Diabetic nephropathy is a microvascular complication of diabetes that involves the progressive decline of kidney function over time. It is defined by albuminuria and declining renal function in a patient with diabetes without other causes of kidney disease. The pathogenesis is related to chronic hyperglycemia causing structural changes in the glomerulus and kidney. Treatment aims to control blood glucose, blood pressure, lipids, restrict protein intake, and stop smoking to prevent decline or slow progression of kidney disease. Screening for nephropathy involves annual urine and serum tests.
Chronic kidney disease (CKD) involves the progressive and irreversible loss of kidney function over time. It is defined by the presence of kidney damage, pathological abnormalities, or a glomerular filtration rate (GFR) below 60 ml/min for three or more months. CKD affects about 10% of the general population and is associated with increased risk of cardiovascular disease as kidney function declines. The leading causes of CKD include diabetes, hypertension, cardiovascular disease, obesity, age, acute kidney injury, autoimmune diseases, and nephrotoxic medications like NSAIDs. Later stages of CKD may require dialysis or kidney transplantation to replace lost kidney function and prevent further health complications.
Chronic kidney disease (CKD) is defined as gradual loss of kidney function over months to years. Key risk factors include diabetes, hypertension, family history, and smoking. CKD is usually asymptomatic in early stages. Treatment focuses on controlling blood pressure and blood glucose, limiting proteinuria, treating anemia and bone disease, and slowing progression. The goals are to delay complications by optimizing blood pressure control with ACE inhibitors, ARBs, and other agents and managing associated conditions like anemia, dyslipidemia, mineral bone disorders.
Chronic kidney disease (CKD) is the gradual loss of kidney function over time. Early stages have no symptoms, but later stages can cause leg swelling, fatigue, vomiting, appetite loss, or confusion. CKD is classified into 5 stages based on glomerular filtration rate. It has many causes like diabetes, hypertension, glomerulonephritis. Symptoms include high blood pressure, azotemia, hyperkalemia, anemia, and fluid overload. Diagnosis involves medical history, physical exam, urine test, and ultrasound. Treatment focuses on controlling symptoms through diet, medication, dialysis, and possibly kidney transplant. Those with advanced CKD may need referral to a kidney specialist.
This document discusses diabetic nephropathy, which affects 300 million people worldwide and is a leading cause of end-stage renal disease. It progresses through 5 stages from early diabetes with hyperfiltration to end-stage renal disease requiring renal replacement therapy. Screening involves testing for microalbuminuria and management focuses on strict glycemic and blood pressure control as well as ACE inhibitors or ARBs to preserve kidney function. The goal is to prevent progression of kidney damage through lifestyle modifications and medical treatment.
Approach and management of chronic kidney disease sandeepMohit Aggarwal
Chronic kidney disease is a spectrum of conditions associated with progressive kidney function decline and damage. It is increasingly prevalent due to rising rates of diabetes and hypertension. Management involves identifying the underlying cause, calculating GFR to stage severity, investigating for complications, and slowing progression. Treatment focuses on managing complications through diet, medication, and preparing patients for renal replacement therapies like dialysis and transplantation if kidney failure occurs. The goal is optimizing quality of life and outcomes through a coordinated multidisciplinary approach.
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.
Chronic kidney disease (CKD) involves the progressive and irreversible loss of kidney function over time. It is defined by the presence of kidney damage, pathological abnormalities, or a glomerular filtration rate (GFR) below 60 ml/min for three or more months. CKD affects about 10% of the general population and is associated with increased risk of cardiovascular disease as kidney function declines. The leading causes of CKD include diabetes, hypertension, cardiovascular disease, obesity, age, acute kidney injury, autoimmune diseases, and nephrotoxic medications like NSAIDs. Later stages of CKD may require dialysis or kidney transplantation to replace lost kidney function and prevent further health complications.
Chronic kidney disease (CKD) is defined as gradual loss of kidney function over months to years. Key risk factors include diabetes, hypertension, family history, and smoking. CKD is usually asymptomatic in early stages. Treatment focuses on controlling blood pressure and blood glucose, limiting proteinuria, treating anemia and bone disease, and slowing progression. The goals are to delay complications by optimizing blood pressure control with ACE inhibitors, ARBs, and other agents and managing associated conditions like anemia, dyslipidemia, mineral bone disorders.
Chronic kidney disease (CKD) is the gradual loss of kidney function over time. Early stages have no symptoms, but later stages can cause leg swelling, fatigue, vomiting, appetite loss, or confusion. CKD is classified into 5 stages based on glomerular filtration rate. It has many causes like diabetes, hypertension, glomerulonephritis. Symptoms include high blood pressure, azotemia, hyperkalemia, anemia, and fluid overload. Diagnosis involves medical history, physical exam, urine test, and ultrasound. Treatment focuses on controlling symptoms through diet, medication, dialysis, and possibly kidney transplant. Those with advanced CKD may need referral to a kidney specialist.
This document discusses diabetic nephropathy, which affects 300 million people worldwide and is a leading cause of end-stage renal disease. It progresses through 5 stages from early diabetes with hyperfiltration to end-stage renal disease requiring renal replacement therapy. Screening involves testing for microalbuminuria and management focuses on strict glycemic and blood pressure control as well as ACE inhibitors or ARBs to preserve kidney function. The goal is to prevent progression of kidney damage through lifestyle modifications and medical treatment.
Approach and management of chronic kidney disease sandeepMohit Aggarwal
Chronic kidney disease is a spectrum of conditions associated with progressive kidney function decline and damage. It is increasingly prevalent due to rising rates of diabetes and hypertension. Management involves identifying the underlying cause, calculating GFR to stage severity, investigating for complications, and slowing progression. Treatment focuses on managing complications through diet, medication, and preparing patients for renal replacement therapies like dialysis and transplantation if kidney failure occurs. The goal is optimizing quality of life and outcomes through a coordinated multidisciplinary approach.
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.
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting over 3 months. CKD is evaluated based on glomerular filtration rate (GFR) and markers of kidney damage. Progression is defined as a sustained decline in GFR or a 25% drop from baseline. Management focuses on preventing progression through blood pressure control, ACE inhibitors/ARBs, glycemic control, salt restriction, and lifestyle changes like exercise and smoking cessation. Complications include anemia, bone disease, vitamin D deficiency, acidosis, cardiovascular disease, and increased risk of infection. Dialysis is initiated when symptoms develop or control of volume, pressure, or nutrition cannot be maintained.
