their guidelines if present. Intravenous iron is more effective than oral iron for treating anemia in CKD patients. Erythropoies
This document discusses the physiology and clinical management of PTH and mineral metabolism disorders in patients with chronic kidney disease (CKD). It provides an overview of calcium, phosphorus, vitamin D, and PTH regulation and how their homeostasis is disrupted in CKD. Secondary hyperparathyroidism leads to elevated PTH levels and disturbances in calcium and phosphorus. If not properly managed, this can result in renal osteodystrophy, vascular calcification, and increased risk of cardiovascular events and mortality. The document reviews therapeutic options like phosphate binders and vitamin D analogs to control mineral levels and treat secondary hyperparathyroidism in CKD patients.
Anemia is common in cancer patients, occurring in 30-86% of cases depending on malignancy type and Hb level definition of anemia. Anemia can be caused by the disease itself through cytokine-mediated effects on erythropoiesis or nutritional deficiencies, or be treatment-related due to chemotherapy, radiotherapy or other drugs. Erythropoietin treatment is effective at reducing transfusion needs and improving quality of life by increasing Hb levels and reducing fatigue in the majority of anemic cancer patients. However, some patients do not respond due iron deficiency or other factors. Iron supplementation can help improve response rates to EPO treatment.
This document summarizes the current state of anemia management in chronic kidney disease patients. It discusses the magnitude of anemia as a problem in CKD patients, outlines the clinical management including first-line treatments like blood saving techniques and second-line treatments like erythropoiesis-stimulating agents and iron supplementation. It also explores future therapy options, noting investigational drugs that aim to stabilize hypoxia-inducible factor or mimic erythropoietin's effects. The document reviews clinical trial data on these new agents and discusses limitations of current erythropoietin-based approaches.
The patient is a 71-year-old female who presented to the emergency room with shortness of breath, feeling faint, and dizziness. She has a history of diabetes, hypertension, chronic kidney disease, and myelodysplastic syndrome. Laboratory tests showed low red blood cell counts and hemoglobin due to bone marrow failure from her myelodysplastic syndrome. She was given two units of red blood cells due to her anemia. Her diagnoses is symptomatic anemia from her myelodysplastic syndrome, which carries a poor prognosis including a high risk of developing leukemia.
This document contains the results of laboratory tests performed on a 62-year-old female. The tests measured levels of components in the blood including hemoglobin, white blood cells, platelets, proteins, liver enzymes, glucose, lipids, electrolytes, kidney and liver function. Most results were within normal ranges, though the patient had elevated erythrocyte sedimentation rate and low levels of vitamin D and B12.
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This document discusses thalassemia in Bangladesh and advances in the management of beta thalassemia major. It notes that Bangladesh has high carrier and frequency rates of thalassemia major and hemoglobin E. The key advances in managing beta thalassemia major discussed include regular blood transfusions to maintain optimal hemoglobin levels, iron monitoring and chelation therapy to remove excess iron, and hematopoietic stem cell transplantation which can cure thalassemia major in some cases. Complications from iron overload continue to be a major challenge in the long term management of patients.
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This document summarizes the current state of anemia treatment in chronic kidney disease (CKD) patients. It discusses the magnitude of the problem, clinical management including use of erythropoiesis-stimulating agents (ESAs), and future therapies. ESAs are currently the mainstay of treatment but have limitations like requiring high doses and increased risks at higher hemoglobin levels. Newer approaches being researched include stabilizing hypoxia-inducible factor to stimulate endogenous erythropoietin production, modulating the iron-regulating hormone hepcidin, and gene therapy to introduce the erythropoietin gene directly.
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This document summarizes management strategies for non-transfusion dependent thalassemia (NTDT). It discusses transfusion therapy, iron chelation therapy using deferasirox, splenectomy, and fetal hemoglobin induction using hydroxyurea or hypomethylating agents. Novel therapeutic approaches discussed include modulating hepcidin, using JAK2 inhibitors, apo-transferrin therapy, and targeted fetal hemoglobin induction through factors like BCL11A. The document provides recommendations on when to initiate various treatments and how to monitor patients receiving therapy.
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Erythropoetin - From Bench to Bedside
1. “Erythropoietin – From Bench to
Bedside "
K.Sampath kumar,MD,DM,FRCP
Meenakshi Mission Hospital
Madurai,India
2. Focus of my talk
• Biology of Erythropoietin [EPO]
• Why EPO should come from Kidneys? Why
not Lungs ?
