Protein Energy Malnutrition (PEM), also known as Protein-Energy Wasting (PEW) or Kidney Disease Wasting (KDW), is a state of decreased body protein and energy stores. PEM is common in patients with kidney disease, affecting up to 40-70% of those with end-stage renal disease. Factors contributing to PEM include poor nutritional intake, increased protein losses, and increased protein catabolism. A thorough nutritional assessment involves evaluating dietary intake, body composition, laboratory values, and scoring systems. Proper nutritional assessment and therapy are important for managing PEM and its negative effects in patients with kidney disease.
1. Protein energy wasting (PEW) is a state of nutritional and metabolic derangements in patients with chronic kidney disease characterized by loss of body protein and energy stores leading to loss of muscle and fat mass.
2. PEW is caused by hypercatabolic status, uremic toxins, malnutrition, inflammation, and is highly prevalent in hemodialysis patients where it is associated with adverse outcomes.
3. Mechanisms of PEW include activation of the ubiquitin-proteasome system, caspase-3, lysosomes and myostatin which can be initiated by complications of CKD like metabolic acidosis and inflammation.
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication in chronic kidney disease caused by reduced kidney function and mineral metabolism abnormalities. This leads to high phosphate, activation of parathyroid hormone, and bone abnormalities from renal osteodystrophy to vascular calcification. Treatment focuses on controlling phosphate levels through binders like sevelamer and cinacalcet to reduce parathyroid hormone in order to prevent bone disease and fractures while minimizing cardiovascular risks.
This document provides an overview of renal nutrition for non-renal dietitians. It discusses the basics of kidney function including measurement of glomerular filtration rate and stages of chronic kidney disease. Prevalence of CKD and end stage renal disease are noted. The roles and responsibilities of renal dietitians are outlined. Guidelines for protein and fluid intake at different stages of CKD are presented. Management of complications like potassium levels, edema and malnutrition are covered. A case study is provided to demonstrate application of renal nutrition principles.
Participants will be able to
Discuss the markers of malnutrition in CKD
Identify causes of malnutrition in CKD
Discuss current recommendations for treatment of malnutrition in CKD
This document discusses chronic kidney disease mineral and bone disorder (CKD-MBD). It begins by defining CKD-MBD and describing the pathogenesis involving abnormalities in calcium, phosphorus, PTH, and vitamin D metabolism. It then discusses the clinical features, investigations, and laboratory target levels. The final section covers treatment approaches including dietary phosphorus restriction, phosphate binders, vitamin D analogs, and calcimimetics to manage secondary hyperparathyroidism and hyperphosphatemia. It also addresses treating adynamic bone disease.
Dr. Ahmed Mohamed Albeyaly is a nephrology specialist and moderator in Dakahlia Health directorate. The document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD), which is a systemic disorder affecting bone disease, soft tissue calcification, and abnormalities in mineral metabolism that result from kidney disease and kidney failure. The document covers pathogenesis of CKD-MBD, classifications of bone disease seen in CKD patients, diagnosis through laboratory tests and imaging, and treatment approaches including controlling calcium, phosphorus, PTH, and vitamin D levels.
This document provides an overview of integrated renal care and the role of renal diet and nutritional counseling. It discusses the stages of chronic kidney disease and care processes. Key points include:
- Nutritional assessment and counseling are important parts of renal care provided by a renal dietitian.
- Diet must be individualized based on a patient's kidney disease stage, lab results, nutrition status and other factors.
- Diet focuses on managing calories, protein, carbohydrates, fat, sodium, fluids, phosphorus and other minerals.
- Malnutrition is common in kidney disease and dialysis, so nutritional monitoring and counseling are essential.
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.
1. Protein energy wasting (PEW) is a state of nutritional and metabolic derangements in patients with chronic kidney disease characterized by loss of body protein and energy stores leading to loss of muscle and fat mass.
2. PEW is caused by hypercatabolic status, uremic toxins, malnutrition, inflammation, and is highly prevalent in hemodialysis patients where it is associated with adverse outcomes.
3. Mechanisms of PEW include activation of the ubiquitin-proteasome system, caspase-3, lysosomes and myostatin which can be initiated by complications of CKD like metabolic acidosis and inflammation.
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication in chronic kidney disease caused by reduced kidney function and mineral metabolism abnormalities. This leads to high phosphate, activation of parathyroid hormone, and bone abnormalities from renal osteodystrophy to vascular calcification. Treatment focuses on controlling phosphate levels through binders like sevelamer and cinacalcet to reduce parathyroid hormone in order to prevent bone disease and fractures while minimizing cardiovascular risks.
This document provides an overview of renal nutrition for non-renal dietitians. It discusses the basics of kidney function including measurement of glomerular filtration rate and stages of chronic kidney disease. Prevalence of CKD and end stage renal disease are noted. The roles and responsibilities of renal dietitians are outlined. Guidelines for protein and fluid intake at different stages of CKD are presented. Management of complications like potassium levels, edema and malnutrition are covered. A case study is provided to demonstrate application of renal nutrition principles.
Participants will be able to
Discuss the markers of malnutrition in CKD
Identify causes of malnutrition in CKD
Discuss current recommendations for treatment of malnutrition in CKD
This document discusses chronic kidney disease mineral and bone disorder (CKD-MBD). It begins by defining CKD-MBD and describing the pathogenesis involving abnormalities in calcium, phosphorus, PTH, and vitamin D metabolism. It then discusses the clinical features, investigations, and laboratory target levels. The final section covers treatment approaches including dietary phosphorus restriction, phosphate binders, vitamin D analogs, and calcimimetics to manage secondary hyperparathyroidism and hyperphosphatemia. It also addresses treating adynamic bone disease.
Dr. Ahmed Mohamed Albeyaly is a nephrology specialist and moderator in Dakahlia Health directorate. The document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD), which is a systemic disorder affecting bone disease, soft tissue calcification, and abnormalities in mineral metabolism that result from kidney disease and kidney failure. The document covers pathogenesis of CKD-MBD, classifications of bone disease seen in CKD patients, diagnosis through laboratory tests and imaging, and treatment approaches including controlling calcium, phosphorus, PTH, and vitamin D levels.
This document provides an overview of integrated renal care and the role of renal diet and nutritional counseling. It discusses the stages of chronic kidney disease and care processes. Key points include:
- Nutritional assessment and counseling are important parts of renal care provided by a renal dietitian.
- Diet must be individualized based on a patient's kidney disease stage, lab results, nutrition status and other factors.
- Diet focuses on managing calories, protein, carbohydrates, fat, sodium, fluids, phosphorus and other minerals.
- Malnutrition is common in kidney disease and dialysis, so nutritional monitoring and counseling are essential.
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.
Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
This document discusses dietary guidelines for kidney health. It notes that kidneys play a key role in nutrient homeostasis and that loss of kidney function disrupts this. For chronic kidney disease (CKD) patients, guidelines recommend a daily protein intake of 0.6-0.8g/kg, limiting fat intake to 30% of calories, and restricting sodium and phosphorus intake. While protein restriction may slow CKD progression, large trials like MDRD found little overall benefit. A plant-based, low-protein diet that is low in phosphorus and sodium may be most suitable for CKD patients. Focusing on overall dietary patterns like the DASH diet may be more practical than individual nutrient restrictions.
This document summarizes medical nutrition therapy for chronic kidney disease and end-stage renal disease. It discusses the pathophysiology and stages of chronic kidney disease, complications that can arise at different levels of kidney function, and nutritional management strategies and guidelines for protein, fluid, electrolyte, and energy intake at various stages of kidney disease and on different types of dialysis.