Chronic glomerulonephritis is characterized by progressive scarring of the glomeruli and kidneys that leads to reduced kidney function over time. If left untreated, it can progress to end-stage renal disease requiring dialysis or kidney transplantation. The rate of progression depends on the underlying cause of the chronic glomerulonephritis. Treatment aims to slow progression through controlling blood pressure and proteinuria with ACE inhibitors, ARBs, and other medications. Dietary modifications and management of complications help preserve kidney function for as long as possible.
1) Diabetic nephropathy is characterized by persistent albuminuria, declining GFR, and presence of retinopathy. It involves thickening of basement membranes and expansion of the mesangial matrix.
2) It progresses through five stages from hyperfiltration to end-stage renal disease. Glycemic control, blood pressure management, and ACE inhibitors or ARBs can slow its progression.
3) Treatment involves tight glycemic and blood pressure control, lipid lowering, dietary protein restriction, anemia management, and renal replacement therapy through hemodialysis, peritoneal dialysis, or transplantation if end-stage is reached.
1) Diabetic nephropathy is characterized by persistent albuminuria, declining GFR, and presence of retinopathy. It involves thickening of basement membranes and expansion of the mesangial matrix.
2) It progresses through five stages from hyperfiltration to end-stage renal disease. Glycemic control, blood pressure management, and ACE inhibitors or ARBs can slow progression.
3) For patients reaching end-stage renal disease, treatment options include hemodialysis, peritoneal dialysis, and kidney transplantation. Kidney transplantation has the best outcomes, but survival is still worse for diabetics than non-diabetics.
This document summarizes chronic kidney disease (CKD), dividing it into 5 stages based on glomerular filtration rate (GFR). It describes the etiologies of CKD including primary and secondary glomerular diseases, tubulointerstitial nephritis, obstructive nephropathies, vascular diseases, and hereditary diseases. The clinical features of CKD include fluid and electrolyte imbalance, acid-base disturbances, uremia, disturbances in calcium and phosphate metabolism, anemia, hypertension, dyslipidemia, endocrine dysfunction, and growth impairment. Management involves treating the underlying cause, slowing progression with ACE inhibitors, and treating complications like anemia, fluid overload, hyperkalemia, metabolic acid
This document discusses chronic kidney disease (CKD) in pediatrics. It defines CKD as kidney damage lasting at least 3 months as determined by structural abnormalities and/or a glomerular filtration rate below 60 mL/min/1.73m2. The stages of CKD are described based on GFR. Common causes in children include congenital abnormalities and glomerulonephritis. The pathogenesis involves hyperfiltration injury and other factors like proteinuria that accelerate kidney damage. Management aims to address complications through careful monitoring, nutrition, treatment of mineral bone disorders, and controlling blood pressure and electrolyte abnormalities.
Chapter 6 Endocrine disorders by Dr. DerejepdfRebiraWorkineh
Chronic kidney disease (CKD) is common in patients with diabetes and is diagnosed through elevated albuminuria and reduced estimated glomerular filtration rate (eGFR). CKD attributed to diabetes occurs in 20-40% of patients and can progress to end-stage renal disease requiring dialysis. Diabetic retinopathy, caused by chronic hyperglycemia, is the most common cause of blindness and is assessed through eye exams. Neuropathy is assessed through history and examination of sensation, with annual 10-g monofilament testing to check for high-risk feet. Foot care includes inspection, assessment of deformities and pulses, and referral for ongoing surveillance in high-risk patients to prevent ulcers and amputations.
- Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is usually caused by primary glomerular disease but can be secondary to other medical conditions.
- Diagnosis requires proteinuria >3.5g/day and hypoalbuminemia <2.5g/dL. Management involves salt and fluid restriction, diuretics, ACE inhibitors to reduce proteinuria, and corticosteroids which induce remission in 80-90% of adults. Frequent relapses or steroid resistance may require additional immunosuppressive drugs. Complications include infection, thromboembolism, and renal failure.
This document provides an overview of the management of chronic kidney disease (CKD). It defines CKD and outlines its classification based on cause, glomerular filtration rate, and albuminuria levels. The epidemiology, pathophysiology, clinical features, diagnostic evaluation, and management of CKD are discussed. Treatment aims to address reversible causes, prevent disease progression, and manage complications. Referral to a nephrologist is recommended for advanced CKD stages or complex cases.
This document provides an overview of the management of chronic kidney disease (CKD). It defines CKD and outlines criteria for diagnosis based on markers of kidney damage and glomerular filtration rate (GFR). It describes tools for screening and staging CKD, including estimated GFR (eGFR) calculators and urine albumin-to-creatinine ratio. Common clinical manifestations of CKD like fluid and electrolyte disorders, anemia, bone disease, and cardiovascular complications are summarized. Treatment strategies are covered for managing complications involving hypertension, acid-base abnormalities, mineral and bone disorders, anemia, and diabetes in CKD patients.
Chronic kidney disease (CKD) is defined as kidney damage or decreased kidney function that lasts for at least 3 months. It is a progressive loss of kidney function over time that can lead to complications if left untreated. CKD is caused by conditions that damage the kidneys such as diabetes and hypertension. Symptoms are often vague until later stages when kidney function is significantly decreased. Treatment focuses on controlling blood pressure and blood sugars to slow the progression of kidney damage.
This document provides information about diabetes mellitus. It begins with an introduction and overview of diabetes symptoms and complications. It then discusses the different types of diabetes (type 1, type 2, gestational, pre-diabetes), diagnosis methods, and treatment options including medications like insulin, sulfonylureas, thiazolidinediones, biguanides, and meglitinides. Complications of diabetes such as retinopathy, neuropathy, and nephropathy are also summarized. The document provides details on diabetes prevalence globally and risk factors. It concludes with descriptions of hypoglycemia and diabetic ketoacidosis.
This document provides information on managing renal failure in primary care. It presents a case study of a 46-year-old woman with chronic kidney disease due to uncontrolled diabetes and hypertension. Key steps in management include controlling blood pressure and diabetes, addressing complications like anemia and bone disease, and referring to nephrology if glomerular filtration rate drops below 30 or complications require treatment. The take-home message is that lifestyle modification, monitoring for complications, and early nephrology referral can help slow chronic kidney disease progression.
1) Hyperfiltration of remaining nephrons following renal surgery or transplantation can lead to progressive kidney damage over time due to increased workload.
2) Multiple factors like diabetes, hypertension, genetic diseases, and various glomerular diseases can promote hyperfiltration injury through mechanical and metabolic effects on the kidneys.
