Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Nefropatía diabética. Nuevos aspectos
Dr. Francisco Gómez Pérez
Jefe del Departamento de Endocrinología y Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán”
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Manejo de la diabetes en el anciano
Dr. Guillermo E. Umpierrez
Professor of Medicine in the Division of Endocrinology at Emory University School of Medicine, Section Head, Diabetes and Endocrinology. USA. Editor en Jefe del BJM Open Diabetes Research and Care.
This document summarizes information on diabetic ketoacidosis (DKA). It discusses that DKA occurs when there is a lack of insulin and excess of counterregulatory hormones. Common precipitating factors include infections. Symptoms include polyuria, polydipsia, weight loss, vomiting, and altered mental status. Diagnosis involves finding hyperglycemia, ketonemia, and acidosis on labs and tests. Treatment focuses on hydration, insulin administration, electrolyte replacement, and bicarbonate in some cases. Prognosis is generally good if treated properly but elderly patients, those in a coma, or with severe hypotension have a higher risk of death. Ongoing research continues on optimizing treatment
This document provides information on diabetic nephropathy and diabetic kidney disease (DKD) for healthcare professionals. It covers the causes and risk factors of DKD, how to screen for and diagnose it, treatment options, and guidelines for when to refer patients to specialists. It emphasizes the importance of controlling blood glucose and blood pressure to prevent and slow the progression of DKD. Lifestyle modifications and medication adjustments may be needed for patients with reduced kidney function.
This document summarizes a presentation on diabetic nephropathy given by Dr. Jafar Al-Said at the GCC Diabetes Conference in Bahrain in March 2016. It discusses the epidemiology, pathogenesis, progression, diagnosis and management of diabetic nephropathy. Specifically, it covers topics such as the definition of diabetic nephropathy, risk factors contributing to its development like genetics and hemodynamics, pathological features, the relationship between diabetes, cardiovascular disease and chronic kidney disease, and treatment approaches including lifestyle modifications, blood pressure and glucose control, and use of RAAS inhibitors.
Challenges in Diagnosis and Management of Diabetic Kidney Disease - Dr. GawadNephroTube - Dr.Gawad
This document discusses challenges in diagnosing and managing diabetic kidney disease. It emphasizes that renal problems in diabetic patients are not always due to diabetic nephropathy and may be caused by other conditions. A thorough evaluation is needed to determine the underlying cause, including considering patient history, type of diabetes, presence of retinopathy, characteristics of proteinuria and hematuria, rate of renal impairment, hypertension, and potential contributing factors. A renal biopsy may be warranted if the presentation is atypical or suggests an alternative diagnosis.
Diabetic nephropathy has become a leading cause of end-stage renal failure. Approximately 40% of patients with diabetes develop nephropathy, which is characterized by persistent albuminuria, elevated blood pressure, and decline in kidney function. Good glycemic and blood pressure control can delay the onset and slow the progression of diabetic nephropathy. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are effective in treating diabetic nephropathy through their blood pressure lowering effects and additional renal protection. Intensive management of all cardiovascular risk factors can further slow the progression of kidney damage in patients with diabetes.
Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria and a progressive decline in kidney function. It is the leading cause of end-stage renal disease. Risk factors include poor blood glucose control, high blood pressure, smoking, and family history of kidney disease. The pathophysiology involves changes in the kidney's small blood vessels caused by high blood glucose levels over time. Common signs and symptoms include edema, trouble sleeping, weakness, and itching skin. Medical diagnosis involves blood and urine tests to assess kidney function and detect albuminuria. Management focuses on tight blood glucose and blood pressure control through medication, diet, exercise and lifestyle changes to slow disease progression and prevent complications like heart disease.
This document discusses diabetic nephropathy and its treatment. It begins by describing how diabetic nephropathy progresses from hyperfiltration to proteinuria to declining kidney function over many years. It then discusses treatments including tight blood pressure and glucose control as well as ACE inhibitors and ARBs to slow disease progression. While ACEi and ARBs are beneficial, their combination leads to increased side effects like higher potassium with unclear benefits and potential harms.
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Manejo de la diabetes en el anciano
Dr. Guillermo E. Umpierrez
Professor of Medicine in the Division of Endocrinology at Emory University School of Medicine, Section Head, Diabetes and Endocrinology. USA. Editor en Jefe del BJM Open Diabetes Research and Care.
This document summarizes information on diabetic ketoacidosis (DKA). It discusses that DKA occurs when there is a lack of insulin and excess of counterregulatory hormones. Common precipitating factors include infections. Symptoms include polyuria, polydipsia, weight loss, vomiting, and altered mental status. Diagnosis involves finding hyperglycemia, ketonemia, and acidosis on labs and tests. Treatment focuses on hydration, insulin administration, electrolyte replacement, and bicarbonate in some cases. Prognosis is generally good if treated properly but elderly patients, those in a coma, or with severe hypotension have a higher risk of death. Ongoing research continues on optimizing treatment
This document provides information on diabetic nephropathy and diabetic kidney disease (DKD) for healthcare professionals. It covers the causes and risk factors of DKD, how to screen for and diagnose it, treatment options, and guidelines for when to refer patients to specialists. It emphasizes the importance of controlling blood glucose and blood pressure to prevent and slow the progression of DKD. Lifestyle modifications and medication adjustments may be needed for patients with reduced kidney function.
This document summarizes a presentation on diabetic nephropathy given by Dr. Jafar Al-Said at the GCC Diabetes Conference in Bahrain in March 2016. It discusses the epidemiology, pathogenesis, progression, diagnosis and management of diabetic nephropathy. Specifically, it covers topics such as the definition of diabetic nephropathy, risk factors contributing to its development like genetics and hemodynamics, pathological features, the relationship between diabetes, cardiovascular disease and chronic kidney disease, and treatment approaches including lifestyle modifications, blood pressure and glucose control, and use of RAAS inhibitors.
Challenges in Diagnosis and Management of Diabetic Kidney Disease - Dr. GawadNephroTube - Dr.Gawad
This document discusses challenges in diagnosing and managing diabetic kidney disease. It emphasizes that renal problems in diabetic patients are not always due to diabetic nephropathy and may be caused by other conditions. A thorough evaluation is needed to determine the underlying cause, including considering patient history, type of diabetes, presence of retinopathy, characteristics of proteinuria and hematuria, rate of renal impairment, hypertension, and potential contributing factors. A renal biopsy may be warranted if the presentation is atypical or suggests an alternative diagnosis.
Diabetic nephropathy has become a leading cause of end-stage renal failure. Approximately 40% of patients with diabetes develop nephropathy, which is characterized by persistent albuminuria, elevated blood pressure, and decline in kidney function. Good glycemic and blood pressure control can delay the onset and slow the progression of diabetic nephropathy. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are effective in treating diabetic nephropathy through their blood pressure lowering effects and additional renal protection. Intensive management of all cardiovascular risk factors can further slow the progression of kidney damage in patients with diabetes.
Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria and a progressive decline in kidney function. It is the leading cause of end-stage renal disease. Risk factors include poor blood glucose control, high blood pressure, smoking, and family history of kidney disease. The pathophysiology involves changes in the kidney's small blood vessels caused by high blood glucose levels over time. Common signs and symptoms include edema, trouble sleeping, weakness, and itching skin. Medical diagnosis involves blood and urine tests to assess kidney function and detect albuminuria. Management focuses on tight blood glucose and blood pressure control through medication, diet, exercise and lifestyle changes to slow disease progression and prevent complications like heart disease.
This document discusses diabetic nephropathy and its treatment. It begins by describing how diabetic nephropathy progresses from hyperfiltration to proteinuria to declining kidney function over many years. It then discusses treatments including tight blood pressure and glucose control as well as ACE inhibitors and ARBs to slow disease progression. While ACEi and ARBs are beneficial, their combination leads to increased side effects like higher potassium with unclear benefits and potential harms.
Dr. Nabieh Al-Hilali discusses diabetic nephropathy, noting that over 387 million people currently suffer from diabetes. Microalbuminuria has traditionally been used to detect diabetic nephropathy but lacks sensitivity and specificity. Several novel biomarkers are emerging as potentially better indicators of disease progression, including serum cystatin C, markers of inflammation like TNF receptors, fatty acid binding proteins, and peptide fragments in urine. While more research is still needed, these new biomarkers may improve ability to predict which patients will develop kidney disease and open opportunities for preventative treatment.
Hypertension and Diabetic Kidney Disease Progression Hypertension and Diabe...MedicineAndHealthUSA
Hypertension and diabetic kidney disease progression are linked, and reducing proteinuria is key to slowing kidney disease. The document discusses how conditions like hypertension and diabetes that cause kidney damage have increased in the US population. Landmark trials found that lowering blood pressure and proteinuria reduced kidney disease progression and cardiovascular risks. Initial therapy for kidney or diabetes patients should be an ACE inhibitor or ARB to target blood pressure under 130/80 mmHg.
Reduciendo eventos cardiovasculares en pacientes con DM2: nuevas evidencias
23/06/16 18:00h Casa del Corazón, Madrid
http://ecvdm2.secardiologia.es
#ECVDM2
Resultados de nuevos estudios: más allá de la no inferioridad
Dr. Luis Masmiquel Comas, Endocrinólogo. Hospital Son Llàtzer (Palma de Mallorca)
This document discusses diabetic nephropathy, including its causes, risk factors, stages, diagnosis, progression, and treatment strategies. It notes that diabetic nephropathy is a major complication of diabetes and a leading cause of end-stage renal disease. Key points include that strict control of blood pressure, blood glucose, diet, and lifestyle factors can help prevent or slow the progression of kidney damage caused by diabetes.
