This document proposes revisions to ICD-9-CM codes for chronic kidney disease to better classify stages of disease severity, distinguish between CKD and end-stage renal disease, indicate presence of proteinuria, and identify disease etiology. The proposed changes would improve risk assessment, determine appropriate treatments, examine healthcare utilization and costs, and enhance CKD research.
Diabetes is a significant healthcare problem in the US, affecting over 18 million Americans. Long-term complications from diabetes, including diabetic nephropathy, neuropathy, and retinopathy, are devastating and place a huge economic burden on the healthcare system. Current treatment options focus on controlling blood pressure and glucose to slow progression, but new therapies are needed to directly target the underlying disease processes and prevent complications. Early detection through regular screening is critical to predict and delay the onset of diabetic microvascular complications.
The FIGARO-DKD trial found that:
1) Finerenone significantly reduced the risk of the primary cardiovascular outcome (composite of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, or hospitalization for heart failure) by 13% compared to placebo in patients with chronic kidney disease and type 2 diabetes.
2) The cardiovascular benefit was primarily driven by a reduction in hospitalization for heart failure despite excluding patients with symptomatic heart failure with reduced ejection fraction.
3) Finerenone did not significantly reduce the risk of a sustained 40% decline in eGFR but did trend toward improving the clinically accepted outcome of a sustained 57% decline in eGFR compared to placebo.
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.
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.
This document summarizes strategies for preventing chronic kidney disease (CKD). It discusses several key risk factors for CKD, including diabetes, hypertension, obesity, and smoking. It then outlines primary and secondary prevention approaches. For primary prevention, lifestyle modifications and controlling risk factors like blood pressure and blood sugar are emphasized. For secondary prevention in patients with existing kidney disease, tight control of blood pressure and glucose is important, along with use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers to slow disease progression. Clinical trials demonstrate that controlling these modifiable risk factors can significantly reduce the risk of end-stage renal disease.
Diabetes is a significant healthcare problem in the US, affecting over 18 million Americans. Long-term complications from diabetes, including diabetic nephropathy, neuropathy, and retinopathy, are devastating and place a huge economic burden on the healthcare system. Current treatment options focus on controlling blood pressure and glucose to slow progression, but new therapies are needed to directly target the underlying disease processes and prevent complications. Early detection through regular screening is critical to predict and delay the onset of diabetic microvascular complications.
The FIGARO-DKD trial found that:
1) Finerenone significantly reduced the risk of the primary cardiovascular outcome (composite of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, or hospitalization for heart failure) by 13% compared to placebo in patients with chronic kidney disease and type 2 diabetes.
2) The cardiovascular benefit was primarily driven by a reduction in hospitalization for heart failure despite excluding patients with symptomatic heart failure with reduced ejection fraction.
3) Finerenone did not significantly reduce the risk of a sustained 40% decline in eGFR but did trend toward improving the clinically accepted outcome of a sustained 57% decline in eGFR compared to placebo.
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.
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.
This document summarizes strategies for preventing chronic kidney disease (CKD). It discusses several key risk factors for CKD, including diabetes, hypertension, obesity, and smoking. It then outlines primary and secondary prevention approaches. For primary prevention, lifestyle modifications and controlling risk factors like blood pressure and blood sugar are emphasized. For secondary prevention in patients with existing kidney disease, tight control of blood pressure and glucose is important, along with use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers to slow disease progression. Clinical trials demonstrate that controlling these modifiable risk factors can significantly reduce the risk of end-stage renal disease.