3) Management strategies aim to prevent or reduce hyperfiltration through measures like low-protein diets, weight loss, ACE inhibitors, lipid lowering agents, and calcium channel blockers to protect kidney function long-term.
This document summarizes chronic kidney disease (CKD), defining it as abnormalities of kidney structure or function lasting over 3 months that impact health. CKD is classified based on cause, glomerular filtration rate (GFR) category, and albuminuria levels. Key aspects of CKD addressed include pathophysiology, GFR estimation and staging, risk factors, clinical abnormalities associated with decreased kidney function like fluid/electrolyte issues and anemia, leading causes, and management including treating complications and renal replacement therapy for late stages.
This document provides information on chronic kidney disease (CKD) and dialysis. It discusses:
1. The functions of the kidneys and how CKD develops due to gradual loss of kidney function over time.
2. The stages of CKD progression and treatment strategies at each stage, including managing risk factors, complications, and preparing for renal replacement therapy.
3. The two main types of renal replacement therapy - hemodialysis which uses an artificial kidney to filter waste from the blood, and peritoneal dialysis which uses the peritoneal membrane in the abdomen.
- A 55-year-old woman presented with swelling of the face and lower limbs for one month, as well as shortness of breath on exertion for 20 days and decreased appetite.
- Investigations showed nephrotic range proteinuria, hypoalbuminemia, and a renal biopsy consistent with minimal change disease.
- Minimal change disease should be considered and treatment involves corticosteroids, with frequent monitoring due to the risk of relapses.
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function present for more than 3 months. CKD is staged based on glomerular filtration rate (GFR) from stage 1 (normal or high GFR) to stage 5 (kidney failure). Common causes of CKD in India include diabetes, hypertension, and glomerulonephritis. Symptoms vary depending on stage but may include fatigue, pruritus, nausea, and electrolyte imbalances. Treatment includes controlling risk factors, nutritional management, dialysis if needed, and potentially kidney transplantation for end stage renal disease.
Chronic kidney disease ppt presentation for classsumathiparagati
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function present for more than 3 months. CKD is staged based on glomerular filtration rate from stage 1 to 5. The leading causes of CKD in India are diabetes, hypertension, and glomerulonephritis. Treatment includes controlling risk factors, nutritional therapy, dialysis, and kidney transplantation. Dialysis techniques include hemodialysis and peritoneal dialysis. Kidney transplantation is the treatment of choice for end-stage renal disease but requires lifelong immunosuppression.
1. The document discusses conditions other than cirrhosis that can result in diffuse surface nodularity of the liver or portal hypertension such as chronic Budd-Chiari syndrome, chronic portal vein thrombosis, sarcoidosis, and pseudocirrhosis of treated breast cancer metastases or fulminant hepatic failure.
2. It provides imaging examples and characteristics of these non-cirrhotic conditions that can mimic cirrhosis on imaging. For example, pseudocirrhosis of treated breast cancer metastases shows diffuse hepatic nodularity and signs of portal hypertension but the history of breast cancer and prior imaging helps identify the correct diagnosis.
3. Nodular regenerative hyperplasia, congenital hepatic fibrosis, and
This document summarizes ultrasound findings for cirrhosis of the liver. Key findings include coarse echotexture and nodular surface of the liver. Regenerating nodules appear isoechoic or hypoechoic. Portal hypertension is a complication and is evidenced by dilated portal veins, low portal flow, and portosystemic collaterals visible on ultrasound. Doppler ultrasound can detect changes in portal flow from normal hepatopetal to reversed hepatofugal flow in advanced cases.
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting over 3 months. CKD is evaluated based on glomerular filtration rate (GFR) and markers of kidney damage. Progression is defined as a sustained decline in GFR or a 25% drop from baseline. Management focuses on preventing progression through blood pressure control, ACE inhibitors/ARBs, glycemic control, salt restriction, and lifestyle changes like exercise and smoking cessation. Complications include anemia, bone disease, vitamin D deficiency, acidosis, cardiovascular disease, and increased risk of infection. Dialysis is initiated when symptoms develop or control of volume, pressure, or nutrition cannot be maintained.
Chronic glomerulonephritis is characterized by progressive scarring of the glomeruli and kidneys that leads to reduced kidney function over time. If left untreated, it can progress to end-stage renal disease requiring dialysis or kidney transplantation. The rate of progression depends on the underlying cause of the chronic glomerulonephritis. Treatment aims to slow progression through controlling blood pressure and proteinuria with ACE inhibitors, ARBs, and other medications. Dietary modifications and management of complications help preserve kidney function for as long as possible.
1) Diabetic nephropathy is characterized by persistent albuminuria, declining GFR, and presence of retinopathy. It involves thickening of basement membranes and expansion of the mesangial matrix.
2) It progresses through five stages from hyperfiltration to end-stage renal disease. Glycemic control, blood pressure management, and ACE inhibitors or ARBs can slow its progression.
3) Treatment involves tight glycemic and blood pressure control, lipid lowering, dietary protein restriction, anemia management, and renal replacement therapy through hemodialysis, peritoneal dialysis, or transplantation if end-stage is reached.
1) Diabetic nephropathy is characterized by persistent albuminuria, declining GFR, and presence of retinopathy. It involves thickening of basement membranes and expansion of the mesangial matrix.
2) It progresses through five stages from hyperfiltration to end-stage renal disease. Glycemic control, blood pressure management, and ACE inhibitors or ARBs can slow progression.
3) For patients reaching end-stage renal disease, treatment options include hemodialysis, peritoneal dialysis, and kidney transplantation. Kidney transplantation has the best outcomes, but survival is still worse for diabetics than non-diabetics.
This document summarizes chronic kidney disease (CKD), dividing it into 5 stages based on glomerular filtration rate (GFR). It describes the etiologies of CKD including primary and secondary glomerular diseases, tubulointerstitial nephritis, obstructive nephropathies, vascular diseases, and hereditary diseases. The clinical features of CKD include fluid and electrolyte imbalance, acid-base disturbances, uremia, disturbances in calcium and phosphate metabolism, anemia, hypertension, dyslipidemia, endocrine dysfunction, and growth impairment. Management involves treating the underlying cause, slowing progression with ACE inhibitors, and treating complications like anemia, fluid overload, hyperkalemia, metabolic acid
This document discusses chronic kidney disease (CKD) in pediatrics. It defines CKD as kidney damage lasting at least 3 months as determined by structural abnormalities and/or a glomerular filtration rate below 60 mL/min/1.73m2. The stages of CKD are described based on GFR. Common causes in children include congenital abnormalities and glomerulonephritis. The pathogenesis involves hyperfiltration injury and other factors like proteinuria that accelerate kidney damage. Management aims to address complications through careful monitoring, nutrition, treatment of mineral bone disorders, and controlling blood pressure and electrolyte abnormalities.