Diabetic nephropathy is a chronic kidney disease characterized by gradually increasing urinary albumin excretion, high blood pressure, declining kidney function, and presence of diabetic retinopathy. It develops in 20-40% of people with diabetes and is the leading cause of end-stage renal disease. The pathophysiology involves metabolic and hemodynamic pathways as well as genetic factors. Hyperglycemia causes kidney damage through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and other mechanisms. Hemodynamic changes from hypertension increase glomerular pressure and permeability. Genetic factors like ACE polymorphisms also influence risk. Progression is associated with proteinuria, anemia
Nutrition of patients undergoing dialysisManiz Joshi
This document discusses nutritional assessment and dietary recommendations for dialysis patients. It outlines several methods for assessing nutritional status, including physical exams, body composition measurements, functional tests, and biochemical markers like serum albumin and prealbumin. Optimal intake levels are provided for proteins, sodium, fluids, potassium, phosphorus, and various vitamins. Maintaining adequate nutrition through diet and supplements is important for dialysis patients given losses during treatment and high risk of malnutrition.
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
The document discusses nutrition care for patients with chronic kidney disease (CKD) and those undergoing hemodialysis (HD). It outlines the stages of CKD based on glomerular filtration rate. The nutrition care process involves assessment, diagnosis, intervention, and monitoring. Key dietary recommendations for CKD and HD patients include restricting protein, sodium, and phosphorus while maintaining adequate energy, carbohydrates, and fat intake. Regular nutrition counseling and monitoring of nutritional status indicators are important for managing the disease and preventing complications.
This document provides information on chronic kidney disease (CKD) and its treatment with dialysis. It discusses the physiological functions of the kidneys, causes of CKD including diabetes, stages of CKD and associated signs/symptoms. It also describes different treatment options for stage 5 CKD including kidney transplantation and dialysis (hemodialysis and peritoneal dialysis). The document outlines components of Mrs. Joaquin's medical nutrition therapy and assesses her weight and calculates her edema-free weight.
This document provides information on medical nutrition therapy for a patient with end-stage renal disease undergoing hemodialysis. The patient has a GFR of 12 mL/min and receives hemodialysis twice a week. The goals of medical nutrition therapy are to prevent deficiencies, control fluid balance and electrolytes, and prevent complications related to calcium and phosphorus levels. The dietitian provides calculations to determine the patient's energy, protein, fluid and electrolyte needs and prescribes an appropriate diet.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/Ed5naxEDwnQ
Arabic Language version of this lecture is available at:
https://youtu.be/eYe0ORMdnaI
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/h3HRvWGUj5A
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
This document provides information on chronic kidney disease (CKD) diagnosis and management. It discusses common clinical features of CKD, which are often vague until late stages. It outlines the approach to investigating patients, including lab tests and imaging studies. Management focuses on slowing progression, treating complications, and timely planning for renal replacement therapy if needed. Goals include controlling risk factors like hypertension and diabetes, treating anemia, bone disease, and other issues. Dialysis criteria include refractory symptoms, complications, or glomerular filtration rate below 10 ml/min/1.73m2.
Renal anemia is common in patients with chronic kidney disease and end stage renal disease, and can lead to reduced quality of life and increased health risks. Anemia is typically diagnosed and managed according to guidelines when hemoglobin levels fall below 12.5 g/dL for men and 11 g/dL for women with CKD. The causes of anemia include insufficient erythropoietin production and iron deficiency. Treatment involves iron supplementation and administration of erythropoiesis-stimulating agents (ESAs) to increase hemoglobin levels. Close monitoring is required due to potential side effects of ESA therapy and risks of iron overload.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/Nl2xKEmvRWk
Arabic Language version of this lecture is available at:
https://youtu.be/K14fWBNdEco
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Diabetic kidney disease, also called diabetic nephropathy, is a type of chronic kidney disease caused by damage to the kidneys as a result of diabetes. Over time, high blood glucose levels associated with diabetes can damage the tiny filters in the kidneys called glomeruli. This can progressively reduce their ability to filter waste from the blood, potentially leading to kidney failure. Symptoms of diabetic kidney disease may include swelling, poor sleep or concentration, nausea or weakness. It can be diagnosed through urine and blood tests and managed through strict control of blood sugar and blood pressure levels.
This document discusses hypertension and kidney diseases. It begins with an outline covering topics like the definition, measurement, evaluation, and management of hypertension as well as its relation to other conditions. It then focuses on the relationship between kidney diseases and blood pressure. It discusses how high blood pressure can damage kidneys and be both a cause and effect of kidney disease. It covers prevalence of hypertension in chronic kidney disease (CKD) stages, pathogenesis, risk factors, and therapy goals. Cardiovascular disease is a primary cause of death in CKD patients due to factors like inflammation and mineral metabolism abnormalities. Goals for treating hypertension in CKD depend on level of proteinuria.
This document discusses diabetic nephropathy, which is kidney damage caused by diabetes. It begins with an introduction on the increasing prevalence of diabetes in India and how about 25-40% of diabetics develop end stage renal disease or chronic kidney disease. The natural history of kidney disease progression through 5 stages is described from early increased filtration to end stage requiring dialysis or transplant. Risk factors, screening methods, management including controlling blood glucose and blood pressure, and treatment options like dialysis and transplant are covered.
The patient is a 49-year-old woman with end-stage renal disease and diabetes who presented with altered mental status. She receives hemodialysis three times per week for a few years. Recently, she has been increasingly tired, weak, and unable to perform daily activities with poor appetite and nausea. On examination, she was pale and swollen with low hemoglobin. Tests found elevated creatinine, BUN, and electrolyte abnormalities. The most probable diagnosis is inadequate hemodialysis, as her symptoms and labs are consistent with worsening uremia due to insufficient solute clearance from her dialysis sessions. Kt/V is a measure of dialysis adequacy that accounts for urea clearance and patient
Nutritional management of renal diseasesWajid Rather
The document discusses the major roles of the kidney in metabolic regulation including water-electrolyte homeostasis, calcium-phosphate balance, waste product removal, acid-base balance, erythropoietin production, and blood pressure regulation. It then summarizes the goals of nutritional therapy in renal failure and discusses nutritional problems patients with renal failure often experience like anorexia and metabolic abnormalities. Guidelines for protein intake, energy intake, fluid intake, sodium intake, and potassium intake are provided for non-dialysis patients, patients undergoing hemodialysis, and patients undergoing peritoneal dialysis.
This document provides an overview of nutritional assessment. It discusses the goals of assessment as identifying malnutrition, obesity, and devising treatment plans. Assessment includes clinical history, physical exam, screening tools, anthropometrics, lab tests, and body composition analysis. Specific assessment measures are described in detail such as the subjective global assessment screening tool, body mass index, serum proteins, and creatinine tests. The document provides reference values and factors that influence various assessment markers.
This document discusses nutrition in surgical patients. It begins by outlining the goals of nutritional support, which include identifying patients at risk of malnutrition, preventing or reversing catabolism, and meeting energy requirements. It then covers topics like malnutrition, nutritional assessment tools, estimating energy needs, and administration of enteral and parenteral nutrition. The key points are that nutritional support should begin preoperatively for high-risk patients or if oral intake won't resume within 7 days post-op, and the enteral route is preferred over parenteral nutrition when possible.
Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
This document discusses dietary guidelines for kidney health. It notes that kidneys play a key role in nutrient homeostasis and that loss of kidney function disrupts this. For chronic kidney disease (CKD) patients, guidelines recommend a daily protein intake of 0.6-0.8g/kg, limiting fat intake to 30% of calories, and restricting sodium and phosphorus intake. While protein restriction may slow CKD progression, large trials like MDRD found little overall benefit. A plant-based, low-protein diet that is low in phosphorus and sodium may be most suitable for CKD patients. Focusing on overall dietary patterns like the DASH diet may be more practical than individual nutrient restrictions.
This document summarizes medical nutrition therapy for chronic kidney disease and end-stage renal disease. It discusses the pathophysiology and stages of chronic kidney disease, complications that can arise at different levels of kidney function, and nutritional management strategies and guidelines for protein, fluid, electrolyte, and energy intake at various stages of kidney disease and on different types of dialysis.
Diabetic nephropathy is a chronic kidney disease characterized by gradually increasing urinary albumin excretion, high blood pressure, declining kidney function, and presence of diabetic retinopathy. It develops in 20-40% of people with diabetes and is the leading cause of end-stage renal disease. The pathophysiology involves metabolic and hemodynamic pathways as well as genetic factors. Hyperglycemia causes kidney damage through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and other mechanisms. Hemodynamic changes from hypertension increase glomerular pressure and permeability. Genetic factors like ACE polymorphisms also influence risk. Progression is associated with proteinuria, anemia
Nutrition of patients undergoing dialysisManiz Joshi
This document discusses nutritional assessment and dietary recommendations for dialysis patients. It outlines several methods for assessing nutritional status, including physical exams, body composition measurements, functional tests, and biochemical markers like serum albumin and prealbumin. Optimal intake levels are provided for proteins, sodium, fluids, potassium, phosphorus, and various vitamins. Maintaining adequate nutrition through diet and supplements is important for dialysis patients given losses during treatment and high risk of malnutrition.
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
The document discusses nutrition care for patients with chronic kidney disease (CKD) and those undergoing hemodialysis (HD). It outlines the stages of CKD based on glomerular filtration rate. The nutrition care process involves assessment, diagnosis, intervention, and monitoring. Key dietary recommendations for CKD and HD patients include restricting protein, sodium, and phosphorus while maintaining adequate energy, carbohydrates, and fat intake. Regular nutrition counseling and monitoring of nutritional status indicators are important for managing the disease and preventing complications.
This document provides information on chronic kidney disease (CKD) and its treatment with dialysis. It discusses the physiological functions of the kidneys, causes of CKD including diabetes, stages of CKD and associated signs/symptoms. It also describes different treatment options for stage 5 CKD including kidney transplantation and dialysis (hemodialysis and peritoneal dialysis). The document outlines components of Mrs. Joaquin's medical nutrition therapy and assesses her weight and calculates her edema-free weight.
This document provides information on medical nutrition therapy for a patient with end-stage renal disease undergoing hemodialysis. The patient has a GFR of 12 mL/min and receives hemodialysis twice a week. The goals of medical nutrition therapy are to prevent deficiencies, control fluid balance and electrolytes, and prevent complications related to calcium and phosphorus levels. The dietitian provides calculations to determine the patient's energy, protein, fluid and electrolyte needs and prescribes an appropriate diet.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/Ed5naxEDwnQ
Arabic Language version of this lecture is available at:
https://youtu.be/eYe0ORMdnaI
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/h3HRvWGUj5A
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
This document provides information on chronic kidney disease (CKD) diagnosis and management. It discusses common clinical features of CKD, which are often vague until late stages. It outlines the approach to investigating patients, including lab tests and imaging studies. Management focuses on slowing progression, treating complications, and timely planning for renal replacement therapy if needed. Goals include controlling risk factors like hypertension and diabetes, treating anemia, bone disease, and other issues. Dialysis criteria include refractory symptoms, complications, or glomerular filtration rate below 10 ml/min/1.73m2.
Renal anemia is common in patients with chronic kidney disease and end stage renal disease, and can lead to reduced quality of life and increased health risks. Anemia is typically diagnosed and managed according to guidelines when hemoglobin levels fall below 12.5 g/dL for men and 11 g/dL for women with CKD. The causes of anemia include insufficient erythropoietin production and iron deficiency. Treatment involves iron supplementation and administration of erythropoiesis-stimulating agents (ESAs) to increase hemoglobin levels. Close monitoring is required due to potential side effects of ESA therapy and risks of iron overload.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/Nl2xKEmvRWk
Arabic Language version of this lecture is available at:
https://youtu.be/K14fWBNdEco
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Diabetic kidney disease, also called diabetic nephropathy, is a type of chronic kidney disease caused by damage to the kidneys as a result of diabetes. Over time, high blood glucose levels associated with diabetes can damage the tiny filters in the kidneys called glomeruli. This can progressively reduce their ability to filter waste from the blood, potentially leading to kidney failure. Symptoms of diabetic kidney disease may include swelling, poor sleep or concentration, nausea or weakness. It can be diagnosed through urine and blood tests and managed through strict control of blood sugar and blood pressure levels.
This document discusses hypertension and kidney diseases. It begins with an outline covering topics like the definition, measurement, evaluation, and management of hypertension as well as its relation to other conditions. It then focuses on the relationship between kidney diseases and blood pressure. It discusses how high blood pressure can damage kidneys and be both a cause and effect of kidney disease. It covers prevalence of hypertension in chronic kidney disease (CKD) stages, pathogenesis, risk factors, and therapy goals. Cardiovascular disease is a primary cause of death in CKD patients due to factors like inflammation and mineral metabolism abnormalities. Goals for treating hypertension in CKD depend on level of proteinuria.
This document discusses diabetic nephropathy, which is kidney damage caused by diabetes. It begins with an introduction on the increasing prevalence of diabetes in India and how about 25-40% of diabetics develop end stage renal disease or chronic kidney disease. The natural history of kidney disease progression through 5 stages is described from early increased filtration to end stage requiring dialysis or transplant. Risk factors, screening methods, management including controlling blood glucose and blood pressure, and treatment options like dialysis and transplant are covered.
The patient is a 49-year-old woman with end-stage renal disease and diabetes who presented with altered mental status. She receives hemodialysis three times per week for a few years. Recently, she has been increasingly tired, weak, and unable to perform daily activities with poor appetite and nausea. On examination, she was pale and swollen with low hemoglobin. Tests found elevated creatinine, BUN, and electrolyte abnormalities. The most probable diagnosis is inadequate hemodialysis, as her symptoms and labs are consistent with worsening uremia due to insufficient solute clearance from her dialysis sessions. Kt/V is a measure of dialysis adequacy that accounts for urea clearance and patient
Nutritional management of renal diseasesWajid Rather
The document discusses the major roles of the kidney in metabolic regulation including water-electrolyte homeostasis, calcium-phosphate balance, waste product removal, acid-base balance, erythropoietin production, and blood pressure regulation. It then summarizes the goals of nutritional therapy in renal failure and discusses nutritional problems patients with renal failure often experience like anorexia and metabolic abnormalities. Guidelines for protein intake, energy intake, fluid intake, sodium intake, and potassium intake are provided for non-dialysis patients, patients undergoing hemodialysis, and patients undergoing peritoneal dialysis.
This document provides an overview of nutritional assessment. It discusses the goals of assessment as identifying malnutrition, obesity, and devising treatment plans. Assessment includes clinical history, physical exam, screening tools, anthropometrics, lab tests, and body composition analysis. Specific assessment measures are described in detail such as the subjective global assessment screening tool, body mass index, serum proteins, and creatinine tests. The document provides reference values and factors that influence various assessment markers.