This document summarizes the five types of cardiorenal syndromes (CRS). Type 1 is acute or chronic heart failure leading to kidney dysfunction. Type 2 is chronic kidney disease contributing to heart disease. Type 3 is acute kidney injury causing acute cardiac injury or dysfunction. Type 4 is chronic kidney disease causing chronic cardiac damage. Type 5 occurs when a systemic condition like sepsis or cirrhosis affects both the heart and kidneys. The document discusses the pathogenesis, risk factors, diagnosis and treatment approaches for each type of CRS.
a-comprehensive-approach-to-kidney-disease-and-hypertension by HazwanMohd Hanafi
This document discusses kidney disease and hypertension. It begins by outlining the key functions of the kidneys, including regulating blood pressure through the renin-angiotensin-aldosterone system. It then examines the causes and classifications of acute and chronic kidney disease. Chronic kidney disease is a growing problem due to its asymptomatic nature in early stages. The document reviews factors that can damage the kidneys and lead to reduced glomerular filtration rate. It also discusses how chronic kidney disease and reduced kidney function are linked to increased risk of cardiovascular disease, anemia, and bone disease like renal osteodystrophy. Hypertension is both a common cause and complication of chronic kidney disease. Tight blood pressure control is important to slow
This document discusses the role of glyptins (DPP-4 inhibitors) in the management of type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD). It notes that T2DM is a leading cause of CKD globally and that strict glycemic control is important for treating diabetic nephropathy. However, patients with CKD are at higher risk of hypoglycemia from antidiabetic medications. The document examines whether glyptins may be renoprotective and safer to use in CKD patients compared to other drugs due to their low risk of hypoglycemia. It reviews studies on the use of sitagliptin and other glyptins in T2
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.
This document discusses the challenges of managing diabetes in patients with chronic kidney disease (CKD). It notes that diabetes is a leading cause of CKD progression and that CKD increases mortality risk in diabetes patients. Managing glucose levels in CKD patients is difficult due to risks of hypoglycemia from insulin clearance issues and need to adjust oral medications for kidney function. The CARMELINA trial demonstrated the renal safety of the DPP-4 inhibitor linagliptin in high cardio-renal risk patients, showing no increase in sustained decrease in eGFR or other renal outcomes compared to placebo over 2 years.
DKD is a leading cause of ESRD in the US, affecting 30-40% of those with diabetes. Poor glycemic control and hypertension are major risk factors for developing and progressing DKD. Clinical trials have shown that intensive control of blood glucose and blood pressure can delay and prevent kidney disease. New drugs targeting the kidney are showing promise in reducing albuminuria and slowing kidney function decline in DKD patients.
This document summarizes a presentation on the benefits of SGLT2 inhibitors (SGLT2i) for patients with diabetes and kidney disease. It discusses how SGLT2i lower intraglomerular pressure and protect the kidneys by reducing hyperfiltration. Clinical trials show SGLT2i slow the progression of kidney disease and reduce cardiovascular risks compared to other treatments like ACE inhibitors or ARBs alone. The document concludes SGLT2i provide renal and cardiovascular benefits and are an important new treatment for preserving kidney function in patients with diabetes.
The document discusses the history and development of dialysis for treating acute renal failure. It describes how Dr. Haas invented the first dialysis machine for humans in 1928 but all 6 of his initial patients died. Dr. Kolff then created the second human dialysis machine in 1943 and was able to successfully treat his first patient. The document also examines biomarkers like KIM-1 and NGAL that can help diagnose acute kidney injury earlier than creatinine. It analyzes the RIFLE criteria for classifying the severity of acute renal failure.
This document presents guidelines from Kidney Disease: Improving Global Outcomes (KDIGO) for the diagnosis, evaluation, prevention and treatment of chronic kidney disease - mineral and bone disorder (CKD-MBD). KDIGO is an independent nonprofit foundation that develops clinical practice guidelines to improve care for kidney disease patients worldwide. The guidelines were developed by an international work group and evidence review team using the GRADE framework. The guidelines cover diagnosis of CKD-MBD through biochemical abnormalities, bone changes, and vascular calcification, as well as treatment targeting phosphorus, PTH levels, bone, and kidney transplant bone 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.
The document discusses diabetic nephropathy, which is a progressive kidney disease caused by damage to the capillaries in the kidneys' glomeruli due to diabetes. It is characterized by protein in the urine and scarring of the glomeruli. The document outlines the 5 stages of diabetic nephropathy from early microalbuminuria to end-stage kidney disease. It discusses the pathology, risk factors like high blood pressure and hyperglycemia, genetic predispositions, and the role of hemodynamic changes and connective tissue growth factor in the pathogenesis. Improved control of blood sugar and blood pressure can slow the progression of diabetic nephropathy.