Diabetic nephropathy is a leading cause of end-stage renal disease worldwide. Strict control of blood glucose, blood pressure, angiotensin system inhibitors, and other risk factors can help prevent or slow the progression of kidney damage. The stages include early hyperfiltration, development of microalbuminuria, progression to macroalbuminuria and renal failure. Management focuses on glycemic control, blood pressure reduction, angiotensin blockade, cholesterol control, and management of anemia and cardiovascular risk factors to preserve kidney function for as long as possible.
My Nephrology Registrar Seminar Talk from September 2013
Topics Covered
Pathogenesis of Diabetic Nephropathy
Other Renal Disease in Diabetes
Treatment of Diabetic Kidney Disease + The Joint Renal Diabetic Clinic
This document discusses the management of diabetic nephropathy. It begins with defining diabetic nephropathy as a clinical syndrome characterized by persistent albuminuria, progressive decline in glomerular filtration rate, elevated blood pressure, worse glycemic control, hypertension, and genetic predisposition. It then outlines the typical progression of diabetic kidney disease and reviews risk factors. Current treatment strategies are aimed at strict glycemic control, blood pressure control, reducing proteinuria, and preserving renal function through ACE inhibitors, ARBs, and lifestyle modifications like weight loss and smoking cessation. Newer treatments continue to be explored, but therapeutic intervention works best when begun early and glycemia, blood pressure, and proteinuria are well controlled.
This document discusses diabetic kidney disease and intensive glucose control. It begins with the author's conflicts of interest related to pharmaceutical companies. It then reviews several major studies on intensive glucose control including the DCCT, UKPDS, ADVANCE, ACCORD, and VADT trials. The studies showed reductions in microvascular complications with intensive control but mixed results for cardiovascular outcomes, with the ACCORD trial finding higher mortality in the intensive control group. Overall the document examines the evidence from major trials on benefits and risks of tight glycemic control.
Hígado graso no alcohólico en niños y adolescentes obesosCuerpomedicoinsn
The document discusses non-alcoholic fatty liver disease (NAFLD) and its relationship to obesity and insulin resistance. It notes that NAFLD affects around 20% of adults and 5% of children, and is strongly associated with obesity. A small portion of NAFLD cases progress to non-alcoholic steatohepatitis (NASH), which can potentially lead to scarring, cirrhosis, and liver failure over many years if not treated or reversed. Lifestyle changes such as weight loss and increased physical activity are recommended for treatment.
- T2DM accounts for 90-95% of all diagnosed diabetes cases. It is a growing epidemic affecting 246 million people worldwide in 2007.
- The main pathophysiology of T2DM includes insulin resistance in muscle, liver and fat tissues as well as insulin deficiency due to impaired insulin secretion from pancreatic beta cells over time.
- Current treatment options for T2DM like metformin, sulfonylureas and thiazolidinediones have limitations such as side effects of weight gain, hypoglycemia, edema and heart failure which impact efficacy and safety.
Diabetic nephropathy medical managementNilesh Jadhav
1. Diabetic nephropathy is a chronic kidney disease caused by damage to the kidneys over many years as a result of diabetes. It is the most common cause of end-stage renal disease.
2. Management of diabetic nephropathy focuses on optimal control of blood glucose, blood pressure, lipids through medication, lifestyle changes, and monitoring for progression of kidney disease.
3. RAAS blockade using ACE inhibitors, ARBs, or renin inhibitors is important treatment but requires monitoring of potassium and kidney function. Referral to a nephrologist is recommended for atypical cases or rapid decline in kidney function.
Recent advancement in managing diabetic nephropathypp_shivgunde
This document discusses recent advances in managing and understanding diabetic nephropathy. It begins with an introduction to diabetes and chronic kidney disease prevalence and prognosis. It then covers the pathophysiology of diabetic nephropathy and the current standard tripartite approach of intensive blood glucose control, blood pressure control, and RAAS blockade. Novel therapeutic modalities such as exploiting the renin-angiotensin-aldosterone axis through dual or combined blockade and aldosterone antagonism are also discussed.
Empagliflozin and Cardiovascular OutcomesUyen Nguyen
1) The EMPA-REG OUTCOME trial evaluated the cardiovascular outcomes of empagliflozin compared to placebo in over 7000 patients with type 2 diabetes at high risk of cardiovascular events.
2) Empagliflozin was found to significantly reduce the risk of the primary composite outcome of cardiovascular death, non-fatal myocardial infarction, or non-fatal stroke compared to placebo.
3) Additional benefits observed with empagliflozin included a significant reduction in all-cause mortality, cardiovascular mortality, and hospitalization for heart failure.
1) The document discusses a Phase 3 clinical trial investigating the effects of the ASK1 inhibitor selonsertib (SEL) in patients with diabetic kidney disease (DKD).
2) The trial did not meet its primary endpoint of a 50% improvement in eGFR from baseline to week 48. However, exploratory analyses found SEL induced acute but reversible eGFR declines followed by stabilization or improvement in eGFR slope over time.
3) Adverse events including acute kidney injury and fluid overload were similar between SEL and placebo groups. The study was limited by its short duration and data issues from two sites.
Diabetic nephropathy considered one of the most common complications of DM. This presentation answer the question are some diabetic patient immune to diabetic nephroapthy
This document provides information about diabetes statistics, pathophysiology, diagnosis, management, and complications. Some key points:
- 29.1 million Americans have diabetes, with costs totaling $245 billion in 2012. Rates are highest among racial/ethnic minorities.
- Type 1 diabetes results from autoimmune destruction of pancreatic beta cells causing absolute insulin deficiency. Type 2 is caused by insulin resistance and relative insulin deficiency.
- Diagnosis is based on HbA1c levels, fasting plasma glucose, and oral glucose tolerance tests. Goals are to maintain HbA1c under 7% and limit pre- and post-prandial hyperglycemia.
- Strict glucose control can reduce risk
Diabetes is a chronic disease characterized by high blood sugar levels that can damage organs and blood vessels. There are three main types of diabetes: type 1, type 2, and gestational diabetes. The goals of diabetes management are to control blood sugar levels through lifestyle modifications like diet, exercise, smoking cessation, and medication if needed. Treatment involves medical nutrition therapy, oral medications or insulin injections, glucose monitoring, and managing complications. The standard targets for blood sugar control are an A1C under 7% for most adults and under 7.5% for children.
Type 2 diabetes mellitus (T2DM) is a chronic condition characterized by insulin resistance and an inability to properly regulate blood sugar levels. The two most important risk factors for T2DM are a family history of diabetes and obesity, though age, race, diet, and exercise level also impact risk. Common symptoms include frequent urination, nerve damage, and dark skin patches. Treatment involves lifestyle changes like diet and exercise as well as medications like metformin, which improves insulin sensitivity and decreases glucose production in the liver. Patients are counseled on managing diabetes-related risks and provided support through organizations and groups.
El documento discute los beneficios de la rehabilitación para adultos mayores con síndrome metabólico. La rehabilitación integral que incluye ejercicio físico, terapia cognitiva y orientación nutricional puede mejorar la fuerza muscular, reducir la inflamación y mejorar la sensibilidad a la insulina. Los programas de ejercicio deben incluir actividad aeróbica y de resistencia de intensidad moderada de 3 a 5 veces por semana para mejorar la salud y reducir la discapacidad en esta población.
Este documento discute los mejores métodos anticonceptivos hormonales para mujeres que han tenido diabetes gestacional. Explica que los métodos combinados y de solo progestina son generalmente seguros, pero que los de solo progestina pueden asociarse a un mayor riesgo de diabetes durante la lactancia o con el uso prolongado de inyectables como el AMPD. Finalmente, concluye que las opciones anticonceptivas son variadas siguiendo las guías de la OMS, pero se debe realizar un seguimiento cuidadoso de la salud para minimizar el riesgo de
Dr. Nabieh Al-Hilali discusses diabetic nephropathy, noting that over 387 million people currently suffer from diabetes. Microalbuminuria has traditionally been used to detect diabetic nephropathy but lacks sensitivity and specificity. Several novel biomarkers are emerging as potentially better indicators of disease progression, including serum cystatin C, markers of inflammation like TNF receptors, fatty acid binding proteins, and peptide fragments in urine. While more research is still needed, these new biomarkers may improve ability to predict which patients will develop kidney disease and open opportunities for preventative treatment.
Hypertension and Diabetic Kidney Disease Progression Hypertension and Diabe...MedicineAndHealthUSA
Hypertension and diabetic kidney disease progression are linked, and reducing proteinuria is key to slowing kidney disease. The document discusses how conditions like hypertension and diabetes that cause kidney damage have increased in the US population. Landmark trials found that lowering blood pressure and proteinuria reduced kidney disease progression and cardiovascular risks. Initial therapy for kidney or diabetes patients should be an ACE inhibitor or ARB to target blood pressure under 130/80 mmHg.
Reduciendo eventos cardiovasculares en pacientes con DM2: nuevas evidencias
23/06/16 18:00h Casa del Corazón, Madrid
http://ecvdm2.secardiologia.es
#ECVDM2
Resultados de nuevos estudios: más allá de la no inferioridad
Dr. Luis Masmiquel Comas, Endocrinólogo. Hospital Son Llàtzer (Palma de Mallorca)
This document discusses diabetic nephropathy, including its causes, risk factors, stages, diagnosis, progression, and treatment strategies. It notes that diabetic nephropathy is a major complication of diabetes and a leading cause of end-stage renal disease. Key points include that strict control of blood pressure, blood glucose, diet, and lifestyle factors can help prevent or slow the progression of kidney damage caused by diabetes.
Diabetic nephropathy is a leading cause of end-stage renal disease worldwide. Strict control of blood glucose, blood pressure, angiotensin system inhibitors, and other risk factors can help prevent or slow the progression of kidney damage. The stages include early hyperfiltration, development of microalbuminuria, progression to macroalbuminuria and renal failure. Management focuses on glycemic control, blood pressure reduction, angiotensin blockade, cholesterol control, and management of anemia and cardiovascular risk factors to preserve kidney function for as long as possible.