Chapter 6 Endocrine disorders by Dr. DerejepdfRebiraWorkineh
Chronic kidney disease (CKD) is common in patients with diabetes and is diagnosed through elevated albuminuria and reduced estimated glomerular filtration rate (eGFR). CKD attributed to diabetes occurs in 20-40% of patients and can progress to end-stage renal disease requiring dialysis. Diabetic retinopathy, caused by chronic hyperglycemia, is the most common cause of blindness and is assessed through eye exams. Neuropathy is assessed through history and examination of sensation, with annual 10-g monofilament testing to check for high-risk feet. Foot care includes inspection, assessment of deformities and pulses, and referral for ongoing surveillance in high-risk patients to prevent ulcers and amputations.
- Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is usually caused by primary glomerular disease but can be secondary to other medical conditions.
- Diagnosis requires proteinuria >3.5g/day and hypoalbuminemia <2.5g/dL. Management involves salt and fluid restriction, diuretics, ACE inhibitors to reduce proteinuria, and corticosteroids which induce remission in 80-90% of adults. Frequent relapses or steroid resistance may require additional immunosuppressive drugs. Complications include infection, thromboembolism, and renal failure.
This document provides an overview of the management of chronic kidney disease (CKD). It defines CKD and outlines its classification based on cause, glomerular filtration rate, and albuminuria levels. The epidemiology, pathophysiology, clinical features, diagnostic evaluation, and management of CKD are discussed. Treatment aims to address reversible causes, prevent disease progression, and manage complications. Referral to a nephrologist is recommended for advanced CKD stages or complex cases.
This document provides an overview of the management of chronic kidney disease (CKD). It defines CKD and outlines criteria for diagnosis based on markers of kidney damage and glomerular filtration rate (GFR). It describes tools for screening and staging CKD, including estimated GFR (eGFR) calculators and urine albumin-to-creatinine ratio. Common clinical manifestations of CKD like fluid and electrolyte disorders, anemia, bone disease, and cardiovascular complications are summarized. Treatment strategies are covered for managing complications involving hypertension, acid-base abnormalities, mineral and bone disorders, anemia, and diabetes in CKD patients.
Chronic kidney disease (CKD) is defined as kidney damage or decreased kidney function that lasts for at least 3 months. It is a progressive loss of kidney function over time that can lead to complications if left untreated. CKD is caused by conditions that damage the kidneys such as diabetes and hypertension. Symptoms are often vague until later stages when kidney function is significantly decreased. Treatment focuses on controlling blood pressure and blood sugars to slow the progression of kidney damage.
This document provides information about diabetes mellitus. It begins with an introduction and overview of diabetes symptoms and complications. It then discusses the different types of diabetes (type 1, type 2, gestational, pre-diabetes), diagnosis methods, and treatment options including medications like insulin, sulfonylureas, thiazolidinediones, biguanides, and meglitinides. Complications of diabetes such as retinopathy, neuropathy, and nephropathy are also summarized. The document provides details on diabetes prevalence globally and risk factors. It concludes with descriptions of hypoglycemia and diabetic ketoacidosis.
This document provides information on managing renal failure in primary care. It presents a case study of a 46-year-old woman with chronic kidney disease due to uncontrolled diabetes and hypertension. Key steps in management include controlling blood pressure and diabetes, addressing complications like anemia and bone disease, and referring to nephrology if glomerular filtration rate drops below 30 or complications require treatment. The take-home message is that lifestyle modification, monitoring for complications, and early nephrology referral can help slow chronic kidney disease progression.
1) Hyperfiltration of remaining nephrons following renal surgery or transplantation can lead to progressive kidney damage over time due to increased workload.
2) Multiple factors like diabetes, hypertension, genetic diseases, and various glomerular diseases can promote hyperfiltration injury through mechanical and metabolic effects on the kidneys.
3) Management strategies aim to prevent or reduce hyperfiltration through measures like low-protein diets, weight loss, ACE inhibitors, lipid lowering agents, and calcium channel blockers to protect kidney function long-term.
This document summarizes chronic kidney disease (CKD), defining it as abnormalities of kidney structure or function lasting over 3 months that impact health. CKD is classified based on cause, glomerular filtration rate (GFR) category, and albuminuria levels. Key aspects of CKD addressed include pathophysiology, GFR estimation and staging, risk factors, clinical abnormalities associated with decreased kidney function like fluid/electrolyte issues and anemia, leading causes, and management including treating complications and renal replacement therapy for late stages.
This document provides information on chronic kidney disease (CKD) and dialysis. It discusses:
1. The functions of the kidneys and how CKD develops due to gradual loss of kidney function over time.
2. The stages of CKD progression and treatment strategies at each stage, including managing risk factors, complications, and preparing for renal replacement therapy.
3. The two main types of renal replacement therapy - hemodialysis which uses an artificial kidney to filter waste from the blood, and peritoneal dialysis which uses the peritoneal membrane in the abdomen.
- A 55-year-old woman presented with swelling of the face and lower limbs for one month, as well as shortness of breath on exertion for 20 days and decreased appetite.
- Investigations showed nephrotic range proteinuria, hypoalbuminemia, and a renal biopsy consistent with minimal change disease.
- Minimal change disease should be considered and treatment involves corticosteroids, with frequent monitoring due to the risk of relapses.
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function present for more than 3 months. CKD is staged based on glomerular filtration rate (GFR) from stage 1 (normal or high GFR) to stage 5 (kidney failure). Common causes of CKD in India include diabetes, hypertension, and glomerulonephritis. Symptoms vary depending on stage but may include fatigue, pruritus, nausea, and electrolyte imbalances. Treatment includes controlling risk factors, nutritional management, dialysis if needed, and potentially kidney transplantation for end stage renal disease.
Chronic kidney disease ppt presentation for classsumathiparagati
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function present for more than 3 months. CKD is staged based on glomerular filtration rate from stage 1 to 5. The leading causes of CKD in India are diabetes, hypertension, and glomerulonephritis. Treatment includes controlling risk factors, nutritional therapy, dialysis, and kidney transplantation. Dialysis techniques include hemodialysis and peritoneal dialysis. Kidney transplantation is the treatment of choice for end-stage renal disease but requires lifelong immunosuppression.