The document discusses the paradoxical relationship between obesity and mortality in patients with kidney disease undergoing dialysis. Several studies are reviewed that found higher BMI in dialysis patients was associated with lower risks of death and hospitalization, unlike the general population where obesity increases health risks. The studies accounted for various factors and found even extreme obesity was protective. Weight gain over time was also associated with reduced mortality risk. The reasons for this reverse epidemiology are unclear but proposed mechanisms include increased stores of nutrients and anti-inflammatory proteins in adipose tissue.
This document proposes revisions to ICD-9-CM codes for classifying chronic kidney disease (CKD). It outlines stages of CKD based on glomerular filtration rate and proteinuria levels. The current codes do not distinguish CKD from end-stage renal disease (ESRD) or capture disease severity. The proposed changes would add codes to classify CKD stages 1-5, indicate presence of proteinuria, and code for underlying etiologies. This enhanced classification system could help determine patient risk, guide treatment, and assess quality of care for CKD.
Chronic kidney disease is defined as either kidney damage or decreased glomerular filtration rate (GFR) below 60 mL/min/1.73m2 lasting at least 3 months. The causes of chronic kidney disease include diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. Management involves monitoring progression, treating complications, and planning for renal replacement therapy if kidney failure develops. Preventing progression to end-stage renal disease focuses on tight control of blood pressure, cholesterol, blood sugar, diet, and use of ACE inhibitors.
This document proposes revisions to ICD-9-CM codes for chronic kidney disease (CKD) to improve identification, staging, and management of patients. It recommends:
1) Separating codes for end-stage renal disease (ESRD) on dialysis/transplant from CKD codes
2) Adding 5 codes (586.1-586.5) to stage CKD by severity of glomerular filtration rate reduction
3) Adding a 5th digit to CKD codes to indicate presence of proteinuria or albuminuria
4) Instructing use of CKD codes along with disease-specific codes (e.g. diabetes, glomerulonephritis) to identify et
This document proposes revisions to ICD-9-CM codes for chronic kidney disease (CKD) to improve identification and classification of CKD stages and related risk factors. The proposed changes include: 1) Distinguishing CKD from end-stage renal disease and dialysis vs. transplant status, 2) Classifying CKD severity into 5 stages based on glomerular filtration rate, 3) Indicating presence or absence of proteinuria for each CKD stage, and 4) Coding CKD etiology and related comorbidities. The goals are to better assess patient risk, determine treatment needs, examine health care utilization and costs, and advance CKD research.
1. Chronic kidney disease (CKD) is defined as kidney damage or decreased kidney function lasting at least 3 months. It is staged based on glomerular filtration rate (GFR) from normal kidney function to kidney failure.
2. The most common causes of CKD are diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. As CKD progresses, patients experience complications such as anemia, bone disease, cardiovascular disease, and metabolic acidosis.
3. Management of CKD focuses on slowing progression, treating complications, and preparing for renal replacement therapy if kidney failure occurs. Key interventions include blood pressure control, diabetes management, treatment of anemia, and dietary modifications.
This document discusses chronic kidney disease (CKD), including its definition as structural or functional abnormalities of the kidneys for over 3 months, stages of progression from normal kidney function to kidney failure, prevalence, clinical practice guidelines for diagnosis and management, classification based on etiology and diagnosis, and remaining treatment options for end-stage renal disease.
1. Chronic kidney disease (CKD) affects 1 in 10 people in the UK and is often unrecognized as it commonly occurs alongside other conditions like cardiovascular disease or diabetes.
2. CKD is defined as abnormalities of the kidneys persisting for over 3 months, determined by markers of kidney damage or a glomerular filtration rate (GFR) of under 60 ml/min/1.73m^2.