My Nephrology Registrar Seminar Talk from September 2013
Topics Covered
Pathogenesis of Diabetic Nephropathy
Other Renal Disease in Diabetes
Treatment of Diabetic Kidney Disease + The Joint Renal Diabetic Clinic
This document discusses the management of diabetic nephropathy. It begins with defining diabetic nephropathy as a clinical syndrome characterized by persistent albuminuria, progressive decline in glomerular filtration rate, elevated blood pressure, worse glycemic control, hypertension, and genetic predisposition. It then outlines the typical progression of diabetic kidney disease and reviews risk factors. Current treatment strategies are aimed at strict glycemic control, blood pressure control, reducing proteinuria, and preserving renal function through ACE inhibitors, ARBs, and lifestyle modifications like weight loss and smoking cessation. Newer treatments continue to be explored, but therapeutic intervention works best when begun early and glycemia, blood pressure, and proteinuria are well controlled.
This document discusses diabetic kidney disease and intensive glucose control. It begins with the author's conflicts of interest related to pharmaceutical companies. It then reviews several major studies on intensive glucose control including the DCCT, UKPDS, ADVANCE, ACCORD, and VADT trials. The studies showed reductions in microvascular complications with intensive control but mixed results for cardiovascular outcomes, with the ACCORD trial finding higher mortality in the intensive control group. Overall the document examines the evidence from major trials on benefits and risks of tight glycemic control.
Hígado graso no alcohólico en niños y adolescentes obesosCuerpomedicoinsn
The document discusses non-alcoholic fatty liver disease (NAFLD) and its relationship to obesity and insulin resistance. It notes that NAFLD affects around 20% of adults and 5% of children, and is strongly associated with obesity. A small portion of NAFLD cases progress to non-alcoholic steatohepatitis (NASH), which can potentially lead to scarring, cirrhosis, and liver failure over many years if not treated or reversed. Lifestyle changes such as weight loss and increased physical activity are recommended for treatment.
- T2DM accounts for 90-95% of all diagnosed diabetes cases. It is a growing epidemic affecting 246 million people worldwide in 2007.
- The main pathophysiology of T2DM includes insulin resistance in muscle, liver and fat tissues as well as insulin deficiency due to impaired insulin secretion from pancreatic beta cells over time.
- Current treatment options for T2DM like metformin, sulfonylureas and thiazolidinediones have limitations such as side effects of weight gain, hypoglycemia, edema and heart failure which impact efficacy and safety.
Diabetic nephropathy medical managementNilesh Jadhav
1. Diabetic nephropathy is a chronic kidney disease caused by damage to the kidneys over many years as a result of diabetes. It is the most common cause of end-stage renal disease.
2. Management of diabetic nephropathy focuses on optimal control of blood glucose, blood pressure, lipids through medication, lifestyle changes, and monitoring for progression of kidney disease.
3. RAAS blockade using ACE inhibitors, ARBs, or renin inhibitors is important treatment but requires monitoring of potassium and kidney function. Referral to a nephrologist is recommended for atypical cases or rapid decline in kidney function.
Recent advancement in managing diabetic nephropathypp_shivgunde
This document discusses recent advances in managing and understanding diabetic nephropathy. It begins with an introduction to diabetes and chronic kidney disease prevalence and prognosis. It then covers the pathophysiology of diabetic nephropathy and the current standard tripartite approach of intensive blood glucose control, blood pressure control, and RAAS blockade. Novel therapeutic modalities such as exploiting the renin-angiotensin-aldosterone axis through dual or combined blockade and aldosterone antagonism are also discussed.
Empagliflozin and Cardiovascular OutcomesUyen Nguyen
1) The EMPA-REG OUTCOME trial evaluated the cardiovascular outcomes of empagliflozin compared to placebo in over 7000 patients with type 2 diabetes at high risk of cardiovascular events.
2) Empagliflozin was found to significantly reduce the risk of the primary composite outcome of cardiovascular death, non-fatal myocardial infarction, or non-fatal stroke compared to placebo.
3) Additional benefits observed with empagliflozin included a significant reduction in all-cause mortality, cardiovascular mortality, and hospitalization for heart failure.
1) The document discusses a Phase 3 clinical trial investigating the effects of the ASK1 inhibitor selonsertib (SEL) in patients with diabetic kidney disease (DKD).
2) The trial did not meet its primary endpoint of a 50% improvement in eGFR from baseline to week 48. However, exploratory analyses found SEL induced acute but reversible eGFR declines followed by stabilization or improvement in eGFR slope over time.
3) Adverse events including acute kidney injury and fluid overload were similar between SEL and placebo groups. The study was limited by its short duration and data issues from two sites.
Diabetic nephropathy considered one of the most common complications of DM. This presentation answer the question are some diabetic patient immune to diabetic nephroapthy
This document provides information about diabetes statistics, pathophysiology, diagnosis, management, and complications. Some key points:
- 29.1 million Americans have diabetes, with costs totaling $245 billion in 2012. Rates are highest among racial/ethnic minorities.
- Type 1 diabetes results from autoimmune destruction of pancreatic beta cells causing absolute insulin deficiency. Type 2 is caused by insulin resistance and relative insulin deficiency.
- Diagnosis is based on HbA1c levels, fasting plasma glucose, and oral glucose tolerance tests. Goals are to maintain HbA1c under 7% and limit pre- and post-prandial hyperglycemia.
- Strict glucose control can reduce risk
Diabetes is a chronic disease characterized by high blood sugar levels that can damage organs and blood vessels. There are three main types of diabetes: type 1, type 2, and gestational diabetes. The goals of diabetes management are to control blood sugar levels through lifestyle modifications like diet, exercise, smoking cessation, and medication if needed. Treatment involves medical nutrition therapy, oral medications or insulin injections, glucose monitoring, and managing complications. The standard targets for blood sugar control are an A1C under 7% for most adults and under 7.5% for children.
Type 2 diabetes mellitus (T2DM) is a chronic condition characterized by insulin resistance and an inability to properly regulate blood sugar levels. The two most important risk factors for T2DM are a family history of diabetes and obesity, though age, race, diet, and exercise level also impact risk. Common symptoms include frequent urination, nerve damage, and dark skin patches. Treatment involves lifestyle changes like diet and exercise as well as medications like metformin, which improves insulin sensitivity and decreases glucose production in the liver. Patients are counseled on managing diabetes-related risks and provided support through organizations and groups.
El documento discute los beneficios de la rehabilitación para adultos mayores con síndrome metabólico. La rehabilitación integral que incluye ejercicio físico, terapia cognitiva y orientación nutricional puede mejorar la fuerza muscular, reducir la inflamación y mejorar la sensibilidad a la insulina. Los programas de ejercicio deben incluir actividad aeróbica y de resistencia de intensidad moderada de 3 a 5 veces por semana para mejorar la salud y reducir la discapacidad en esta población.
Este documento discute los mejores métodos anticonceptivos hormonales para mujeres que han tenido diabetes gestacional. Explica que los métodos combinados y de solo progestina son generalmente seguros, pero que los de solo progestina pueden asociarse a un mayor riesgo de diabetes durante la lactancia o con el uso prolongado de inyectables como el AMPD. Finalmente, concluye que las opciones anticonceptivas son variadas siguiendo las guías de la OMS, pero se debe realizar un seguimiento cuidadoso de la salud para minimizar el riesgo de
El documento presenta información sobre el síndrome metabólico, incluyendo sus definiciones iniciales, componentes y asociación con enfermedades cardiovasculares y diabetes. También resume los hallazgos clave de varios estudios como INSPIRE ME IAA sobre la distribución de la grasa corporal y su relación con la tolerancia a la glucosa y riesgo cardiometabólico.
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
SIMPOSIO: Tratando la obesidad seriamente
Mitos y realidades de los procedimientos estéticos en la obesidad
Dr. Edgar Bazaldúa Cobas
Medicina Estética y Bariatría
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
TALLER: Discusión con el experto: Nuevas recomendaciones en los estándares del cuidado del paciente con diabetes, emitidos por la ASOCIACIÓN AMERICANA DE DIABETES (ADA) 2016 y 2017, una discusión de los mismos
Dr. Ismael Javier Chavira López
Jefe del Servicio de Endocrinología, Hospital General de México “Dr. Eduardo Liceaga”
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Entendiendo los resultados de los estudios clínicos con fármacos antidiabéticos en la disminución de eventos cardiovasculares
Dra. Paloma Almeda Valdés
Departamento de Endocrinología y Metabolismo, Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán”
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
TALLER: Escalas o calculadoras para la determinación del riesgo cardiovascular en los pacientes con o sin síndrome metabólico
Dra. Sandra Elizondo Argueta
Esp. Medicina Interna, Dirección de Prestaciones Médicas, División de Proyectos Especiales en Salud, IMSS, Miembro AMESI
Dra. Diana Castellanos Rodríguez
Esp. Medicina Interna, Servicio de Medicina Interna, Hospital de Alta Especialidad Bicentenario de la Independencia. ISSSTE. Miembro AMESI
Dra. Pilar Rangel
Esp. Medicina Interna, Jefa de la Unidad de Calidad, Hospital General “Dr. Enrique Cabrera”. Miembro AMESI
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Enfermedades del sueño y diabetes
Dr. Humberto Medina Chávez
Medicina Interna y Geriatría
Clínica de Trastornos de sueño, Facultad de Medicina, UNAM
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Repercusiones metabólicas de los desórdenes de la composición corporal
Dra. Edna J. Nava González
Presidenta del Colegio Mexicano de Nutriólogos
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Futuro en el tratamiento de la DM2
Dr. Guillermo E. Umpierrez
Professor of Medicine in the Division of Endocrinology at Emory University School of Medicine, Section Head, Diabetes and Endocrinology. USA. Editor en Jefe del BJM Open Diabetes Research and Care
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
SIMPOSIO: De la Sociedad de Prevención Cardiovascular y el Instituto Nacional de CardiologÍa
Presentación de la NOM en dislipidemia versión 2017 [Estatinas en prevención primaria y secundaria, metas a lograr con el tratamiento del LDL-C, nuevos fármacos incluidos, PCSK9]
Dr. Héctor Hernández y Hernández
Cardiólogo Certificado, Presidente de la Asociación de Prevención del Riesgo Cardiovascular
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
TALLER: Educación en diabetes, en realidad ¿a quién le toca educar al paciente y cuál sería la mejor estrategia?