1. The document discusses conditions other than cirrhosis that can result in diffuse surface nodularity of the liver or portal hypertension such as chronic Budd-Chiari syndrome, chronic portal vein thrombosis, sarcoidosis, and pseudocirrhosis of treated breast cancer metastases or fulminant hepatic failure.
2. It provides imaging examples and characteristics of these non-cirrhotic conditions that can mimic cirrhosis on imaging. For example, pseudocirrhosis of treated breast cancer metastases shows diffuse hepatic nodularity and signs of portal hypertension but the history of breast cancer and prior imaging helps identify the correct diagnosis.
3. Nodular regenerative hyperplasia, congenital hepatic fibrosis, and
This document summarizes ultrasound findings for cirrhosis of the liver. Key findings include coarse echotexture and nodular surface of the liver. Regenerating nodules appear isoechoic or hypoechoic. Portal hypertension is a complication and is evidenced by dilated portal veins, low portal flow, and portosystemic collaterals visible on ultrasound. Doppler ultrasound can detect changes in portal flow from normal hepatopetal to reversed hepatofugal flow in advanced cases.
1. The document discusses the diagnosis and treatment of acute ischemic stroke. It outlines the time windows for treatment with intravenous thrombolysis, which is most effective within 4.5 hours of symptom onset.
2. Early diagnosis is critical in stroke care due to the concept of "time is brain". Delays in treatment can lead to further neuronal damage and worse outcomes. The goals are to perform a CT scan within 20 minutes of arrival and initiate thrombolysis within 60 minutes.
3. Post-thrombolytic management focuses on monitoring for hemorrhagic complications and providing supportive care to reduce disability from the stroke.
hepaticcoma.pdf is important for medical studentsDrYaqoobBahar
Hepatic coma is an advanced complication of liver failure characterized by reversible decreased neurologic function and loss of consciousness due to the liver's failure to detoxify toxic substances. It is caused by chronic liver disease, fulminant hepatic failure, or portosystemic shunts. Patients experience disturbances in consciousness, neurological signs, and mental changes. Treatment focuses on treating the underlying cause, decreasing ammonia production, and controlling risk factors through supportive care, lactulose, rifaximin, and L-ornithine/L-aspartate supplementation. Complications can include brain herniation, organ failure, and brain edema.
1) Abdominal tuberculosis poses a diagnostic challenge due to its nonspecific symptoms. It is increasingly common and can involve the gastrointestinal tract, peritoneum, lymph nodes or solid organs.
2) Tubercle bacilli typically spread from the lungs or ingested materials to the abdominal cavity via the bloodstream or lymphatics. This can cause caseating granulomas and lesions in the abdomen.
3) Common presentations include abdominal pain, fever, weight loss, and ascites or abdominal masses. Imaging shows lymphadenopathy, bowel thickening or strictures, and ascites. Diagnosis relies on clinical suspicion plus histology, microbiology or response to antitubercular treatment.
- Abdominal tuberculosis can affect the peritoneum, gastrointestinal tract, abdominal lymph nodes, and solid organs like the liver, pancreas, and spleen. It is most commonly seen in the ileoceal region.
- On imaging, tubercular peritonitis can appear as wet ascites, fibrotic omental thickening, or dry adhesions. Lymphadenopathy often shows peripheral rim enhancement.
- Gastrointestinal tuberculosis frequently involves the terminal ileum and cecum, appearing as thickened valves, contracted cecum, or strictures on barium studies or CT.
Diagnosis and managment of pulmonary embolismDrYaqoobBahar
A pulmonary embolism is a sudden blockage in a lung artery, usually caused by a blood clot breaking off and traveling to the lungs. PE is a common cause of death in hospitalized patients. Risk factors include genetic mutations, cancer, obesity, smoking, and surgery. Symptoms may include dyspnea, chest pain, and cough. Diagnosis involves assessing risk factors, blood tests, imaging like CT scans, and echocardiograms. Treatment involves immediate anticoagulation with blood thinners, potentially thrombolytic therapy for severe cases, and inferior vena cava filters for high-risk patients. Anticoagulation may continue for several months depending on the underlying cause of clotting.
This document discusses peripartum cardiomyopathy, which is a type of dilated cardiomyopathy of unknown origin that presents with left ventricular systolic dysfunction. It can occur in 1 in 4,000 live births in the United States. The precise causes are unclear but may involve viral infection, immune response abnormalities, or prolonged use of tocolytics. Symptoms include dyspnea, chest pain, and edema. Diagnosis involves excluding other potential causes through ECG, echocardiogram, biomarkers and imaging. Treatment focuses on heart failure medications, anticoagulants if needed, and assisted devices. Prognosis is generally good with 50% fully recovering but risks include persistent symptoms or progression to heart failure.
Heart failure is a clinical syndrome where the heart is unable to pump sufficiently to maintain blood flow to meet the body's needs. It can be caused by structural or functional defects in the heart. The most common causes are coronary artery disease, high blood pressure, and diabetes. While it affects about 2% of adults globally, the risk increases to 6-10% for those over age 65. Treatment involves controlling underlying causes, removing precipitating factors, and managing symptoms through diuretics, ACE inhibitors, beta blockers, and other medications.
Pulmonary edema refers to excess fluid accumulation in the lungs. It can be caused by increased hydrostatic pressure, permeability changes, or a mix of both. Common causes include heart failure, fluid overload, near drowning, trauma, and certain drugs. Symptoms include shortness of breath, cough, wheezing, and anxiety. Diagnosis involves physical exam, imaging like chest x-rays, and tests to check for underlying conditions. Treatment focuses on addressing the underlying cause, giving oxygen, diuretics, and other medications to reduce fluid buildup. Ventilatory support may be needed in severe cases.
Pulmonary edema refers to excess fluid accumulation in the lungs. It has four main categories based on pathophysiology: increased hydrostatic pressure, interstitial edema, alveolar flooding, and permeability edema. Causes include heart failure, mitral regurgitation, near-drowning, and renal failure. Symptoms include difficulty breathing, cough, and anxiety. Diagnosis involves clinical exam, BNP levels, chest x-ray, and echocardiogram. Treatment focuses on addressing the underlying cause with oxygen, diuretics, nitrates, and sometimes ventilation support.
1. Acute variceal hemorrhage refers to bleeding from enlarged veins (varices) in the esophagus or stomach that is caused by portal hypertension from liver cirrhosis. Variceal bleeding is a severe complication and is the cause of bleeding in 70% of upper GI bleeds in cirrhotic patients.