This document discusses nutrition in surgical patients. It begins by outlining the goals of nutritional support, which include identifying patients at risk of malnutrition, preventing or reversing catabolism, and meeting energy requirements. It then covers topics like malnutrition, nutritional assessment tools, estimating energy needs, and administration of enteral and parenteral nutrition. The key points are that nutritional support should begin preoperatively for high-risk patients or if oral intake won't resume within 7 days post-op, and the enteral route is preferred over parenteral nutrition when possible.
This document discusses nutrition in critical care patients. It recommends that critically ill patients who are at high nutritional risk based on a NUTRIC or NRS 2002 score of 5 or higher should receive specialized nutrition support, preferably through enteral feeding. Enteral feeding is preferred over parenteral nutrition when possible. The goals of nutrition support are to provide 1.2-2.0 g/kg/day of protein and aim for 25 kcal/kg/day of calories. Achieving adequate protein provision may improve outcomes over providing only trophic or permissive underfeeding. Monitoring of nutrition support is important to help meet goals and avoid overfeeding complications.
1. For Case 1 (COPD patient with BMI 25 and no weight loss), the nutritional program will focus on oral diet and nutrition education with oral nutritional supplements twice daily if needed.
2. For Case 2 (COPD patient with pneumonia, BMI 17, and fever), the program will provide enteral nutrition via a nasogastric tube at 20-25 kcal/day initially, increasing as tolerated. Micronutrients including antioxidants and vitamins will be supplemented.
3. For Case 3 (mechanically ventilated COPD patient in shock), the program will start enteral nutrition within 24-48 hours at a rate of 25-30 kcal/day, increasing as tolerated. The formula will
This document discusses nutrition and protein-energy wasting in patients undergoing hemodialysis. It outlines that patients on dialysis are often depleted of protein and energy stores due to deficient nutrition or protein/energy wasting. The terminology "protein-energy wasting syndrome" describes the loss of body protein and fuel reserves in patients with end-stage kidney disease. Assessment of nutritional status includes dietary assessment of appetite and weight changes, physical assessment of weight and BMI trends, and laboratory assessment including serum albumin and BUN levels. Causes of protein-energy wasting include decreased intake, hypercatabolism, and factors related to dialysis. Dietary recommendations aim to provide at least 1.2 g/kg of protein and 30-35 k
Nutrition is important for surgical patients. Malnutrition can compound complications, while well-nourished patients tolerate surgery better. Several factors are used to assess a patient's nutritional status prior to surgery, including weight loss, serum albumin levels, and medical history. For patients who cannot eat adequately after surgery, enteral or parenteral nutrition may be needed to meet nutrient demands and support healing. Enteral nutrition involves feeding through a stomach or intestinal tube, while parenteral nutrition is administered intravenously.
Nutrition is essential for surgery patients as surgical procedures and fasting can quickly lead to malnutrition. Patients with severe protein depletion are more likely to experience postoperative complications like pneumonia and infection. Nutritional status should be assessed through history, diet assessment, physical exam, and lab tests. Malnutrition is caused by reduced food intake, malabsorption, altered metabolism, and more. Nutritional requirements vary but are generally 25-30 calories/kg/day and 1.5-2 grams of protein/kg/day. Nutrition can be provided enterally through tubes or parenterally through IVs. Enteral nutrition is preferred over parenteral when possible.
Daily minimum nutritional requirements of the critically illRalekeOkoye
The document discusses the daily minimum nutritional needs of critically ill patients. It defines key terms like critically ill patient and malnutrition. It describes the nutritional changes, assessment of nutritional state, and predictors of outcome during critical illness. It provides guidelines for calculating nutritional requirements including carbohydrates, proteins, fats, vitamins, and minerals. It discusses enteral nutrition as the preferred route of administration when possible, and provides guidelines for safe enteral feeding including early initiation and proper tube positioning.
Importance of nutritional management during hospitalizationBushra Tariq
The document discusses the importance of nutritional management for hospitalized patients. It notes that up to 50% of hospitalized patients experience some degree of malnutrition. Providing adequate nutrition support through enteral or parenteral nutrition can improve patient outcomes, reduce recovery time, and lower healthcare costs. The document provides guidelines for estimating caloric and protein needs for critically ill patients and recommends early enteral nutrition within 24-48 hours when possible to support gut health and integrity.
The document discusses the management of obesity through various means. It begins by defining obesity and assessing severity using body mass index (BMI) measurements. It then covers the etiology of obesity through factors like macronutrient properties, metabolism, hormones, and genetics. Various medical problems associated with obesity are outlined. Treatment options discussed include lifestyle changes, medications, and bariatric surgery. Criteria for surgical treatment and important preoperative preparations are also summarized.
The document discusses the management of obesity through various means. It begins by defining obesity and assessing severity using body mass index (BMI) measurements. It then covers the etiology of obesity through factors like macronutrient properties, energy expenditure, hormones, and genetic predispositions. Various medical problems associated with obesity are outlined. Treatment options discussed include lifestyle changes, medications, and bariatric surgery. Surgical criteria and extensive preoperative preparation procedures are also described.
The document discusses the management of obesity through various means including assessing severity, etiology, medical problems associated with obesity, medical management, guidelines for treatment, and surgical management. It provides details on criteria for surgical treatment, preoperative preparation, and types of bariatric surgeries.
The document discusses the management of obesity through assessing severity, etiology, and medical problems associated with obesity. It defines body mass index (BMI) categories and notes BMI, waist circumference, and waist-to-hip ratio can identify patients at risk. Factors like genetics, metabolism, hormones like leptin and ghrelin, and lifestyle influence energy balance and obesity development. Medical issues linked to obesity include various cancers, cardiovascular and metabolic diseases, and osteoarthritis.
Protien Energy Malnutrition and Obesity.pdfRahulKishor4
Protein-energy malnutrition (PEM) and obesity are both types of malnutrition that result from imbalances in nutrient intake and energy expenditure. PEM specifically refers to deficiencies in protein and calories over long periods and can manifest as kwashiorkor or marasmus. Obesity is defined as abnormal or excessive fat accumulation that presents health risks. Groups vulnerable to PEM include children, pregnant/lactating women, older adults, and those with chronic illnesses. PEM is diagnosed based on growth monitoring, dietary history, and anthropometric measurements. Prevention focuses on nutrition education, supplementation, and treating infections early. Risk factors for obesity include age, genetics, physical inactivity, diet, and socioeconomic status. Obesity is assessed using body mass index
This document discusses malnutrition in older patients. It begins by outlining ACOVE quality indicators for malnutrition, which provide standards of care for screening, assessing, and treating malnutrition in community-dwelling and hospitalized older adults. It then reviews how physiological changes in aging can increase risk of malnutrition due to changes in body composition, metabolism and organ function. Finally, it identifies common risk factors for malnutrition in older patients and drugs that can contribute to malnutrition by reducing appetite or interfering with nutrient absorption.
This document provides guidelines on nutrition in the intensive care unit (ICU). It defines patients at risk of malnutrition in the ICU, how to assess nutritional status, determine energy needs, choose feeding routes, and adapt nutrition based on clinical conditions. It discusses initiating and progressing nutrition administration, determining macronutrient needs, and paying special attention to glutamine and omega-3 fatty acids. The guidelines also address nutrition for patients with conditions like dysphagia, trauma, surgery, sepsis, and obesity that are common in the ICU.