(¿redes sociales?, ¿qué aplicaciones?)
Introducción
Dr. César Ochoa
Profesor de Investigación Clínica, Western University of Health Science, Pomona, CA, USA – Western Diabetes Institute
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
SIMPOSIO: Rehabilitación cardiaca en pacientes con síndrome metabólico y discapacidad
Enfermedad vascular cerebral
Dra. Azucena Guadalupe Rodríguez Reyes
Adscrita al INR “Dr. Luis Guillermo Ibarra”. Certificada por el Consejo de Medicina de Rehabilitación, Alta Especialidad en la UNAM. Prof. Universitario
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
¿Hacia dónde van los algoritmos de la ADA/EASD, AACE y ALAD en el tratamiento DM2. Control glucémico y protección cardiovascular como objetivo?
Dr. Guillermo E. Umpiérrez
Professor of Medicine in the Division of Endocrinology at Emory University School of Medicine, Section Head, Diabetes and Endocrinology. USA. Editor en Jefe del BJM Open Diabetes Research and Care.
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Genética y plasticidad epigenética en el desarrollo de dislipidemia en mexicanos
Dr. José De Jesús Peralta Romero
Investigador Asociado// SNI I// Medico Cirujano, M en C y Dr en C. en Biomedicina Molecular, Unidad de Investigación Medica en Bioquímica, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, IMSS
Basado en la información proporcionada, algunas sugerencias para este paciente podrían ser:
- Recomendar ejercicios en casa que no requieran equipo como estiramientos, ejercicios de resistencia con el propio peso corporal, baile siguiendo videos musicales en YouTube, etc. Esto le permitiría hacer actividad física de forma segura y disfrutable en su hogar.
- Sugerir caminatas en zonas seguras cercanas a su domicilio, acompañado si es posible, para ir incrementando de a poco la duración y ritmo a medida
El documento presenta información sobre el uso de insulina en el tratamiento de la diabetes. Explica los diferentes tipos de insulina según su duración y pico de acción, así como esquemas de tratamiento con insulina basal y prandial. También ofrece recomendaciones sobre la aplicación correcta de la insulina, incluyendo el uso de agujas, jeringas y sitios de inyección.
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
SIMPOSIO: Nuevos conceptos moleculares en la fisiopatología del síndrome metabólico y diabetes
Fenotipo de exhaustación inmunológica en pacientes con obesidad
Dr. Raúl Flores Mejía
Investigador del Sistema Nacional de Investigadores, Inmunología Médica, Escuela Superior de Medicina, IPN
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Cambios Hormonales y metabólicos después de cirugía
metabolica: ¿Cómo entenderlos?
Dr. Arturo A. Rodríguez González
Clínica Integral de Cirugía para la Obesidad y Enfermedades Metabólicas, Hospital General “Dr. Rubén Leñero”, Ssa D.F. México
1) Los macrófagos en la obesidad visceral cambian su fenotipo de anti a pro inflamatorio, generando una inflamación crónica de bajo grado que causa resistencia a la insulina.
2) Los monocitos de individuos con síndrome metabólico tienen una menor expresión de transportadores de glucosa y una mayor producción de especies reactivas de oxígeno después de la activación.
3) Las alteraciones metabólicas asociadas al síndrome metabólico parecen afectar negativamente las funciones inmunológicas
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.
This document discusses diabetic nephropathy and provides updates on the topic. It notes that diabetes is a leading global epidemic and cause of end-stage renal failure. Almost one third of people with type 2 diabetes develop kidney disease. The natural history and stages of progression of diabetic nephropathy are described. The definition, pathogenesis, risk factors, and treatment of diabetic nephropathy are summarized, including the roles of genetics, hypertension, the renin-angiotensin system, and other biochemical pathways in disease development and progression.
Drugs having Pleiotropic effects, Nutraceuticals and role of antioxidants ant...SwaroopaNallabariki
This document discusses several drugs that have pleiotropic effects beyond their primary mechanism of action, including statins, SGLT2 inhibitors, metformin, thiazolidinediones, cardiac glycosides, and antithrombotic drugs. It also discusses the role of antioxidants in disease prevention and treatment. Statins have beneficial effects including improving endothelial function, reducing inflammation and oxidative stress, stabilizing plaques, and inhibiting smooth muscle proliferation. SGLT2 inhibitors and thiazolidinediones improve glycemic control and have additional vascular benefits. Metformin reshapes the gut microbiota. Antioxidants help counteract free radical damage linked to diseases. Nutraceuticals and antioxidants’ properties influence their bioavailability
Diabetic kidney disease remains a major global health problem. Recent research has provided insights into the pathophysiology and has identified new diagnostic and therapeutic approaches. Several large clinical trials have shown that sodium-glucose cotransporter-2 inhibitors, glucagon-like peptide-1 receptor agonists, mineralocorticoid receptor antagonists, and endothelin receptor antagonists can reduce kidney disease progression and cardiovascular events in patients with diabetes and kidney disease. Ongoing trials are further evaluating combination therapies and the benefits of these agents in non-diabetic kidney disease and heart failure.
1. HDAC inhibitors have been shown to be renoprotective in diabetes by preventing the accumulation of extracellular matrix proteins in the glomerular mesangium and tubulointerstitium.
2. Histone hyperacetylation by the nonselective HDAC inhibitor trichostatin A prevents TGF-β1-induced downregulation of E-cadherin and upregulation of collagen I in human renal proximal tubular epithelial cells.
3. TGF-β1 expression is increased in experimental diabetic animal models and in human diabetic nephropathy, and plays a key role in the development of renal changes through inducing epithelial-mesenchymal transition and extracellular matrix accumulation.
This document discusses renal protective agents for treating lupus nephritis and ANCA-associated vasculitis. It outlines classical agents like RAAS inhibitors, diuretics, and metformin. It also discusses promising future agents including finerenone, SGLT2 inhibitors, GLP1 receptor antagonists, and endothelin receptor antagonists. While these newer agents show potential for preserving renal function and reducing immunosuppressant exposure, the document notes that more research is still needed before widespread use due to challenges like excluding autoimmune patients from trials and long-term effects requiring further study.
NSAIDs can be categorized into four groups based on their selectivity for inhibiting COX-1 and COX-2 enzymes. Selective COX-2 inhibitors were developed to reduce gastrointestinal side effects, but were later found to increase cardiovascular risks. NSAIDs can affect several body systems including the gastrointestinal, hepatic, renal and cardiovascular systems. Common side effects include ulcers, bleeding, elevated liver enzymes, acute kidney injury and increased risk of heart attack or stroke. The document discusses the mechanisms of these side effects and considerations for prescribing NSAIDs.
Diabetic nephropathy involves complex interactions between metabolic and hemodynamic factors that cause damage to the glomerulus and tubulointerstitium. Several pathways contribute to renal injury, including the renin-angiotensin system, specifically ACE2 which converts angiotensin II to the vasodilator angiotensin 1-7. In diabetes, ACE2 expression is reduced in the kidney. Excess extracellular matrix production also contributes via TGF-β signaling, which is modulated by the protein CDA1. Nephrin, a key slit diaphragm protein, is reduced in diabetes and its reduction correlates with increased albuminuria. Optimal glycemic and blood pressure
Gagal ginjal kronis dari sudut pandang keperawatan paliatif octo zulkarnain
1. Chronic kidney disease (CKD) is the gradual loss of kidney function over time. It is classified into 5 stages based on glomerular filtration rate.
2. Common causes of CKD include hypertension, diabetes, glomerulonephritis, and urinary tract obstructions.
3. Manifestations include generalized edema, pulmonary crackles, anemia, weight loss, hyperkalemia, and others resulting from hormonal imbalances and fluid retention as kidney function declines.
Renal disorders can cause complications like chronic kidney disease (CKD) that increase risks during dental procedures and surgery. Patients with CKD are more likely to experience bleeding due to platelet and blood vessel dysfunction, and also have increased risk of infection. They may also develop dental problems such as periodontal disease, tooth discoloration and loss of enamel. When undergoing surgery, CKD patients are at higher risk of complications including bleeding, infections, cardiovascular and thrombotic events due to changes in fluid, electrolyte and acid-base balance as well as altered drug metabolism and clearance. Careful preoperative evaluation and management involving nephrologists can help reduce these perioperative risks.
This document summarizes a journal club discussion on the role of peroxisome proliferator-activated receptor gamma (PPARγ) agonists in treating diabetes and cardiovascular disease. PPARγ agonists like thiazolidinediones improve insulin resistance and reduce inflammation. They may protect blood vessels by inhibiting smooth muscle cell proliferation and migration involved in atherosclerosis and restenosis. While clinical trials show PPARγ agonists reduce cardiovascular risk factors, their side effects like fluid retention require monitoring, and further outcomes research is still needed to establish their long-term cardiovascular benefits and safety.
This document summarizes a study comparing antioxidant status and inflammatory markers in type 2 diabetic male and female subjects with nephropathy. The study found that inflammatory markers IL-6 and TNF-α were higher in type 2 diabetic females with nephropathy compared to males. Antioxidant levels of Gpx were lower in both males and females with nephropathy but more decreased in females. The study concludes that oxidative stress and inflammation play a role in the development of nephropathy in type 2 diabetes, with females exhibiting greater levels of inflammation and oxidative stress than males.