2. Varices develop due to increased pressure in the portal vein system from cirrhosis. Once varices form, there is a risk of 15% annual bleeding for large varices. Bleeding can often be controlled with medical and endoscopic therapy but there is a high risk (60%) of rebleeding without intervention.
3. Varices are classified based on location
Hypertension emergencies require rapid reduction of blood pressure to prevent end organ damage. Hypertensive urgency can be managed as an outpatient but emergencies require hospitalization. Initial evaluation assesses for signs of damage to heart, kidneys, brain, or vasculature. Parenteral drugs like nicardipine, labetalol, and esmolol are used to lower blood pressure 10-15% within 1 hour and further to 160/100 mmHg in 2-6 hours, with goals tailored to specific conditions like stroke, heart failure, or aortic dissection. Oral agents like clonidine or nifedipine may be used after initial parenteral treatment to control blood pressure before discharge
Hypertension emergencies require rapid reduction of blood pressure to prevent end organ damage. Hypertensive urgency can be managed as an outpatient with oral medications, while emergencies require hospitalization and intravenous drugs. Initial evaluation assesses for signs of heart, brain, kidney and vascular damage. Parenteral drugs like nicardipine, labetalol and esmolol are used but sodium nitroprusside is no longer first-line due to risks. Treatment goals depend on the specific organ involved and reduce pressure by 10-25% within 1-2 hours.
1) Myxedema coma is a rare life-threatening condition that occurs when a patient with severe, long-standing hypothyroidism experiences physiological decompensation, usually brought on by an external precipitating event like infection.
2) It is characterized by hypothermia, unconsciousness, decreased metabolism and oxygen consumption. Patients often present with symptoms of both the underlying hypothyroidism and the precipitating condition.
3) Treatment involves supportive care, thyroid hormone replacement, glucocorticoids, and treating any underlying infections or precipitating conditions. Patients require intensive monitoring and care due to involvement of multiple organ systems.
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2. DEFINITION
• Diabetic nephropathy is defined as:
• albuminuria (albumin excretion rate>300 mg/24 hours, which
equates to 24-hour urinary protein >0.5 g)
• declining renal function in a patient with known diabetes who
does not have a urinary tract infection, heart failure, or any other
renal disease
• Presence of diabetic retinopathy
3. • is the leading cause of chronic kidney disease (CKD) and ESRD requiring
renal replacement therapy.
• CKD in individuals with DM is associated with an increased risk of
cardiovascular disease, and the prognosis of individuals with diabetes on
dialysis is poor.
• Individuals with diabetic nephropathy commonly have diabetic retinopathy.
• The presence of CKD in individuals with DM and no retinopathy should
prompt investigation for alternative causes of kidney disease
• Microvascular Complication
4. PATHOGENESIS
• pathogenesis of diabetic nephropathy is related to chronic hyperglycemia
• Due to effects of soluble factors (growth factors, angiotensin II, endothelin, AGEs),
hemodynamic alterations in the renal microcirculation (glomerular hyperfiltration or
hyperperfusion, increased glomerular capillary pressure), and structural changes in
the glomerulus (increased extracellular matrix, basement membrane thickening,
mesangial expansion, fibrosis).
• Some of these effects may be mediated through angiotensin II and
mineralocorticoid receptors.
• Smoking accelerates the decline in renal function.
• Because only 20–40% of patients with diabetes develop diabetic nephropathy,
additional genetic or environmental susceptibility factors likely contribute
5. PATHOLOGY
• ALWAYS PRESENT
• Glomerular basement membrane thickening.
• Tubular basement membrane thickening.
• Mesangial expansion with predominance of increased mesangial matrix.
• Interstitial expansion with predominance of increased extracellular matrix material.
• OFTEN OR USUALLY PRESENT
• Kimmel stiel-Wilson nodules (nodular glomerulosclerosis)
• Global glomerulosclerosis
• Focal segmental glomerulosclerosis
• Atubular glomeruli
• Foci of tubular atrophy
• Afferent and efferent arteriolar hyalinosis
6. PATHOLOGY
• SOMETIMES PRESENT
• Hyaline caps or fibrin caps (Highly characteristic of diabetic
nephropathy)
• Capsular drops (Highly characteristic of diabetic nephropathy)
• Atherosclerosis.
• Glomerular micro-aneurysms
7. FACTORS PROMOTING THE DEVELOPMENT
AND PROGRESSION OF NEPHROPATHY
• Blood pressure
• Poor glycaemic control
• Dyslipidaemia
• Smoking
• High protein intake
• Small kidneys
• Genetic factors
10. 1. HYPERFILTRATION
• Increased Glomerular Filtration Rate (GFR >90ml min),
• Adjust with age, 20% from baseline
• Concomitant renal hypertrophy (glomerular and tubular)
• Various factors contributing are:
• Intra renal hemodynamic abnormalities
• TGF-B
• Increased salt absorption
• Osmotic load and toxic effect of high sugar levels on kidney
cells
11. 2. SILENT STAGE
• The GFR has returned to normal with no evidence of albuminuria
• Glomerular damage occurs in the form of basement membrane
thickening and mesangial expansion.
• Ambulatory BP monitoring studies have shown modest rise in BP
and absence of nocturnal dip
12. 3. INCIPENT NEPHROPATHY/
MICROALBUMINURIA
• Now called moderately increased albuminuria
• Urine AER has increased to 30 to 300 mg/24 hrs
• Renal functions could be normal or reduced
• 30-50% of patients may show reversal of microalbuminuria
• Persistent microalbuminuria, if untreated, will progress to end-
stage renal disease (ESRD).
• Therefore, all diabetes patients should be screened for
microalbuminuria on a routine basis.
13. 4. MACROALBUMINURIA/ OVERT
NEPHROPATHY
• Severely increased albuminuria
• The urine AER is more than 300 mg of albumin in a 24-hour
period.
• Over two thirds of patient in this stage have Hypertension.
• If untreated a vicious cycle of progressive renal impairment
develops leading to ESRD.
14. 5. UREMIA
• GFR has fallen to <15 ml/min and renal replacement
therapy (i.e., haemodialysis, peritoneal dialysis, kidney
transplantation) is needed
• Sign and symptoms of uremia
18. CLINICAL MANIFESTATIONS
• Stages 1–4 CKD are asymptomatic.