Basic Intravenous Therapy 4: Total Parenteral NutritionRonald Magbitang
Lecture Presentation in Basic Intravenous Therapy Seminar regards anothe type of IV fluid the TPN, nutrition in this regard given intravenously, how to go about, the considerations and precautions in giving TPN
Similar to Protein energy malnutrition in CKD (20)
This document discusses immune mediated glomerulonephritis (lupus nephritis). It covers the pathophysiology, novel biomarkers for lupus nephritis, a retrospective study from 1993-2010, treatment approaches for different classes of lupus nephritis including induction and maintenance therapies, class V pure lupus nephritis, lupus nephritis in pregnancy, and monitoring of patients.
Magnesium plays an important role in cardiovascular health and its levels are often disrupted in chronic kidney disease patients. Magnesium helps regulate blood pressure and vascular tone and deficiency can lead to vascular calcification. Managing magnesium levels is important for reducing cardiovascular risks in those with impaired kidney function.
This document discusses asymptomatic hyperuricemia and whether or not it should be treated. It covers the physiology of uric acid production and excretion by the kidneys. While acute hyperuricemia nephropathy, uric acid nephrolithiasis, and hyperuricemia after renal transplantation are clear reasons to treat, the evidence for treating asymptomatic hyperuricemia to prevent chronic gouty nephropathy, cardiovascular issues, insulin resistance, hypertension, and inflammation is unclear. Treatment may be warranted if uric acid levels are very high (≥ 8) or if the patient is symptomatic, but otherwise the decision to treat asymptomatic hyperuricemia remains uncertain based on current evidence.
This document discusses dialytic support for patients with acute kidney injury (AKI). It begins by outlining classifications and definitions of AKI severity. It then addresses many open questions regarding renal replacement therapy (RRT) for AKI, such as when to start, what modality to use, and when to stop. The document reviews various RRT modalities and considerations for their use. It provides guidelines on determining when to initiate RRT based on lab values and clinical criteria. Overall, the document aims to help clinicians navigate the many decisions that must be made in providing RRT for AKI patients.
Kidney transplantation has evolved significantly since the first attempts in the 1930s. Live donor kidney transplantation provides advantages over deceased donor transplants including better outcomes. A comprehensive evaluation of potential live kidney donors is essential and includes medical, surgical, immunological, and psychosocial assessments. Careful evaluation aims to minimize risks to donor health while maximizing the benefits of transplantation for recipients. Ongoing research continues to further develop and improve the live donor evaluation and transplantation process.
This document provides an overview and discussion of vascular calcification. It begins with an introduction stating that vascular calcification is highly correlated with cardiovascular morbidity and mortality in patients with chronic kidney disease. It then outlines the agenda and provides definitions of the two main types of vascular calcification. Subsequent sections discuss the mechanisms of vascular calcification including ectopic osteogenesis and elastin degradation. Factors involved and inducers of vascular calcification such as calcium/phosphate levels, uremic toxins, and oxidative stress are described. The document concludes by examining several endogenous calcification inhibitors and their therapeutic potential, such as fetuin-A, osteopontin, and magnesium.
1) Coronary artery calcification is significant and progressive in a majority of patients with early chronic kidney disease. There is an association between arterial calcification and increased risk of all-cause mortality in chronic kidney disease patients on dialysis.
2) While the data are not entirely consistent, some studies have found relatively less progression of vascular calcification with sevelamer versus calcium-containing phosphate binders among patients with chronic kidney disease.
3) One randomized controlled trial found that among hemodialysis patients treated with either calcium acetate or sevelamer for 1 year, there was similar progression of coronary artery calcification with intensive lowering of LDL-C levels in both groups.
This document discusses dysglycemia and chronic kidney disease (CKD). It begins with an agenda that covers background, pathophysiology, glycemic control, and insulin therapy and conclusions. It then discusses how diabetes is the most common cause of end-stage renal disease. It explains how dysglycemia includes sustained hyperglycemia and acute glucose fluctuations. The kidney plays an important role in glucose homeostasis by filtering, reabsorbing, and producing glucose. Both hyperglycemia and glucose variability can drive diabetic kidney disease through various pathways like protein kinase C activation and oxidative stress. Maintaining good glycemic control through lowering HbA1c can significantly reduce microvascular and cardiovascular complications in patients with CKD.
Diabetic nephropathy is a major complication of diabetes that can progress to kidney failure. The document discusses the pathophysiology, risk factors, stages of progression, biomarkers and pathology of diabetic nephropathy. Key factors that contribute to its development include genetic susceptibility, hypertension, activation of the renin-angiotensin-aldosterone system, increased levels of growth factors like TGF-β, and chronic high blood glucose levels which can activate biochemical pathways like protein kinase C. Left untreated, diabetic nephropathy can progress through five stages and ultimately lead to end-stage renal disease.
AKI is a common problem in ICU patients, occurring in up to 18% of hospitalized patients with normal kidney function. Risk factors include conditions that reduce blood flow to the kidneys like sepsis or hypotension. The kidneys are vulnerable to toxins and drugs due to their high blood flow and the tubules' role in reabsorbing and secreting materials. Early detection of AKI using markers like serum creatinine and urine output is important for management, which aims to treat the underlying cause, ensure proper fluid balance and nutrition, and consider renal replacement therapy for severe cases.
AKI is a common problem in ICU patients, occurring in up to 18% of hospitalized patients with normal kidney function. Risk factors for developing AKI include those that expose the kidneys to toxins and drugs like high blood flow and reabsorption. The kidneys have high energy demands and reabsorb water, increasing toxin concentration, putting them at risk. AKI is detected using rises in creatinine and decreases in urine output, though new markers are being studied. Management involves treating underlying causes, fluid management, and potentially renal replacement therapy, which has a high mortality of up to 70% in severe cases requiring it.
1. Hemodialysis can have acute complications such as hypotension, muscle cramps, headaches, nausea and vomiting, and dialysis disequilibrium syndrome.
2. Hypotension during hemodialysis can be caused by plasma volume contraction and is treated with normal saline or D10%.
3. Muscle cramps are also common and usually involve the lower extremities, occurring near the end of treatments. High serum CPK is a frequent finding.
Hemodialysis is a process that uses a semi-permeable membrane to remove waste and excess fluid from the blood of patients with kidney failure. It requires anticoagulation to prevent clotting and knowledge of what substances need to be removed from the blood. Early experiments with dialysis date back to the 18th century, but the first successful hemodialysis treatment in a human was performed by Nils Alwall in 1937 using the Alwall Kidney. Modern hemodialysis utilizes synthetic high or low flux membranes and a dialysate solution to clear waste from the blood through diffusion, convection, osmosis and ultrafiltration. Indications for initiating hemodialysis include symptoms of u
This document discusses various pulmonary-renal syndromes, including Wegener's granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome, Goodpasture's syndrome, lupus nephritis, uremic lung, post-infectious glomerulonephritis, hemolytic uremic syndrome, cryoglobulinemia, and IgA nephropathy. It provides details on the pathologies, presentations, diagnostic criteria, treatments, and prognoses for each condition. The key takeaway is that pulmonary-renal syndromes can be fatal if bleeding is occurring from both the lungs and kidneys, so aggressive treatment in the ICU is needed in such cases.
The document discusses several myths and realities regarding systemic lupus erythematosus (SLE). It notes that while early deaths were once caused by active SLE, later deaths are now primarily due to cardiovascular disease. It also clarifies that fatigue and pain are often due to other conditions like fibromyalgia rather than active SLE. Additionally, the document states that ANA-negative lupus can still exist and SLE can develop after age 50, contradicting common misconceptions.
The document discusses various known and unknown uremic toxins that accumulate in patients with chronic kidney disease. It describes small water-soluble compounds like urea, guanidines, oxalate, phosphorus, and metabolic acids. It also covers protein-bound compounds such as p-cresol, homocysteine, and discusses how their removal during dialysis is hampered due to strong protein binding. The document provides details on the effects of these uremic toxins and potential strategies to enhance their removal or reduce their levels.