3. People with CKD should be monitored for progression and referred to a nephrologist if their GFR declines rapidly or they have advanced CKD with a GFR under 30 ml/min/1.73m^2.
Uremia refers to the pathological manifestations that result from severe azotemia or high levels of urea in the blood due to kidney failure. The onset of uremia symptoms can vary depending on how quickly kidney function is lost. Both uremia and the uremic syndrome describe a very high plasma urea concentration caused by renal failure. As kidney function declines in chronic kidney disease, patients may experience fluid and electrolyte abnormalities, endocrine and metabolic issues, neurological problems, cardiovascular and pulmonary issues, dermatological changes, gastrointestinal disturbances, and hematological and immunological abnormalities. Many of these complications improve with dialysis treatment, while some persist even with optimal therapy.
Important Roles for Primary Care Providers in Treating Chronic Kidney DiseaseJames Rose
The document discusses the roles of primary care providers and patients in addressing chronic kidney disease, noting that 31 million Americans have CKD but 90% do not know it, and outlines key risk factors, stages of CKD progression, importance of early detection through regular testing of creatinine and eGFR levels, and strategies for protecting kidney health including controlling comorbid conditions and lifestyle factors. The presentation was given by representatives from The Kidney Trust and National Kidney Foundation to promote better management of CKD.
This document provides an overview of chronic kidney disease (CKD). It begins by defining CKD and different stages of kidney disease severity. Major risk factors for CKD progression include diabetes and hypertension. Early detection and treatment can slow CKD progression and improve outcomes. Treatment focuses on controlling blood pressure and glucose, with ACE inhibitors/ARBs shown to protect kidney function. Lifestyle changes like diet and exercise are also important for management.
This document summarizes the five types of cardiorenal syndromes (CRS). Type 1 is acute or chronic heart failure leading to kidney dysfunction. Type 2 is chronic kidney disease contributing to heart disease. Type 3 is acute kidney injury causing acute cardiac injury or dysfunction. Type 4 is chronic kidney disease causing chronic cardiac damage. Type 5 occurs when a systemic condition like sepsis or cirrhosis affects both the heart and kidneys. The document discusses the pathogenesis, risk factors, diagnosis and treatment approaches for each type of CRS.
a-comprehensive-approach-to-kidney-disease-and-hypertension by HazwanMohd Hanafi
This document discusses kidney disease and hypertension. It begins by outlining the key functions of the kidneys, including regulating blood pressure through the renin-angiotensin-aldosterone system. It then examines the causes and classifications of acute and chronic kidney disease. Chronic kidney disease is a growing problem due to its asymptomatic nature in early stages. The document reviews factors that can damage the kidneys and lead to reduced glomerular filtration rate. It also discusses how chronic kidney disease and reduced kidney function are linked to increased risk of cardiovascular disease, anemia, and bone disease like renal osteodystrophy. Hypertension is both a common cause and complication of chronic kidney disease. Tight blood pressure control is important to slow
This document discusses the role of glyptins (DPP-4 inhibitors) in the management of type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD). It notes that T2DM is a leading cause of CKD globally and that strict glycemic control is important for treating diabetic nephropathy. However, patients with CKD are at higher risk of hypoglycemia from antidiabetic medications. The document examines whether glyptins may be renoprotective and safer to use in CKD patients compared to other drugs due to their low risk of hypoglycemia. It reviews studies on the use of sitagliptin and other glyptins in T2
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.
This document discusses the challenges of managing diabetes in patients with chronic kidney disease (CKD). It notes that diabetes is a leading cause of CKD progression and that CKD increases mortality risk in diabetes patients. Managing glucose levels in CKD patients is difficult due to risks of hypoglycemia from insulin clearance issues and need to adjust oral medications for kidney function. The CARMELINA trial demonstrated the renal safety of the DPP-4 inhibitor linagliptin in high cardio-renal risk patients, showing no increase in sustained decrease in eGFR or other renal outcomes compared to placebo over 2 years.