• Symptoms develop slowly with the progressive decline in
GFR, are nonspecific, and do not manifest until kidney
disease is far advanced (GFR less than 5–10 mL/min/1.73
m2).
• Uremic syndrome.
• Fatigue
• anorexia, nausea
• a metallic taste in the mouth.
19. • Neurologic symptoms such as irritability, memory impairment, insomnia,
restless legs, paresthesias, and twitching may be due to uremia.
• Generalized pruritus (without rash)
• decreased libido and menstrual irregularities
• Pericarditis
• Pleuritic chest pain
20. COMMON PHYSICAL FINDINGS
• Hypertension
• volume overload.
• Uremic signs:
• seen with a profound decrease in GFR (less than 5–10
mL/min/1.73 m2)
• generally sallow and ill appearance
• halitosis (uremic fetor)
• the uremic encepholopathic signs of decreased mental
status, asterixis, myoclonus, and possibly seizures
22. SCREENING AND DIAGNOSIS OF
DIABETIC NEPHROPATHY
• Diabetes should be screened annually with serum creatinine and eGFR and
urine Alb:Creatinine (ACR)
• Starting 5 yrs after diagnosis of type 1
• Starting at the diagnosis of type lI
• Elevated urine ACR confirmed ≥ 2 times and not in setting of UTI ,acute
febrile illness, vigorous exercise, uncontrolled hypertension, and heart failure
• Microalbuminuria: ACR 30-300 mg/mmol
• Macroalbuminuria: ACR >300 mg/mmol
23. • Screening should be done when the person is free from acute
illness and with stable glucose levels
• Early morning urine sample is preferred
• Serum creatinine level should also be measured annually
• Recently serum Cystatin C - A naturally circulating protein, freely
filtered by glomerulus has been suggested as an alternative to
creatinine measurement.
24. CALCULATIONS: EGFR
• Cockcroft-Gault
• Men: CrCl (mL/min) = (140 - age) x wt (kg)
• SCr x 0.81
• Women: multiply by 0.85
• MDRD
• GFR (mL/min per 1.73 m2) = 186 x (SCr x 0.0113)-1.154 x (age)-0.203 x (0.742
if female) x (1.12 if African-American)
25. TREATMENT
• Major therapeutic interventions include –
• Control of blood glucose to near normal level
• Antihypertensive treatment
• Lipid lowering therapy
• Restriction of dietary proteins
• Cessation of smoking
26. • Primary prevention:
• Diabetic Control and Complications Trial showed that intensive glycemic control
reduces the occurrence of microalbuminuria
• ADVANCE study and VETERAN trial recently confirmed similar findings.
• Secondary prevention :
• UKPDS proves that tight glycemic control reduces progression from
microalbuminuria to overt nephropathy
• A recent trial also confirms that ESRD development was retarded by
multifactorial interventions
• Nephropathy:
• Once overt nephropathy develops, results are disappointing regarding
metabolic control in preventing further progression of disease
27. KDIGO GUIDELINES FOR MANAGEMENT
OF HYPERGLYCEMIA AND GENERAL
DIABETES CARE IN CKD
• Target Hemoglobin A1c(HbA1c) of 7.0% to prevent or delay progression of
the microvascular complications of diabetes, including DKD.
• No treatment if HbA1c target is <7.0% in patients at risk of hypoglycemia.
• Target HbA1c can be extended to > 7.0% in individuals with co-morbidities
or limited life expectancy
28. METFORMIN
• Metformin to be continued in people with
• GFR ≥ 45 ml/min/1.73 m(GFR categories G1-Ga)
• Its use should be reviewed in those with GFR 30-44 ml/min/1.73 m(GFR category G3b)
• Discontinued in people with GFR<30 ml/min/1.73 m(GFR categories G4-G5) and risk of
hypoglycemia.
29. DIPEPTIDYL PEPTIDASE INHIBITORS
• Sitagliptin, saxagliptin, linagliptin, alogliptin
• Linagliptan: No adjustment needed
• Sitagliptin :
• (eGFR) of 30 or greater to less than 50 mL/min/1.73 m2: 50 mg once daily,
• eGFR less than 30 mL/min/1.73 m2, a dose of 25 mg once daily is advised.
• Saxagliptin:
• 2.5-5 mg daily in patients with an eGFR greater than 50 mL/min,
• eGFR of 50 mL/min/1.73 m2 or less to 2.5 mg daily.
• Alogliptin also requires a dose reduction:
• from 25 mg daily to 12.5 mg daily in patients with an eGFR of less than 60 mL/min/1.73
m2
• and to 6.25 mg daily if the eGFR is less than 30 mL/min/1.73 m2
31. SGLT2
• Canagliflozin, Dapagliflozin, Empagliflozin
• increased excretion of glucose in the urine, which may help subjects lose up to 5 kg of
weight over a year.
• decreased glucose reabsorption is also accompanied by increased urinary excretion of
sodium, which, in turn, may help with further blood pressure lowering
• it is not recommended in patients with an eGFR < 45 mL/min/1.73 m2.
• Increased glucosuria is believed to increase the risk of urinary tract infections, especially
candidal infections, and more frequently in women
• SGLT-2 inhibitors can reduce albuminuria and, after an initial decline (~3 mL/min per 1.73
m2) in GFR, may slow further decline in kidney function in individuals with and without
T2DM and CKD
32. GLP-1 ANALOGUES
• Liraglutide: is not metabolized by the kidney, and no dose adjustment is necessary
in patients with a decreased GFR
33. BLOOD PRESSURE CONTROL
• ACE-I or ARB's are not recommended for the primary prevention of diabetic
nephropathy in normotensive normo-albuminuric patients with diabetes
• ACE inhibitors and ARB's are effective in slowing the progression of kidney
disease characterized by microalbuminuria in hypertensive patients with type
1 or type 2 diabetes.
• ACE inhibitors, ARBs, and nondihydropyridine calcium channel blockers have
a greater anti-protein-uric effect than other antihypertensive classes in
hypertensive patients with diabetic nephropathy.
34. HTN
• Dihydropyridine calcium channel blockers, when used alone in the
absence of ACE inhibitors or ARB's are less effective than other
agents in slowing progression of diabetic nephropathy.
• ADA states " In patients with type 2 diabetes, hypertension,
macroalbuminuria and renal insufficiency ARBs have shown to
delay progression“
35. KDIGO GUIDELINES FOR MANAGEMENT OF
HYPERTENSION IN DIABETIC NEPHROPATHY
AND PROTIENURIA
• Both diabetic and non-diabetic adults with CKD and urine albumin excretion
<30 mg/24 hours whose office BP is consistently >140/90 mm Hg, be treated
with BP-lowering drugs to maintain a BP that is consistently ≤ 140/90 mm
Hg.