This document discusses ethical considerations and guidelines around initiating or withdrawing dialysis for patients with end-stage renal disease (ESRD). It outlines common principles of ethical decision making including beneficence, non-maleficence, patient autonomy, and justice. Features unique to ESRD patients include the chronicity of artificial survival methods, complexity of their conditions, and long-term burdens of treatment. The document also presents a case study and recommendations from the National Kidney Foundation around dialysis decisions based on patient values and medical usefulness of treatment.
This document discusses the effects of chronic kidney disease (CKD) on the endocrine system and vice versa. It notes that CKD can cause abnormalities in the hypothalamic-pituitary-gonadal axis, leading to issues like erectile dysfunction, low libido and infertility in men. It also disrupts thyroid and growth hormone function. Insulin resistance is common in CKD due to impaired tissue sensitivity. The adrenal glands may have altered cortisol metabolism. Conversely, conditions like acromegaly and hyperparathyroidism can damage the kidneys structurally and impair renal function. The kidneys also have endocrine functions, producing hormones like renin, erythropoietin and activating vitamin
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Top Effective Soaps for Fungal Skin Infections in India
Protein energy malnutrition in CKD
1.
2. Protein Energy Malnutrition
(PEM),
Protein-Energy Wasting
(PEW)
Kidney Disease Wasting
(KDW),
Kidney Disease-Related PEM
By
Mabrouk Ramadan Al-Sheikh
Prof. of nephrology and Internal Medicine
Faculty of Medicine
Tanta University
4. Eat right to feel and live right
Do not starve your patient
Let the food be the medicine and not let the
medicine be the food. “Hippocrates”
نعيش ال ،لنعيش نأكل نحنلنأكل
7. The International Society of Renal Nutrition
and Metabolism (ISRNM) expert panel
defined PEM (2012):
“state of decreased body stores of protein
and energy fuels i.e. body protein and fat
masses”
Definition
8. Definition
Component of PEM are
1. Clinical manifestations: unintentional poor
nutritional intake, unintentional BW loss,
depleted energy (fat tissues) stores, and loss
of somatic protein (low muscle mass).
2. Laboratory investigations: low level of
visceral protein; s. albumin, prealbumin and
transferrin and others.
3. Abnormal anthropometric measurements.
11. Prevalence
Depending in part upon the method used and the
population studied, up to 40 to 70 % of patients with
end-stage renal disease are malnourished.
17. Factors contributing to malnutrition
Malnutrition can be secondary to :
1- Poor nutritional intake:
Overzealous dietary restrictions.
Delayed gastric emptying and diarrhea.
Intercurrent illness .
Hospitalization.
Other medical cormorbidities.
18. Factors contributing to malnutrition
Malnutrition can be secondary to :
1- Poor nutritional intake
Medication causing dyspepsia e.g. phos. binders, iron therapy .
Suppression of oral intake by PD load.
Inadequate dialysis
Decreased food intake on HD days
Monetary restriction
Depression
Altered taste sensation
19. 2- Increased protein losses
Gastrointestinal blood loss:
“100ml blood = 14-17g protein.”
Intradialysis nitrogen loss:
“ HD : 6-8 g amino acid/ procedure”
“PD : 8-12 g protein/day”
Factors contributing to malnutrition
20. 3- Increased protein catabolism
Intercurrent illness and hospitalizations.
Metabolic acidosis.
Catabolism associated with HD
Catabolic effects of hormones “cortisol,
PTH, glucagon”
Dysfunction of GH and IGF endocrine axis.
Factors contributing to malnutrition
21. Squeals of PEM
Malaise, fatigue, poor rehabilitation
Increase susceptibility to infection.
Impaired wound healing.
Increase hospitalization rate.
Increase morbidity and mortality rate.
23. ASSESSMENT OF NUTRITIONAL STATUS
No single gold standard measurement.
Therefore, a panel of measurements is
recommended and including:
1. Assessment of dietary nutritional intake
2. Assessment of body composition.
3. Laboratory values
4. Scoring
24.
25. ASSESSMENT OF NUTRITIONAL STATUS
No single gold standard measurement.
Therefore, a panel of measurements is
recommended and including:
1. Assessment of dietary nutritional intake
2. Assessment of body composition.
3. Laboratory values
4. Scoring
26. I-Nutritional Intake
A- Patient’s interview
• Often provides important clue to patients who
might be malnurished
• Symptoms: nausea, vomiting, anorexia, fatigue,
weight loss or gain
• Pharmacological therapy: steroid therapy, iron
therapy and phos. binder
• Co-morbidity and non uremic diseases e.g. DM,
alcoholism, GI diseases.
• Psychological issues.
27. I-Nutritional Intake
Physical Examination
Should include anthropometry
The patient's actual BW is estimated and should be
compared to the recommended “dry or peer” body
weight.
The percentile change (if any) of the "dry weight"
should also be assessed approximately every month.
28. I-Nutritional Intake
B- Assessment of food intake
• Food questionnaire: the 24 h recall helps the patients to
remember food intake in the previous day and to
quantate it.
• Food record: quantitative and qualitative data on food
intake collected for an average 3 days including 2 two
week day and one week end day (3 days should include
dialysis and non-dialysis day).
• A food diary is very useful, especially if the patient
weighs the portions of food. The intake of protein, fat
and carbohydrate can then be calculated from standard
food tables.
29. I-Nutritional Intake
B- Assessment of food intake:
The semi-quantitative food–frequency questionnaire
(SFFQ): is used to assess the frequency of
consumption of food items and groups during a
specific reference time period, which may or may not
be the period the patient actually bases his(her)
recalls on.
30. I-Nutritional Intake
C-Protein equivalent of total nitrogen
appearance (PNA) & nPNA
Calculating the protein catabolic rate (PCR)
is a good indirect index for dietary
protein intake, expressed g/day.
KDOQI guidelines prefers the name:
protein equivalent of total nitrogen
appearance (PNA), expressed g/day.
Normalized nPNA ,expressed g/Kg/day.
31. I-Nutritional Intake
C-Protein equivalent of total nitrogen
appearance (PNA) & nPNA
Determination of nPNA: Calculated by
Formula Computer Program
Target level =1.0-1.2 g/Kg/day.
Best survival rate at level= 1.0-1.4 g/Kg/day.
An increased overall mortality rate at level
<0.8 or>1.4 g/Kg/day.
32. Interpretation of nPNA
Observation Interpretation Consideration
nPNA exceeds DPI
or is unexpectedly
high
Only tentative
conclusions about
protein intake possible
Catabolic state:
-Inadequate energy intake
-Presence of inflammation or inflammatory
stressors (fever, infection)
-Weight loss
- Metabolic acidosis
-Bioincompatible dialysis membrane.
Inaccurate diet record
Low lean body mass
nPNA less than
DPI or is
unexpectedly low
Only tentative
conclusions about
protein intake possible
Anabolic state:
-Corticosteroid use
- Recovery from infection or illness
- Pregnancy or growth
Inaccurate diet record
Edema or excess body weight
nPNA=DPI nPNA reflects protein
intake
Conclude patient is in nitrogen balance and
nPNA reflects intake if none of the above
apply
33. ASSESSMENT OF NUTRITIONAL STATUS
No single gold standard measurement.
Therefore, a panel of measurements is
recommended and including:
1. Assessment of dietary nutritional intake
2. Assessment of body composition.
3. Laboratory values
4. Scoring
34. II- Body composition
1- Body weight-based measures: BMI, weight for
height, edema-free BW, fat-free BW.