This document summarizes a study comparing antioxidant status and inflammatory markers in type 2 diabetic male and female subjects with nephropathy. The study found that inflammatory markers IL-6 and TNF-α were higher in type 2 diabetic female subjects with nephropathy compared to males. It also found that the antioxidant enzyme glutathione peroxidase was lower in both male and female diabetic nephropathy subjects compared to controls, but was lower in females. The study concludes that oxidative stress and inflammation may play a greater role in the pathogenesis of nephropathy in type 2 diabetic females compared to males.
This document discusses diabetic nephropathy (DN). It begins by defining DN as persistent albuminuria attributable to diabetes, with a relentless decline in GFR and elevated blood pressure. It then reviews the history, epidemiology, risk factors, pathogenesis, natural history, clinical features and investigations of DN. The pathogenesis section describes both metabolic and hemodynamic pathways, involving mechanisms such as hyperglycemia, advanced glycation end products, aldose reductase, and glomerular hyperfiltration. Clinical features may include hypertension, retinopathy and neuropathy. Investigations include urine albumin-creatinine ratio and renal biopsy if needed to diagnose or differentiate DN from other kidney diseases.
Diabetic nephropathy is characterized by gradually increasing urinary albumin excretion, high blood pressure, declining kidney function, and presence of diabetic retinopathy. It develops over many years due to effects of hyperglycemia via polyol pathway flux, increased AGE formation, PKC activation, and hemodynamic changes. Genetic factors also contribute to susceptibility. Screening involves measuring urinary albumin-to-creatinine ratio and eGFR annually. Treatment focuses on tight glycemic control, blood pressure management typically using ACE inhibitors or ARBs, and lifestyle modifications like dietary protein restriction and smoking cessation to slow progression to kidney failure.
This document discusses the pathophysiology of acute and chronic complications of diabetes mellitus. It begins by outlining the objectives of understanding ketoacidosis, hyperosmolar state, and mechanisms of glucose-induced vascular damage. It then provides background on the prevalence and types of diabetes. The main pathophysiological mechanisms discussed are the polyol pathway, formation of advanced glycation end products, activation of protein kinase C, increased flux through the hexosamine pathway, and mitochondrial superoxide production. These lead to microvascular complications like nephropathy, retinopathy and neuropathy as well as macrovascular complications. The document concludes by summarizing diagnostic criteria for diabetic ketoacidosis and hyperosmolar hyperglyce
CONGESTIVE HEART FAILURE
Congestive heart failure is a syndrome that can be caused by a variety of abnormalities
Coronary artery disease
Heart attack
Cardiac myopathy
Conditions that overwork the heart
Hypertension
Valve disease
Thyroid disease
Kidney disease
Congenital birth defects
Diabetes
In the usual form of heart failure, the heart muscle has reduced contractility. This produces a reduction in cardiac output, which then becomes inadequate to meet the peripheral demands of the body.
The document discusses the role of peroxisome proliferator activated receptor gamma (PPARγ) agonists in treating type 2 diabetes and reducing cardiovascular risk. PPARγ agonists like thiazolidinediones improve insulin sensitivity and have beneficial effects on lipids, inflammation, and vascular cell proliferation. They may reduce cardiovascular events in type 2 diabetes through these metabolic and anti-inflammatory mechanisms. However, PPARγ agonists can also cause side effects like fluid retention, weight gain, and congestive heart failure, so their risks and benefits must be carefully weighed.
Diabetic nephropathy is a clinical syndrome characterized by the following :
Persistent albuminuria (>300 mg/d or >200 μg/min) that is confirmed on at least 2 occasions 3-6 months apart.
Progressive decline in the glomerular filtration rate (GFR).
Elevated arterial blood pressure.
Three major histologic changes occur in the glomeruli of persons with diabetic nephropathy:
First, mesangial expansion is directly induced by hyperglycemia, perhaps via increased matrix production or glycation of matrix proteins.
Second, thickening of the glomerular basement membrane (GBM) occurs.
Third, glomerular sclerosis caused by intraglomerular hypertension (induced by dilatation of the afferent renal artery or from ischemic injury induced by hyaline narrowing of the vessels supplying the glomeruli).
These different histologic patterns appear to have similar prognostic significance.
Several issues are key in the medical care of patients with diabetic nephropathy.
These include glycemic control, management of hypertension, and reducing dietary salt intake and phosphorus and potassium restriction in advanced cases.
A meta-analysis from the Cochrane Database shows a large fall in blood pressure with salt restriction, similar to that of single-drug therapy
Similar to Nefropatía diabética. Nuevos aspectos (20)
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
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El duelo por pérdida de la salud
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Depto. Salud Pública, Fac. Medicina UNAM
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“La dieta de la milpa”, un modelo de alimentación saludable
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Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Coaching nutricional
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Adscrita al Servicio de Nutriología Clínica, INCMNSZ
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
La visión interdisciplinaria del tratamiento del síndrome metabólico
Dra. Pilar Martínez Matsumoto
Pediatra y residente Nutriología Clínica, INCMNSZ
1) Los documentos presentan guías y recomendaciones para el diagnóstico y evaluación de la obesidad y el síndrome metabólico, incluyendo la medición del IMC, circunferencia abdominal, y pruebas de laboratorio.
2) Se recomienda que los médicos realicen un diagnóstico de obesidad y brinden asesoramiento sobre cambios en el estilo de vida a más pacientes obesos, especialmente a mujeres, adultos jóvenes y personas con obesidad severa.
3) La Asociación Americana de Endocr
Este documento resume los principales temas relacionados con la actividad física y el sedentarismo. Explica la epidemiología del sobrepeso y la obesidad a nivel mundial, y los factores que influyen en el balance energético. Define la actividad física, el sedentarismo e identifica las recomendaciones internacionales. Analiza la epidemiología de la inactividad física en México y las implicaciones del sedentarismo para la salud. Finalmente, presenta barreras comunes para realizar actividad física y estrategias probadas para
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Evolución nutricional de los adolescentes posterior a cirugía bariátrica
ENCP. Betzabé Salgado Arroyo
Clínica de Obesidad Infantil, HIM “Federico Gómez”
Este documento presenta los resultados de un estudio sobre el manejo integral de la obesidad en pediatría realizado en el Hospital Infantil Federico Gómez. El estudio evaluó a 42 pacientes con obesidad y encontró antecedentes familiares de obesidad, hipertensión, dislipidemia y diabetes. También se observó que los pacientes tenían malos hábitos alimenticios y falta de actividad física. El tratamiento multidisciplinario que incluyó cambios dietéticos, ejercicio y terapia psicológica logró reducir el
El documento destaca la importancia de la nutrición durante los primeros 1000 días de vida, desde la concepción hasta los 2 años. Una adecuada nutrición en esta etapa crítica optimiza el crecimiento y desarrollo y reduce el riesgo de enfermedades a futuro. La nutrición materna previa y durante el embarazo, así como la lactancia materna exclusiva en los primeros 6 meses y una alimentación complementaria saludable, son fundamentales para lograr estos beneficios.
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Obesidad y diabetes: actualidades en la terapia médico nutricional
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CAIPaDi, INCMNSZ
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
¿Por qué el uso indiscriminado de los edulcorantes?
Dra. Nallely Bueno Hernández
Investigadora en Ciencias Médicas, Dirección de Investigación, Hospital General de México “Dr. Eduardo Liceaga”
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Edulcorantes en el síndrome metabólico
MC. Mónica Todd Curie Sánchez Tapia
Posgrado UNAM/INCMNSZ
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Impacto en la salud del consumo de fructosa
Dra. Elizabeth Pérez Cruz
Jefa de la División de Medicina Crítica y Coordinadora de la Clínica de Obesidad, Hospital Juárez de México
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Manejo de NASH en diabetes mellitus
MD-MSc Daniel Elías-López
Endocrinología, Medicina Interna, Alta Especialidad en Diabetes. Departamento de Endocrinología y Metabolismo, INCMNSZ
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Síndrome metabólico y cáncer. ¿Quién encendió la mecha?
Dr. Iván Torre Villalvazo
Investigador en Ciencias Médicas, Depto.
de Fisiología de la Nutrición INCMNSZ
Este documento describe las bases moleculares de la angiogénesis y sus implicaciones patológicas. Explica que las GTPasas de Rho y los factores de intercambio de nucleótidos de guanina (GEFs) juegan un papel clave en la angiogénesis al activar los cambios morfológicos, la secreción de factores y la migración celular necesarios. En particular, algunos RhoGEFs como PDZ RhoGEF y p115 RhoGEF promueven la angiogénesis tumoral y juegan un papel en procesos
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Aspectos relevantes de la alimentación de los mexicanos
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Médico internista. Hosp. Especialidades de la CdMx “Dr. Belisario Domínguez”
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa de Nutrición
Regulación del balance energético (integración de señales)
MNA. Carlos Miguel Avendaño Villela
Depto. de Salud, Universidad Iberoamericana
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
TALLER: Aspectos psicológicos en el abordaje del paciente con
obesidad y síndrome metabólico que favorezcan o no la
adherencia terapéutica
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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.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
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Nefropatía diabética. Nuevos aspectos
1. US Renal Data System- Incidence of ESRD by Primary Diagnosis.
La diabetes es la principal causa de insuficiencia renal en fase substitutiva
2. Mecanismos implicados en el daño renal y la expansión mesangial en la nefropatía
diabética
• Activación de PKC y MAPK
• Aumento de la formación de productos de Amadori.
• Aumento de formación de productos avanzados de glucación. (AGES)
• Aumento del flujo de glucosa a través de la vía de los polioles.
• Incremento de la vía de aldosa reductasa.