• Both diabetic and non-diabetic adults with CKD and with urine albumin
excretion of >30 mg/24 hours whose office BP is consistently > 130/80 mm
Hg, be treated with BP-lowering drugs to maintain a BP that is consistently <
130/80 mm Hg.
• There is insufficient evidence to recommend the combination of an ACE-|
with an ARB to prevent progression of CKD
36. PRECAUTIONS TAKEN WHILE STARTING
AN ACE-I OR AN ARB
• Monitoring of blood pressure, potassium, and serum creatinine level is
important.
• Potassium level up to 5.5 mEg/Land an increase in serum creatinine up to
30% from baseline within the first three months with close monitoring is
tolerable
• Medication needs to be reduced or discontinued if potassium levels remain
elevated at > 5.5mEq/L or if the serum creatinine continues to rise or does
not improve.
• Avoid in people with suspected functional renal artery stenosis
37. ACE-I AND ARBS
• Start at lower dose in people with GFR <45 ml/min/1.73 m
• Assess GFR and measure serum potassium within 1 week of starting or
following any dose escalation
• Temporarily suspend during intercurrent illness, planned IV radiocontrast
administration, bowel preparation prior to colonoscopy, or prior to major
surgery
• Do not routinely discontinue in people with GFR <30 ml/min/1.73 m as they
remain nephroprotective
• Ramipril: decrease cardiovascular risk
38. TREATMENT GOAL FOR LIPIDS IN
DIABETIC NEPHROPATHY
• Mechanism
• Low-density lipoprotein <2.6 mmol/L (100 mg/dL)
• High-density lipoprotein >1 mmol/L (40 mg/dL) in men, >1.3
mmol/L (50 mg/dL) in women
• Triglycerides <1.7 mmol/L (150 mg/dL)
• Dyslipidemia is common in people with diabetes and CKD.
Cardiovascular events are a frequent cause of morbidity and
mortality in this population.
39. KDIGO GUIDELINES FOR MANAGEMENT OF
DYSLIPIDEMIA IN DIABETES AND CKD
• Lowering low-density lipoprotein cholesterol (LDL-C) with statin-based therapies
reduces risk of major atherosclerotic events in patients with CKD including those
with diabetes.
• LDL-C lowering medicines, such as statins or statin+ezetimibe combination reduces
risk of major atherosclerotic events in patients with diabetes and CKD, including
those who have undergone kidney transplant.
• Not recommended to initiate statin therapy in patients with diabetes who are
treated by dialysis
• Atorvastatin is better
40. MANAGEMENT OF ANEMIA IN
DIABETIC NEPHROPATHY
• Iron deficiency, AOCD
• Measure ferritin level
• Anemia Screening: measure Hb levels
• When clinically indicated in patients with GFR >60 ml/min/1.73 m (GFR
categories G1-G2)
• Annually in patients with GFR 30-59 ml/min/1.73 m (GFR categories G3a-
Gb)
• Twice a year in patients with GFR<30 ml/min/1.73 m (GFR categories G4-
G5)
• EPO and darbopoetin, HIF inhibitors
41. DIETARY PROTEIN RESTRICTION
• A low protein diet reduces urinary albumin excretion and hyper-filtration
independent of changes in glucose control and blood pressure.
• KDIGO GUIDELINE FOR PROTIEN INTAKE
• Lowering protein intake to 0.8 g/kg/day in adults ‡ diabetes and GFR<30
ml/min/ 1.73 m2(GFR categories G4-G5) with appropriate education.
• Avoiding high protein intake (>1.3 g/kg/day) in adults with CKD at risk of
progression
42. TREATMENT OF ESRD
• Transplantation(kidney only, simultaneous pancreas with kidney,
pancreas after kidney)
• Hemodialysis
• Continuous ambulatory peritoneal dialysis
43. HEMODIALYSIS
• Renal replacement therapy should be started earlier than in non diabetic patients
• Intradialytic hypotension is common in diabetic patient on dialysis because of
autonomic neuropathy and disturbed left ventricular compliance
• Following approach is used to avoid intradialytic hypotension - Long dialytic
session, omission of antihypertensive drugs before dialytic session, controlled
ultrafiltration, correction of anemia by EPO therapy, alternative modalities such as
CAPD
• High prevalence of cardiovascular complications in diabetic patients entering
dialysis programme
• Dialysis partially reverses the insulin resistance and requirement compared prior to
dialysis
44. PERITONEAL DIALYSIS
• According to heaf and co worker, during the first 2 years, survival is better for
diabetic patient treated with CAPD compared to HD
• Survival advantage no longer demonstrated beyond 2 years as by then
residual renal function has already decayed
• CAPD provides slow and sustained ultra filtration without rapid fluctuation of
fluid volume and electrolyte concentration, a feature that is advantageous for
BP control and prevention of heart failure
45. KIDNEY TRANSPLANT
• Survival of diabetic patients with kidney graft is worse compared to non diabetic patients.
• And survival of diabetic nephropathy patients on dialysis is poorer when compared to
patients with kidney graft.
• Simultaneous kidney with pancreas transplantation(SP) should be the preferred treatment
for type1 DM who meet the selection criteria: Age <55 years and GFR<40.
• Exclusion criteria for SPK: Active smoking, morbid obesity and uncorrected CVD
• Pancreas after kidney transplantation - An alternative strategy, must be considered in a
diabetic patient who has a living kidney donor.
• Firstly the living kidney is transplanted and subsequently once stable renal function is
achieved (GFR>50 ml/min), cadaveric pancreas is transplanted
• Results of Islet cell transplantation are inferior to whole pancreas transplantation
46. • Nephrology consultation should be considered when:
• estimated GFR is <30 mL/min per 1.743 m2
• or with atypical features such as:
• Hematuria
• rapidly declining renal function
• proteinuria > 3 g/day.
• Referral for transplant evaluation should be made when
the GFR approaches 20 mL/min per 1.73 m2
47. • INHALED INSULIN approved by FDA in 2014 - AFREZZA
• Rapid acting insulin taken before each meal or soon after starting the
meal
• Doesn't replace the need of injectable long-acting insulin, hence not
suitable for diabetic emergencies such as DKA
• Common side effects - Low blood sugar, cough, scratchy/sore throat
• Should not be used in smokers and individuals with lung disease