2- Skin and muscle anthropometry:
caliper, skin fold, extremity muscle mass.
3- Total body elements: total body potassium.
4- Energy-beam-based methods: total body N2,
DEXA, BIA, NIR.
5- Other method: underwater weighting.
35. A-BMI
The international classification of adult underweight, overweight and obesity
according to BMI
Classification BMI (kg/m2)
Underweight < 18.5
Severe thinness < 16
Moderate thinness 16-16.99
Mild thinness 17-18.49
Normal average 18.5-24.99
Overweight ≥ 25
Pre-obese 25-29.99
Obese ≥ 30
Obese class I 30-34.99
Obese class II 35-39.99
Obese class III ≥ 40
36. B-Anthropometry
Aim: to compare peer (ideal or average) BW to
the actual BW (special tables).
Anthropometry is practical, simple, rapid,
non-invasive, non-expensive and reproducible
technique for evaluating body fat and muscle
mass.
It can be easily done by dietitian.
37. B-Anthropometry
K/DOQI guidelines :
The anthropometric measurement that are valid for
assessing nutritional status:
1. For body fat : triceps (or biceps) skin fold(TSF) .
2. For muscle mass : mid arm muscle circumference
(MAMC) &mid arm circumference (MAC).
3. For obesity : BMI
4. % of usual body weight (UBW) and % of standard
body weight (SBW).
This measures should be taken immediately post-dialysis
at right side of the body; best carried out by the same
observer
38. As a general rule, the percentile values/normal
limitation to the use of anthropometry is that serial
measurements are best carried out by the same
observer
adequate nutritionValues >95 %
risk of malnutritionvalues 75 % and 95 %
significant
malnutrition
values <75 %
39. More sophisticated measures of body composition
include :
Bioelectric impedance analysis (BIA)
Dual-energy x-ray absorptiometry (DEXA)
A major drawback of these techniques is the
difficulty in distinguishing between fat mass and body
water.
40. At present, anthropometry is the only
method that can be readily performed in most
units.
BIA or DEXA should be reserved for selected
patients.
41. ASSESSMENT OF NUTRITIONAL STATUS
No single gold standard measurement.
Therefore, a panel of measurements is
recommended and including:
1. Assessment of dietary nutritional intake
2. Assessment of body composition.
3. Laboratory values
4. Scoring
42. III-Laboratory evaluation
1. Visceral protein: negative acute phase reactants;
albumin, prealbumin, transferrin and amino
acids.
2. Lipids: chlosterol, TG and other lipids.
3. Somatic protein and nitrogen surrogates: BUN
and serum creatinine.
4. Growth factors: IGF-1 and liptin.
5. Peripheral CBC, lymphocyts.
6. Others.
45. I-Plasma protein measurements
Serum Albumin
Clinical practice guidelines for nutrition were
published by a working group for the NKF/DOQI
recommended that the serum albumin
concentration (obtained either predialysis or
when stable) should be measured monthly.
46. I-Plasma protein measurements
Serum Albumin
Impact of Low serum albumin level:
It is strong predictor of mortality and
hospitalization; risk rises dramatically and
logarithmically as levels decline below 4.0
g/dL.
It has been shown to predict coronary
calcification.
47.
48. I-Plasma protein measurements
Serum transferrin:
Serum transferrin is not good indicator of nutritional
status; perhaps due to fluctuations in iron stores,
presence of inflammation and changes in volume
status.
49. I-Plasma protein measurements
Prealbumin
The plasma concentration of prealbumin (has a
shorter half-life than albumin) provides a consistent
assessment of visceral protein and can be used to
assess the response to nutritional interventions
begun for presumed malnutrition as it.
This protein is normally excreted and metabolized by
the kidney and tends to accumulate in renal failure.
51. I-Plasma protein measurements
Amino acids
There is a variable plasma amino acid pattern
in ESRD.
In general, the levels of the essential and
branched chain AA are decreased, while the
nonessential AA are either within the normal
range or increased.
52. III-Laboratory evaluation
II-Plasma cholesterol concentration
The plasma cholesterol concentration is reduced
in malnourished patients with normal renal
function.
Cholesterol levels are also lower in patients with
ESRDs. In this setting, there is an inverse
relationship between mortality and the
cholesterol concentration.
53. III-Laboratory evaluation
III-Blood urea nitrogen
Reflects the balance between urea generation and
removal
Malnourished patients often show a gradual reduction in
BUN and become wasted.
Low levels commonly seen in dialyzed patients (well
dialyzed or inadequately dialyzed) with poor nutrition.
Low predialysis BUN levels have also been associated
with increased mortality.
It is for this reason, protein catabolic rate is monitored in
dialysis patients, since this parameter can estimate
protein intake in the stable patient.
54. III-Laboratory evaluation
IV-Creatinine production
Since creatinine is produced from
nonenzymatic creatine metabolism in skeletal
muscle, estimating the rate of creatinine
production has been used to assess lean body
mass in stable patients.
Estimated lean body mass was below normal
in 47 and 66 % of hemodialysis and peritoneal
dialysis patients, a presumed reflection of
inadequate nutrition.
55. III-Laboratory evaluation
V- C-Reactive protein
A positive acute phase reactant protein.
It correlates negatively with visceral protein
concentration.
Help to uncover potential covert
inflammation especially if serum level of
albumin or prealbumin is low.
56. ASSESSMENT OF NUTRITIONAL STATUS
No gold standard measurement.
Therefore, a panel of measurements is
recommended and including:
1. Assessment of dietary nutritional intake
2. Assessment of body composition.
3. Laboratory values
4. Scoring
57. Subjective global assessment (SGA)
• Conventional SGA is a simple method depends
on the experience of clinician to make an
overall evaluation of nutritional status.
• Advantages: includes objective data and
several manifestations of poor nutritional
status.
• Limitation: heavy reliance on the clinical
judgment and the inability to tailor a specific
nutritional therapy.
58. Subjective global assessment (SGA)
This is a clinical method for evaluation of
nutritional status; including:-
A- History and symptoms:
1- % of weight loss in the last 6 months
2- Dietary nutrient intake
3- Presence of anorexia, nausea, vomiting, diarrhea
or abdominal pain
4- Functional capacity
5- Metabolic demands in the view of activity
59. Subjective global assessment (SGA)
B-Physical parameters focus on:
• Assessment of subcutanous fat.
• Assessment of muscle wasting in the temporal
area, deltoid and quadriceps.
• Presence of sacral or ankle odema.
• Presence of ascites.
63. Indices of malnutrition in HD patients
1. S. albumin concentration < 4.0 gm/dl.
2. Low s.prealbumin concentration (<30 mg/ dl)
3. Low b. urea & s. creatinine level in patients
with residual renal function.
4. PCR < 0.8gm/Kg/day.
5. Chol. concentration<150mg/dl(3.9mmol/L).
6. Transferrin <150 mg/dl.
64. Indices of malnutrition in HD patients
7. IGF-1 concentration < 300 µg/L.
8. Low predialysis serum K (and possibly
phosphororus) concentration.
9. Marked reduction in anthropometric
measurement
10. Continuous decline in estimated dry weight.
11. BW < 80% of ideal weight.
65.
66. Agenda
• Definition
• Factors contributing to malnutrition
• Disorders of nutrient metabolism in CKD
• Nutritional assessment
• Nutritional therapy
• Conclusion and Recommendations
67. Nutritional therapy
Why malnutrition should be corrected?
Many studies documented that poor
nutritional status increases the morbidity and
mortality CKD patients.