• Aumento del paso de glucosa por la vía de las hexosaminas.
• Aumento de producción de tromboxane y otros eicosanoides.
• Aumento del estrés oxidativo y de carbonilos.
• Aumento de la producción renal de factores de crecimiento proescleróticos TGF-
β, PDGF, IGF-1, HGF, substancias vasoactivas: Ang-II, ET-1 y quimiocinas (IL-8,
MCP-1)
Sperling MA. Type 1 Diabetes, Etiology and Treatment 2003. Humana Press
SINDROME METABOLICO
3. Specific classes of oral hypoglycemic and hypolipidemic agents
are associated with renoprotective effects. RAS blockade
remains the mainstay of treatment. Novel agents that target
different pathophysiologic pathways in diabetic nephropathy
are being investigated.
Algunas medidas orientadas al control de la nefropatía diabética
Dounousi E, et al. Rev Diabet Stud (2015) 12:119-133
4. Esquema preventivo y terapéutico en la nefropatía diabetica
Intervención Meta
Tratamiento renoprotector
ACEi o BRA(Evitar combinar ACEi y BRA) Meta < 130/80 en algunos casos resistentes < 140/90
Antihipertensivo Utilizar en casos con Proteína urinaria de 0.5-1 g/d
TFG que disminuye > 2 ml/min/año
Control glucémico Hba1c 7 %
Restricción de proteínas 0.8 g/Kg/día en TFG < 30 ml/min/1.73m2
Protección cardiorenal adicional
Restricción de sal < 5g/día o mayor
Hipolipemiantes <70-100 mg/dl de LDL-C, < 150 mg/dl Tg
Antiplaquetarios Profilaxis de trombosis
Ejercicio Al menos 30 min/día 5 días/semana
Control de peso Perseguir el peso ideal
Tabaquismo Supresión total del hábito
Modificado de: Satirapoj B, Adler SG Kidney Res Clin Pract 2014;33:121–131
Aspirina
6. NUEVAS OPCIONES DE INTERVENCION EN ESTUDIO EN LA NEFROPATIA DIABETICA
• Antiinflamatorios
- Inhibidores de COX y de xantina oxidasa ??
-Inhibidores de la proteina quimioatrayente de monocitos-1 (MCP-1)
- Inhibidores de TNF-α
-Señalización de NF-β
• Inhibidores de PKC
• Inhibidores de HMG-CoA reductasa
• Papel de receptores de endotelina en la ND
• Señalización Wnt en ND
• Antioxidantes e inhibidores de estrés del retículo
endoplásmico.
• Nuevos enfoques moleculares
-Micro RNAs
- Mecanismos epigenéticos en la ND
7. PAPEL DE COX Y PGE2 EN LA NEFROPATIA DIABETICA
Sharma D et al. Diab Res Clin Pract 2017;1 2 8: 9 1 –1 0 8
PLA2: Phospholipase A2; PGE2: Prostaglandin E2;
COX-1 and COX-2: Cyclooxygenase-1 and 2; EP
receptors: Prostaglandin E2 receptors.
EP Receptors: Receptores de Prostanoides
La inhibición de COX-2 podría tener efectos
benéficos debido a la inhibición de COX-2 en
podocitos y atenuación de la hiperfilttración.
El papel de COX-2 en el daño renal puede
depender de las fuentes de origen de COX, el
mecanismo del daño renal y la expresión y el
subtipo de los receptores de PGE asi como el
momento de la inhibición de COX-2
8. COX-2–selective NSAIDs can cause acute renal failure and should be
avoided or at least used cautiously for short periods of time (with close
monitoring) in patients with chronic renal insufficiency.
In addition, randomized, prospective studies should be undertaken to
evaluate the renal safety of COX-2 selective agents compared with
nonselective COX inhibitors in a large number of high-risk patients.
American Journal of Kidney Diseases, Vol 35, No 5 (May), 2000:
pp 937-940
COX inhibition, reduces proteinuria in patients with kidney disease.
However, by diminishing renal blood flow and intraglomerular pressure
it may also precipitate acute kidney injury in predisposed individuals.
Whether therapeutically targeting pathway members that lie
downstream of the COX enzymes themselves can alter the natural
history of kidney disease remains uncertain.
Inhibicion de prostaglandinas y nefropatía diabética
ONO-AE3-208 (selective inhibitor of EP4) prevents podocyte dedifferentiation induced by transforming growth factor-ß1 (TGF-ß1). The
difference in the renal effects of ONO-AE3-208 and captopril, despite both being accompanied by an equivalent reduction in albuminuria,
suggested to us that the reno-protective effects of EP4 inhibition are not limited to actions on hemodynamic forces. Likewise, the observation
that the reno-protective effect of ONO-AE3-208 was also apparent in non-diabetic SNx rats suggested to us that this effect was also not
restricted to high glucose mediated events. Scientific Reports | 7: 3442 | DOI:10.1038/s41598-017-03237-3 June 2017
9. • HIPERGLUCEMIA
• OBESIDAD FACTORES DE
CRECIMIENTO
• AUMENTO DE AGNE
• LIGANDOS CELULARES
• HIPERTENSION
• CITOCINAS
TLR: Toll-like receptors
MCP-1: Proteina quimioatrayente de
monocitos-1
IL-6: Interleucina-1
NF-β: Factor nuclear β
INFLUENCIA DE DIVERSOS FACTORES SOBRE NF-β
NF-β is a protein complex that
controls transcription of DNA,
cytokine production and cell survival.
NF-κB is found in almost all animal
cell types and is involved in cellular
responses to stimuli such as stress,
cytokines, free radicals, heavy metals,
ultraviolet irradiation, oxidized LDL,
and bacterial or viral antigen
10. eNOS ET-1 VEGF PAI-1 NF-B NAD (P) H OXIDASAS
TGF-
Colágena
Fibronectina
fibrinolisis
ROS
Flujo
sanguíneo
anormal
Permeabilidad
Vascular
Angiogénesis
Oclusión
Capilar
Oclusión
vascular
Expresión de
Genes
proinflamatorios
Efectos
Múltiples
HIPERGLUCEMIA
DIACILGLICEROL
DE FORMAS Y DE PKC
11. Have been associated with vascular alterations such as
increases in:
• Permeability
• Contractility
• Extracellular matrix synthesis
• Cell growth and apoptosis
• Angiogenesis,
• Leukocyte adhesión
• Cytokine activation and inhibition.
Linked to
• Development of pathologies affecting Large vessels
(atherosclerosis, cardiomyopathy) and
• Small vessels
(retinopathy, nephropathy and neuropathy)
PKC:Diversas isoformas:
PKC-α, PKC-β 1 / 2 Y PKC-
12. EFECTO DE LA RUBOXISTAURIN (INHIBIDOR ESPECIFICO DE PKC EN LA NEFROPATIA
DIABETICA
Tuttle KR, et al. Am J Kidney Dis. 2015;65(4):632-638
13. The single pivotal study provided only marginal evidence of efficacy in the ITT population. This was not confirmed in the population of
completers or per protocol. Thus, the study does not provide robust evidence of efficacy and does not comply with the CHMP “Points to
consider document” on application with 1. Meta-analysis; 2. One Pivotal study (CPMP/EWP/2330/99). Further confirmatory evidence of efficacy
is required.
• There was a concern regarding QT prolongation with ruboxistaurin.
• There is a concern regarding CPK increase with RBX and in particular
possible interactions with statins.
• Further, the interaction with tricyclic anti-depressants, neuroleptics
and other non anti-arrhythmic QT prolonging drugs, in view of possible
additive/synergistic effects on Q-T interval prolongation is a matter of
concern.
14. Role of inflammatory cascade and its inhibition by 3-Hydroxy-3-methylglutaryl coenzyme A
(HMG-COA) reductase
PAI-1, ECM and
eNOS) in kidney which finally leads to kidney
damage.
ECM: Extracellular matrix; PAI-1: Plasminogen
activator inhibitor-1;
eNOS: Endothelial nitric oxide synthase.
The small GTP-binding proteins Ras
and Rac1 are molecular switches
exchanging GDP for GTP and
converting external signals in
response to a variety of stimuli.
Ras and Rac1 play an important
role in cell proliferation, cell
differentiation, and cell migration.
Rac1 is directly involved in the
reorganization and changes in the
cytoskeleton during cell motility.
Nitric oxide (NO) stimulates the
Ras – ERK1/2 MAP kinases
15. EFECTOS DE ANGIOTENSINA II Y ENDOTELINA EN RIÑON
Am J Physiol Regul Integr Comp
Physiol 2016; 310: R877–R884
17. Egido J , Rojas-Rivera J, et al. Expert Opinion on Investigational Drugs 2017 doi.org/10.1080/13543784.2017.1325872
EFECTO PROTECTOR DE INHIBIDORES DE ET R EN NEFROPATIA DIABETICA
ATRESANTAN BOSENTAN
Atresantan produce aumento
de peso, retención de lÍquidos
y disminución de hemoglobina
en pacientes con DM y
nefropatía sin embargo sin
evidencia significativa de
edema o insuficiencia cardiaca.
DISMINUCION DE
ALBUMINURIA Y PROTECCIÓN
RENAL
19. MECANISMOS EPIGENETICOS EN NEFROPATIA DIABETICA
TGF-β:Transforming growth
factorβ; RAAS: Renin
angiotensin aldosterone
system; PKC: Protein kinase
C; AGEs: Advanced
glycation end produc
20.
21.