• Practical aspects of usage of EPO in clinic
• Major clinical trials
• Use / Abuse of EPO
• Conclusion
12. Focus of my talk
• Biology of Erythropoietin [EPO]
• Why EPO is produced in Kidneys
• Practical aspects of usage of EPO in clinic
• Major clinical trials
• Cautionary notes
• Conclusion
13. Oxygen sensing at Kidney rather than
Lungs
• > 20% of cardiac output goes to Kidneys
• Richest blood supply per gram of tissue
• Blood supply independent of metabolic
demand
• 10% of oxygen supply only is utilised by
Kidneys
14. Kidney is a biological critmeter
Blood supply
Demand and
O2 Conc
45 % Hematocrit is not a random
Number. It is optimises tissue
Oxygen delivery with correct viscosity
And fluidity
Normal hematocrit
Of 45 %
15. Oxygen sensor
EPO Production
O2
content
RBC mass
Serum
EPO
Na Reabsorption
Tissue
02
21. Develops early and worsens as CKD progresses
9%
17% 15% 10%
5%
8% 8% 15%
14%
20%
43%
62%
100
80
60
40
20
0
<2 2-2.9 3-3.9 >4
Serum Creatinine (mg/dL)
Hct <30%
Hct 30% to 32.9%
Hct 33% to Normal
Percentage of Patients
With Anemia (%)
N=1658
Anemia of CKD
22. Anemia: At Onset of RRT
7% 6%
10%
14%
15% 15%
12%
9%
5%
Mean 27.9 +/- 5.4
Median 27.9
3%
2% 2%
16%
12%
8%
4%
0%
< 20 22-24 26-28 30-32 34-36 38-40
Hematocrit (%)
Obrador, J Am Soc Nephrol 1999, 10:1793-1800
131,484 patients who began dialysis between 4/1/95 and
6/30/97
23. Why should we use EPO?
Anemia Why Anemia correction should be corrected benefits in CKD
in CKD
24. Anemia is Associated with
Poor Survival of Patients with CKD
Due to the negative effects of anemia,1–3 early diagnosis and treatment in
patients with CKD is recommended4,5
• Dynamic, retrospective
cohort study among 8761
patients with CKD at
Kaiser Permanente
Northwest2
• Assessment of outcomes2
– Death
– Cardiovascular (CV)
hospitalization
– End-stage renal disease
(ESRD)
25.0
23.4
17.4
4.0
9.4
Rate per 100 patient-years
15.5
14.5
2.6
12.6
9.6
11.6
10.3
7.6 7.4
11.3
Death
CV hospitalization
ESRD
8.5
5.9 6.2
9.0
10.1
5.3 4.8
8.9
6.5
1.3 1.3 1.0 0.8 0.5 0.4 0.4 0.3
11.0 11.8 12.3 12.8 13.2 13.5 13.9 14.5 15.8
Mean hemoglobin (g/dL) per decile
20.0
15.0
10.0
5.0
0.0
1. Fishbane S. Heart Fail Clin 2008;4:401–410; 2. Thorp ML et al. Nephrology 2009;14:240–246; 3. Kovesdy CP et al. Kidney Int
2006;69:560–564; 4. Hörl WH et al. Nephrol Dial Transplant 2007;22(suppl 3):iii2–6; 5. Gouva C et al. Kidney Int 2004;66:753–760
25. Anemia is an Important Predictor of
CVD
Longitudinal study of 246 patients with 1 year FU
Unit RR 95% CI
Hemoglobin 0.5 g/dl Decrease 1.32 1.11 –
1.59
Systolic BP 5 mm Hg Increase 1.11 1.02 –
1.21
Levin, Am J Kid Dis 1999,
34:125-134
LV Mass
Index
10 g/sq. m. Decrease 0.85 0.76 –
0.96
28. Learning Point 1
• Renal Anemia develops when
GFR falls below 30 ml/min.
29. Point 2
• In CKD 1,2,3 renal anemia is rare.
Rule out other causes
• Exception – Diabetics develop
anemia early – 45 ml/min
30. Point 3
• Pure Renal anemia is
• Normocytic
• Normochromic
Either a low[Fe] or high MCV[B12,F]
Low MCH or MCHC strongly
suggest other contributory factors
[ Iron def or hemoglobinopathy]
34. Anemia in CKD: Iron
Replacement
All CKD patients + renal anemia requiring EPO should be
given supplemental iron to reach targets.