Specifically; low s. creatinine ,albumin
concentration and % of ideal dry BW at time
of initiation of maintenance dialysis are
associated with increased risk of morbidity
and mortality during sub sequent years of HD.
68. Why malnutrition should be corrected?
PEM is one of the strongest predictors of
mortality and morbidity and is the third of the
killing triad in CKD and HD patients
1.CV accidents
2.Infection
3.PEM
Nutritional therapy
69. Interventions to prevent and/or treat malnutrition
in advanced kidney failure
CKD patients:
1- Close supervision and nutritional counseling (especially for patients on protein-
restricted diets).
2- Initiation of dialysis or kidney transplant in advanced CKD patients with
apparent uremic malnutrition despite vigorous attempts to rectify it.
Maintenance dialysis patients:
1- Appropriate amount of dietary protein (> 1.2 g/kg/day) and calorie (> 35
kcal/kg/day) intake.
2- Optimal dose of dialysis (urea reduction ratio > 70%).
Use of biocompatible hemodialysis membranes.
3-Nutritional support in chronic dialysis patients who are unable to meet their
dietary needs:
a-Oral supplements.
b-Tube feeds (if medically appropriate).
c-Intradialytic parenteral nutritional supplements for HD patients.
d-Amino acid dialysate for peritoneal dialysis patients.
e-TPN
70. Nutritional therapy
Strategies for correction of malnutrition
I. Dietary counseling, support and optimization.
II. Adequate dialysis.
III. Nutritional support in chronic HD patient who
are unable to meet their dietary needs:
1- Oral supplementation.
2- Tube feeding(if medically appropriate).
3- IDPN supplements for HD patients.
4- AA dialysate for PD patients.
5-Continuos total parenteral nutrition(TPN)
71. Nutritional therapy
Other interventions
1. Correction of anemia, metabolic acidosis and
SHPT.
2. Anabolic agents :insulin, growth factor, or
androgenic anabolic steroid.
3. Exercise.
4. Treatment of inflammation :statin, vit E.
5. Social work.
6. Pharmacy support.
7. Transplantation.
72. Nutritional therapy
Dietary requirement
The recommended average level of nutritional
intake are listed in the following table.
These recommendations are consistent with
NKF ,KDOQI and EBP guidelines for nutrition
for CKD patient.
75. Nutritional therapy
Needs for individualization
Adherence to the renal diet is difficult & stressful.
Prescribed diet should be individualized to help every
patient in the terms of: cost, palatability,
comorbidities and cultural eating habits.
Too many restriction should be avoided as they may
lead to poor intake.
Reinforcement by all members of the family and
medical stuff.
Compliance should be assessed on regular basis even
monthly .
77. Adequacy of dialysis
Early referral to dialysis is very crucial.
Optimal dose of dialysis(URR>70%).
Use of biocompatible HD membrane.
Keep KT/V =1-1.2
An important consensus:
Adequate dialysis coupled with good
nutrition is the main pillar for best quality of life.
Adequate dialysis corrects uremia & anorexia
which enhance nutrition.
78. Peer rather than actual BW
Protein and caloric recommendation should
be based on the peer BW for healthy subjects
of the same age, sex, height and body frame
size as the patients.
80. Recommendation
• Understanding and application of the nutritional
principles.
• Periodic assessment of nutritional status (once/
month) should be part of the routine care of CKD and
dialysis patients to permit early recognition.
• Providing and institution of appropriate therapy for
the best improvement of nutrition status .
• Renal dietitian should be a member of the medical
personals.
81. Take home message
• PEM is underappreciated, although it largely
preventable and completely curable.
96. Response to reduced dietary protein and
energy intake.
• (A) Normal response. Reduced dietary protein and energy drive an
increase in hunger and
• a fall in REE, loss of protein preferentially from the visceral organs,
and increased insulin sensitivity of muscle.The liver and kidney
provide glucose, and serum albumin is maintained at a normal level.
• (B) Response with PEW. During PEW, the adaptations to increase
hunger and lower REE are blunted in part by an increased half-life of
leptin and ghrelin and in part by inflammation and dialysis. The loss
of protein occurs preferentially from muscle because of the effects of
metabolic acidosis, glucocorticoids, and inflammation, leading to
increased insulin resistance. Dialysis results in the loss of amino
acids, stimulating muscle protein breakdown. Under the influence of
inflammation and metabolic acidosis, the liver makes glutamine for
deamination in the kidney, increases acute-phase reactants, and
reduces serum albumin. The kidney increases glucose production
from glutamine under the influence of metabolic acidosis.
97. Potential causes of frailty and protein-energy wasting
in elderly patients with end stage kidney disease.
98.
99.
100.
101. Clinical consequences of frailty and protein-energy
wasting in elderly patients with end stage kidney
disease.
112. Selected nutritional parameters for varying
levels of kidney disease (K/DOQI guidelines)
Nutritional
Parameters
Stages 1-4 CKD Stage 5
Hemodialysis
Calories (kcal/kg/d) 30 – 35 35 - 60
Protein (g/kg/d) 0.6 – 0.75 1.2
Fat (% total kcal) For patients at risk for CVD, < 10%
saturated fat, 250-300 mg cholesterol/d
Sodium (g/d) < 2 2
Potassium (g/d) Match to laboratory
values
2 - 3
Calcium (g/d) 1.2 2 from diet and
medicines
Phosphorus (mg/d) Match to laboratory
values
800 – 1000
Fluid (ml/d) Unrestricted with
normal urine output
1000 + urine
Editor's Notes
PEW is the result
of multiple mechanisms inherent to CKD, including
undernutrition, systemic inflammation,
comorbidities, hormonal derangements, the dialysis
procedure, and other consequences of uremic toxicity.
PEW may cause infection, CVD, frailty, and
depression, but these complications may also
increase the extent of PEW.
(A) Normal response. Reduced dietary
protein and energy drive an increase in hunger and
a fall in REE, loss of protein preferentially from the visceral
organs, and increased insulin sensitivity of muscle.
The liver and kidney provide glucose, and serum
albumin is maintained at a normal level.
(B) Response
with PEW. During PEW, the adaptations to increase
hunger and lower REE are blunted in part by an increased
half-life of leptin and ghrelin and in part by inflammation
and dialysis. The loss of protein occurs
preferentially from muscle because of the effects of
metabolic acidosis, glucocorticoids, and inflammation,
leading to increased insulin resistance. Dialysis
results in the loss of amino acids, stimulating muscle
protein breakdown. Under the influence of inflammation
and metabolic acidosis, the liver makes glutamine
for deamination in the kidney, increases
acute-phase reactants, and reduces serum albumin.
The kidney increases glucose production from glutamine
under the influence of metabolic acidosis.
Suggested algorithm for clinical assessment and interventions aimed at assessing and treating PEW by manipulating protein intake in patients
with chronic kidney disease. 1Measured with bromcresol green method. 2Head-to-head comparisons of the different supplementation methods for the
treatment of PEW are not available. Individual patient characteristics and tolerance of, adherence to, and affordability of specific supplementation
methods should be considered. 3Efficacy and safety because treatment of PEW is not proven. 4Ideal amount of daily protein intake in PEW is unclear.
5Directed by specific clinical scenario. The efficacy and safety of PEW treatment in patients with non-dialysis-dependent chronic kidney disease is generally
unproven. DEI, daily energy intake; DPI, dietary protein intake; EAA, essential amino acid; eDPI, estimated daily protein intake; KA, keto acid; LPD, lowprotein
diet; PEW, protein-energy wasting; RAAS, renin angiotensin aldosterone system.