22. The RAS including the novel ACE2/Ang(1–7) axis
Karnik SS. British Journal of Pharmacology (2017) 174 737–753 737
23. Efectos potenciales de ACE2 y angiotensina 1-7 sobre la regulación de la presión arterial
Nat. Rev. Cardiol. 11, 413–426 (2014)
24. POSIBLES APLICACIONES EN MEDICINA DE LA ANGIOTENSINA 1-7
Passos-Silva DG, verano-Braga T, Santos RAS. Clinical Science 2013;124:443-456
25. Padda RS, et al. J Diabetes Metab. 2015; 6
Angiotensina 1-7 en la nefropatía diabética
26. CONCEPTO ACTUAL DE LOS RECEPTORES A ANGIOTENSINA 1-7
British Journal of Pharmacology (2017) 174 737–753
27. Los riñones de ratones db/db muestran aumento de la acetilación de FOXO1, y disminución de SIRTUINA1
y PPARα que fueron completamente revertidos por tratamiento con angiotensina 1-7
28. LA AMPLIFICACION DEL RECEPTOR DE ANGIOTENSINA 1-7 NO PROTEGE A LOS RATONES DEL
DESARROLLO DE NEFROPATIA DIABETICA
Wyzoki J, et al. Kidney international 2016
30. REPRESENTACION ESQUEMATICA DEL ESTADO DE MARCADORES DE ESTRÉS OXIDATIVO EN
PRESENCIA DE DIABETES
MDA: malondialdehyde, AOPP: Advanced oxidation protein
products, PCO: protein carbonyls, GSH: reduced glutathione,
and SOD: superoxide dismutase.
Existe un aumento de oxidación y
una disminución del sistema
antioxidante
Journal of Biomarkers 2013http://dx.doi.org/10.1155/2013/378790
31. ESTRÉS OXIDATIVO Y RESPUESTAS CELULARES
Japan Medical Association Journal 2002; 45: 271
32. Deen WM. J. Clin. Invest. 114:1412–1414
Glomerular capillary wall, consisting principally of a fenestrated endothelium, a basement membrane, and epithelial foot
processes. The foot processes form filtration slits spanned by slit diaphragms. Also shown is the endothelial cell coat, or
glycocalyx. Some approximate dimensions are (8, 10): minimum diameter of fenestra, 30 nm; GBM thickness, 200–400 nm
(depending on species); width of filtration slit, 40 nm. The glycocalyx thickness is uncertain
33. P = Podocitos. Las flechas indican la localización de la nefrina
GBM = Membrana basal glomerular
LOCALIZACION GLOMERULAR DE LA NEFRINA (MICROSCOPIA ELECTRÓNICA) EN LAS HENDIDURAS DIAFRAGMATICAS.
DE LOS PODOCITOS
Ruotsalainen V, Jungberg L, Wartiovaara P, et al Proc Nat Acad Sci USA 1999; 96: 7962
34. Toyoda M, Suzuki D, Umezono T, et al, Nephrol Dial Transplant 2004; 19: 380–385
EXPRESIÓN DEL RNAm DE LA NEFRINA HUMANA EN LA NEFROPATIA DIABÉTICA
39. Señales de insulina, inflamación y señales de estrés
En presencia de resistencia a la insulina, mediadores inflamatorios y lípidos activan una cascada de señales que dispara cinasas
inflamatorias como JNK e IKK asi como PKC,S6K,mTOR y ERK. La activación de JNK e IKK resulta en la inhibición de la acción
de insulina en parte a través de la fosforilación en la serina de los substratos del receptor de insulina (IRS) 1 y 2. La energía del
exceso de nutrientes puede inducir estrés del retículo endoplásmico que esta directamente ligado a la activación de vías
inflamatorias que a su vez bloquean la acción de la insulina y regulan transcripcionalmente la producción de citocinas
inflamatorias. Los ROS que se producen durante el estrés de organelos y disfunción mitocondrial contribuyen a estos efectos. La
consecuencias finales son estrés del RE, aumento de la inflamación, inhibición de la acción de insulina y posiblemente de la
acción de Leptina que culminan en disfunción metabólica.
40. Cell 2010;140: 900–917
Hotamisligil GKS
Factores que pueden afectar el funcionamiento del retículo endoplásmico
Failure of the ER’s adaptive capacity results in activation of the unfolded protein response (UPR), which
intersects with many different inflammatory and stress signaling pathways. These pathways are also critical
in chronic metabolic diseases such as obesity, insulin resistance, and type 2 diabetes. The ER and related
signaling networks are emerging as a potential site for the intersection of inflammation and metabolic
disease.
Falla de la capacidad adaptativa del reticuloendoplásmico (ER) resulta en activación de la respuesta de proteínas no
plegadas (UPR) que es afectada por diferentes vías y señales de señalamiento de estrés. Estas vías también son críticas en
enfermedades metabólicas crónicas tales como obesidad, resistencia a la insulina y DMT2. El RE y las redes de
señalamiento están emergiendo como un posible sitio de importancia en enfermedades metabólicas e inflamatorias.
41. Endoplasmic reticulum (ER) stress response
The UPR has three aims: initially to
restore normal function of the cell by
halting protein translation, degrading
misfolded proteins, and activating the
signaling pathways that lead to
increasing the production of
molecular chaperones involved
in protein folding. If these objectives
are not achieved within a certain time
span or the disruption is prolonged,
the UPR aims towards apoptosis.
UPR = Unfolded protein response
PERK function is essential for cell survival following exposure of cells to ER stress, but the mechanisms whereby
PERK signaling promotes cell survival are not thoroughly understood. We have identified the Nrf2 transcription
factor as a novel PERK substrate
IRE1: ER stress sensor and cell fate executor
ATF6 is an endoplasmic reticulum (ER) membrane-anchored transcription factor
42. Al unirse oxLDL al receptor escavenger CD36 dispara la activación de la transcripción del factor PPARγ lo que induce a una
presentación aumentada del receptor en la superficie del macrófago. NFB también es estimulado por oxLDL induciendo la
síntesis de diversas citocinas. Además oxLDL desencadena la activación de cinasas relacionadas con CD36 tales como Lyn,MEKK2,
JNK1 y JNK2
Efecto de oxLDL sobre macrófagos via el receptor scavenger CD36,
NF-kB (factor nuclear potenciador de las cadenas ligeras kappa de las células B activadas) es un complejo proteico que controla la transcripción del ADN. NF-kB se
encuentra en la mayoría de tipos de células animales y está implicado en la respuesta celular frente a estímulos como el estrés, las citoquinas, radiación
ultravioleta, LDL oxidadas y antígenos bacterianos o virales
43. Consequences of VEGF-A increase in diabetic nephropathy
VEGF-induced thickening and distortion of podocyte foot processes in
diabetic mice, observed by scanning electron microscopy. A) Control
diabetic glomerulus; B) Vegf164 overexpressing glomerulus showing
wider foot processes. Scale bars=2 μm.
Tufro A, Veron D,
Semin Nephrol. 2012 July ; 32(4): 385–393.
VEGF-A increases TGFβ, CTGF and established a positive feedback loop, leading to extracellular matrix (ECM) accumulation and GBM
thickening (orange); VEGF-A induces nephrin downregulation and foot process effacement (FPE) (green); VEGF-A stimulates eNOS,
which in the setting of high ROS leads to peroxinitrite (ONOO−) and further ROS generation, a positive feedback loop (blue), the
dashed line represents the normal negative feedback regulation of VEGF-A by NO, not operative in DN. Low NO and high ROS
damage endothelial cells and induce HTN.
44. Vitamin D binding to VDR inhibits targets responsible for declining renal function. The combined inhibition of heparanase
and the RAA axis has proved capable of controlling the onset of proteinuria. In addition, the combined inhibition of
heparanase and the TGFβ pathway may prevent the progression of fibrosis mediated by tubular epithelial–mesenchymal
transi
EFECTO DE VITAMINA D EN LA NEFROPATIA DIABETICA
Masola V et al. J Pathol 2016;238: 7-9
45. Mechanism by which uric acid contributes to the development of
renal and non-renal diseases. RAS, renin–angiotensin system.
Johnson RJ , Nakagawa T, Jalal D , Sánchez-Lozada LG et al.
Nephrol Dial Transplant 2013; 28: 2221–2228
46. Patel1 SR, Malhotra A, White DP, Gottlieb DJ. Et al. Am J Epidemiol. 2006;
164: 947–954.
Mean age-adjusted weight of the Nurses’ Health Study cohort from 1986 to 2002 as a function of
habitual sleep duration
Patel et al.
In analyses adjusted for age and body mass
index, women sleeping 5 hours or less gained 1.14
kg (95% (CI): 0.49, 1.79) more than did those sleeping 7
hours over 16 years, and women sleeping 6 hours
gained 0.71 kg (95% CI: 0.41, 1.00) more.
The relative risks of a 15-kg weight gain were 1.32
(95% CI: 1.19,1.47) and 1.12 (95% CI: 1.06, 1.19) for those
sleeping 5 and 6 hours, respectively. The relative
risks for incident obesity (body mass index: >30
kg/m2) were 1.15 (95% CI: 1.04, 1.26) and 1.06 (95% CI:
1.01, 1.11).
These associations remained significant after
inclusion of important covariates and were not
affected by adjustment for physical activity or
dietary consumption
47. Hydration and Chronic Kidney Disease Progression: A Critical Review of the Evidence
Am J Nephrol 2016;43:281–292
Clark WF, Sontrop JM, Huang SH
48. A number of experimental studies in rats and a few observations in humans suggest
that vasopressin increases GFR and albuminuria, thus inducing a vicious circle as suggested
by Brenner for a high protein diet. Adapted from Brenner.
Am J Nephrol 2016;43:281–292
49. Prevalencia de patrón A o B de acuerdo con la proporción de hidratos de carbono en la dieta
Ronald M Krauss
Annu. Rev. Nutr. 2001. 21:283–95
Men with a predominance of small, dense LDL (pattern B) on the high-fat diet (n D 18) exhibited a twofold greater reduction
in LDL cholesterol than did pattern A men. This was associated with significantly greater reductions in mass of midsized
(LDL2) and small (LDL3) LDL subfractions measured by analytic ultracentrifugation. Only pattern B subjects showed
significant reductions in plasma apoB, and in LDL relative to HDL cholesterol levels
Patron A No aterogénico sin hiperlipidemia
postprandial.