Route: IV or oral in pre-dialysis -CKD or PD-CKD
The preferred route is IV in CKD-HD
K-DOQI 2006
35. Functional Fe Def
Ferritin
Normal
>100
Transf.sat
Low
<20%
Hypochr
cells
>10%
36. Parenteral forms of Iron
Features Iron Dextran Iron Sucrose Ferric
Gluconate
Nature Dextran complex
covering iron
core
Sucrose
covering iron
oxide core
Iron bound with 1
gluconate + 4
sucrose
Mol. Wt 96-265 kd 34 – 60 kd 289 – 440 kd
Direct Iron
Transfer
No No No
Half life 40-60 hours 6 hrs 1 hrs
Vol.
Distribution
6 Liter 3.2 – 7.3 liter 6 liter
Renal Excret. Negligible < 5 % Nil
37. Point 4
• Retics of > 100 x 10 9 /L
suggests active BM but
enhanced blood loss due to
hemolysis or bleed
38. ERA OF ESAs
Darbepoeti
n
t1/2 25–72
hours
Epoetin d
HX575 and SB309
Fishbane S. Curr Opin Nephrol Hypertens 2009;18:112–115
Macdougall IC & Ashenden M. Adv Chron Kid Dis 2009;16:117–130
Epoetin a
t1/2 6–24
hours
Methoxy
PEG-epoetin
b
(CERA)
t1/2 130 hours
Epoetin b
t1/2 6–24
hours
1989 1990 2002 2007
Biosimilar
epoetins
39. Point-5 *****
• Trigger Hb for initiating ESA therapy
should be between 9 or 10 G/dL
• Target Hb LEVEL 10-12 G/dL
Why not a normal hematocrit be targetted in CKD?
Crux of controversy
53. DM/CVA
CANCER
CKD
PHYSIOLO
GY
HD/PD/
TX
GENDER/
GENES
AGE/
ALTIDUDE
DISEASE
SEVERITY
LIFE STYLE
IRON
STATUS
54. Point -6
• Caution while using EPO !
• Active malignancy
• History of Stroke
• CAD/CCF
• Uncontrolled HT
55. EPO: Routes of administration
S.C. I.V.
Bioavailability 48.8% 100%
t 1/2 19-25 hrs 5-11 hrs
Effectiveness More less
Dose
Less More
requirement
Besarab A, et al. Am J Kidney Dis 2002; 40: 439–446
56. IV route
More dose
Less immunogenic
S.C ROUTE
30% less dose
> Half Life
> Immunogenic
57. Retic count < 10
x 10 9/L
BM failure due
to AB mediated
Pure red cell
aplasia
58. • EPO Alfa
• S.C route
?Rubber stoppers
?Polysorbate 80
Antibody against
endo and exo EPO
• B cell
tolerance lost
• Immunogenic
• Transfusion
dep
• PRCA
Trt -Hematide
59.
60. Darbepoetin Alpha
Long-acting protein
2 more carbohydrate chains and up to 8 more sialic acid
residues
Bind to same receptor as EPO
Same mechanism of action as EPO
Super-silation prolong in-vitro activity
Clinical efficacy and Safety profile similar
61. Darbepoetin in Anemia:
Correction Phase
Dialysis patients SC/IV 0.45 μg/kg once weekly
Non- Dialysis patients
0.45 μg/kg once weekly (or)
0.75 μg/kg once every two weeks (or)
1.5 μg/kg once monthly
If in Hb is < 1 g/dl in 4 wks, the dose by 25%.
Dose not more frequently than once in four weeks
If the Hb is > 2 g/dl in 4 wks the dose by 25%.
If the Hb > 12 g/dl, a dose reduction should be made.
62. Darbepoetin in CKD: EPO
Comparison
Significantly faster increase in Hb
* p<0.0001
Lullo, et al. Cardiorenal Med 2012;2:18–25
63. Hemoglobin variability and its
impact on survival
A longitudinal survey of HD patients
showing fluctuations in Hb with its
impact on survival
68. Conclusion
• Do not assume every anemia in CKD is EPO
responsive
• Look for clues for secondary causes
• Do not overcorrect hematocrit in CKD
• Know your patient profile well before EPO
therapy
• Start low and go slow
• Long acting EPO like DarboP is preferable