Patron B Aterogénico con hiperlipidemia
postprandial
50. Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats
Laura G. Sanchez-Lozada,1 Edilia Tapia,1 Adriana Jiménez,1 Pablo Bautista,1 Magdalena Cristobal,1 Tomas Nepomuceno,1 Virgilia Soto,2 Carmen Avila-Casado,2 Takahiko
Nakagawa,3 Richard J. Johnson,3 Jaime Herrera-Acosta,1† and Martha Franco1
In the present study, plasma UA levels correlated with fructose ingestion even in
individual animals as demonstrated by the positive correlation between %
fructose caloric intake and UA at week 8. Previously, we demonstrated that rats
made hyperuricemic by inhibiting uricase with oxonic acid had increased blood
pressure, afferent arteriole thickening,glomerular hypertension, and cortical
vasoconstriction (29). In the present study, we found positive linear relationships
between plasma uric acid and SBP (r 0.54, P 0.01) and arteriolar area (r 0.64, P
0.001) and a negative correlation with ultrafiltration coefficient, a marker of
glomerular vasoconstriction(r 0.41, P 0.05). Therefore, higher UA levels induced
by 60% fructose diet may be partially responsible for the glomerular
hemodynamic alteration
Am J Physiol Renal Physiol 292: F423–F429, 2007.
Departments of 1Nephrology and 2Pathology, Instituto Nacional de Cardiología Ignacio Chávez,
Mexico City, Mexico; and 3Nephrology, Hypertension and Transplantation, University of Florida,
Gainesville, Florida
51. Hazard ratios greater than 1 demonstrate an increased risk for composite outcome with sulfonylurea compared with
metformin.
ACEi=angiotensinconverting enzyme inhibitor;
ARB=angiotensin receptor blocker.
N Engl J Med 2008; 359: 1577–15
METFORMIN SULFONYLUREA
Adjusted hazard ratios for the composite outcome of glomerular filtration rate event or end-stage renal
disease among age, race, HbA1c, and renin–angiotensin– aldosterone system blockade subgroups
Kidney International 2012; 81: 698–706
52. Número de eventos, personas/año, tasas e índices de riesgo ajustados por cada resultado final en relación
con medicamentos antidiabéticos
469 688 participantes con DM tipo 2 edades 25-84 entre abril 2007 a enero de 2015
Hippisley-Cox J, Coupland C. BMJ 2016;352
Hazard ratios adjusted for: sex; age; calendar year; duration since diagnosis of diabetes (five levels); ethnicity (nine levels); Townsend deprivation score; smoking status (five levels); use of
anticoagulants, thiazides, ACE inhibitors, angiotensin 2 blockers; calcium channel blockers; statins; aspirin; existing complications (blindness, hyperglycaemia, hypoglycaemia, amputation, severe
kidney failure); hypertension; cardiovascular disease; atrial fibrillation; chronic renal disease; rheumatoid arthritis; valvular heart disease; peripheral vascular disease; body mass index; systolic
blood pressure; HbA1c; serum creatinine; cholesterol:high density lipoprotein ratio. Hazard ratios also mutually adjusted for use of each of the other diabetes drug classes.
BLINDNESS
RENAL FAILURE
53. Número de eventos, personas/año, tasas e índices de riesgo ajustados por cada resultado final en relación
con medicamentos antidiabéticos
469 688 participantes con DM tipo 2 edades 25-84 entre abril 2007 a enero de 2015
Hippisley-Cox J, Coupland C. BMJ 2016;352
Hazard ratios adjusted for: sex; age; calendar year; duration since diagnosis of diabetes (five levels); ethnicity (nine levels); Townsend deprivation score; smoking status (five levels); use of
anticoagulants, thiazides, ACE inhibitors, angiotensin 2 blockers; calcium channel blockers; statins; aspirin; existing complications (blindness, hyperglycaemia, hypoglycaemia, amputation, severe
kidney failure); hypertension; cardiovascular disease; atrial fibrillation; chronic renal disease; rheumatoid arthritis; valvular heart disease; peripheral vascular disease; body mass index; systolic
blood pressure; HbA1c; serum creatinine; cholesterol:high density lipoprotein ratio. Hazard ratios also mutually adjusted for use of each of the other diabetes drug classes.
BLINDNESS
RENAL FAILURE
54. Annuzzi G, Bozzetto L, Costabile G et al.
Polyphenols improve fasting and postprandial dyslipidemia and reduce oxidative stress: a randomized controlled
trial1–3
Am J Clin Nutr 2014;99:463–7100
56. Comparación de linagliptina y placebo en varios puntos finales relacionados con nefropatía
Am J Kidney Dis. 2015;66:441-449
Cooper ME, Perkovic V, McGill, JB, et al
57.
58.
59. Lang F. Kidney Blood Press
Res 2017;42:483-494
LA INGESTION SUBOPTIMA DE LIQUIDOS PUEDE AUMENTAR LOS NIVELES DE
VASOPRESINA Y GLUCOCORTICOIDES AUMENTANDO LA EXPRESION DE SGK1
FAVORECIENDO LAS PATOLOGIAS QUE SE SEÑALAN
SGK1: Serine/threonine-protein kinase is also known
as serum and glucocorticoid-regulated kinase 1
NFAT5, is a human gene that encodes a transcription factor that
regulates the expression of genes involved in the osmotic stress
63. Sirtuins target many proteins that are not histones they havebeen demonstrated
to bind and deacetylate p53 in vitro and in vivo [32,33,41]. p53 is transcriptional
activator, and its activation results in cell cycle arrest, senescence or the
initiation of programmed cell death. Over expression of sirtuins has been shown
to inhibit p53-dependent apoptosis in response to DNA damage and oxidative
stress [33]. Recently, it has been reported that increased expression of p53 gene
under diabetic
condition is associated with renal apoptosis [42]. We found increasedexpression
of p53 protein in the kidneys of diabetic animals as compared to their respective
controls. However, the expression of p53 is reduced significantly in the kidneys
of diabetic rats on IF regimen. The expression as well as activationof p53 is
thought to be mediated by Sir2 dependent deacetylation. They both share an
inverse relationship as is evident from our results wherein the Sir2 expression is
decreased and at the same time p53 is upregulated.
Intermittent fasting prevents the progression of type I diabetic nephropathy in rats and
changes the expression of Sir2 and p53
FEBS Letters 581 (2007) 1071–1078
64. TRATAMIENTO POTENCIAL DE LA NEFROPATIA DIABETICA CON ANGIOTENSINA 1-7
Padda RS, et al. J Diabetes Metab. 2015; 6
72. Compared with other types of tea, green tea is
unfermented and contains the highest concentration of
catechins, in which EGCG accounts for as much as 50%
of its total polyphenols and has been reported to
possess antioxidative, antiinflammatory, and
anticarcinogenic effects[EGCG is estimated to be 25
times more potent than vitamin E and 100 times more
potent than vitamin C.
Bao H, Peng A. J Translat Int Med
2016;4: 99-103
EFECTOS DEL TE VERDE COMO
ANTIOXIDANTE EN LA ALBUMINURIA
SEVERAL
MECHANISMS
73. Growth hormone (GH)–GH receptor (GHR)–IGF-1 axis in type 1 diabetes
(1) reduced portal insulin levels results in decreased expression of hepatic GHR, impaired IGF-1 production and elevated
IGFBP-1 levels (2). Low bioavailability of IGF-1 leads to compensatory GH hypersecretion via negative feedback loop
mechanism (3). Except in liver, GHR expression in other tissues including kidney is not compromised. Elevated GH levels
in poorly controlled type 1 diabetes associated with elevated GHR and IGF-1 in the kidney (4). Elevated GH levels are
implicated in the renal hyperfiltration, glomerulosclerosis, nephromegaly, and proteinuria (5).
Frontiers in Medicine 2017: (July )
74. MODELO PROPUESTO DE LA ACCION DE LA HORMONA DE CRECIMIENTO SOBRE LOS
PODOCITOS
Los efectos de GH incluyen: desdiferenciacion de podocitos, engrosamiento y/o formación de puentes cruzados de la membrana basa,l deterioro de
los podocitos y puede producir apoptosis e hipertrofia. Todos estos efectos resultan en disminución del número de podocitos y alteración de la función
glomerular. Este efecto puede verse tanto en la acromegalia como en la diabetes tipo 1.
75.
76. Conclusiones
• Existen múltiples líneas de investigación dirigidas a la fisiopatología, prevención y tratamiento de los pacientes
con nefropatía diabética.
• Varias de estas líneas han establecido conocimientos sólidos, muchos de ellos en animales de experimentación
pero aun con pocos estudios clínicos y aun en etapas tempranas de evaluación.
• Las recomendaciones vigentes siguen siendo las que tienen más bases en estudios controlados.
• El control de la glucemia, de la hipertensión arterial, de los lípidos, el evitar medicamentos nefrotóxicos y
controlar adecuadamente cada elemento del síndrome metabólico siguen siendo los mejores lineamientos en la
prevención y tratamiento de los pacientes con diversos grados de compromiso renal.
• La monitorización del control y las posibles complicaciones a intervalos adecuados es de vital importancia.
• El obtener consejo de los especialistas en nefrología es muy importante para los médicos que tratan pacientes
diabéticos sobre todo cuando ya existe evidencia de compromiso renal.
• Es muy importante que el paciente reciba una educación adecuada en relación con los factores de riesgo de esta
y otras complicaciones de la diabetes, y la necesidad de mantener un control estricto y con los exámenes
pertinentes que permitan valorar sud condiciones de salud, para poder detectar tempranamente esta alteración.