DKD is a leading cause of ESRD in the US, affecting 30-40% of those with diabetes. Poor glycemic control and hypertension are major risk factors for developing and progressing DKD. Clinical trials have shown that intensive control of blood glucose and blood pressure can delay and prevent kidney disease. New drugs targeting the kidney are showing promise in reducing albuminuria and slowing kidney function decline in DKD patients.
This document summarizes a presentation on the benefits of SGLT2 inhibitors (SGLT2i) for patients with diabetes and kidney disease. It discusses how SGLT2i lower intraglomerular pressure and protect the kidneys by reducing hyperfiltration. Clinical trials show SGLT2i slow the progression of kidney disease and reduce cardiovascular risks compared to other treatments like ACE inhibitors or ARBs alone. The document concludes SGLT2i provide renal and cardiovascular benefits and are an important new treatment for preserving kidney function in patients with diabetes.
The document discusses the history and development of dialysis for treating acute renal failure. It describes how Dr. Haas invented the first dialysis machine for humans in 1928 but all 6 of his initial patients died. Dr. Kolff then created the second human dialysis machine in 1943 and was able to successfully treat his first patient. The document also examines biomarkers like KIM-1 and NGAL that can help diagnose acute kidney injury earlier than creatinine. It analyzes the RIFLE criteria for classifying the severity of acute renal failure.
This document presents guidelines from Kidney Disease: Improving Global Outcomes (KDIGO) for the diagnosis, evaluation, prevention and treatment of chronic kidney disease - mineral and bone disorder (CKD-MBD). KDIGO is an independent nonprofit foundation that develops clinical practice guidelines to improve care for kidney disease patients worldwide. The guidelines were developed by an international work group and evidence review team using the GRADE framework. The guidelines cover diagnosis of CKD-MBD through biochemical abnormalities, bone changes, and vascular calcification, as well as treatment targeting phosphorus, PTH levels, bone, and kidney transplant bone 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.
The document discusses diabetic nephropathy, which is a progressive kidney disease caused by damage to the capillaries in the kidneys' glomeruli due to diabetes. It is characterized by protein in the urine and scarring of the glomeruli. The document outlines the 5 stages of diabetic nephropathy from early microalbuminuria to end-stage kidney disease. It discusses the pathology, risk factors like high blood pressure and hyperglycemia, genetic predispositions, and the role of hemodynamic changes and connective tissue growth factor in the pathogenesis. Improved control of blood sugar and blood pressure can slow the progression of diabetic nephropathy.
The document discusses the paradoxical relationship between obesity and mortality in patients with kidney disease undergoing dialysis. Several studies are reviewed that found higher BMI in dialysis patients was associated with lower risks of death and hospitalization, unlike the general population where obesity increases health risks. The studies accounted for various factors and found even extreme obesity was protective. Weight gain over time was also associated with reduced mortality risk. The reasons for this reverse epidemiology are unclear but proposed mechanisms include increased stores of nutrients and anti-inflammatory proteins in adipose tissue.
This document proposes revisions to ICD-9-CM codes for classifying chronic kidney disease (CKD). It outlines stages of CKD based on glomerular filtration rate and proteinuria levels. The current codes do not distinguish CKD from end-stage renal disease (ESRD) or capture disease severity. The proposed changes would add codes to classify CKD stages 1-5, indicate presence of proteinuria, and code for underlying etiologies. This enhanced classification system could help determine patient risk, guide treatment, and assess quality of care for CKD.
Chronic kidney disease is defined as either kidney damage or decreased glomerular filtration rate (GFR) below 60 mL/min/1.73m2 lasting at least 3 months. The causes of chronic kidney disease include diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. Management involves monitoring progression, treating complications, and planning for renal replacement therapy if kidney failure develops. Preventing progression to end-stage renal disease focuses on tight control of blood pressure, cholesterol, blood sugar, diet, and use of ACE inhibitors.
This document proposes revisions to ICD-9-CM codes for chronic kidney disease (CKD) to improve identification, staging, and management of patients. It recommends:
1) Separating codes for end-stage renal disease (ESRD) on dialysis/transplant from CKD codes
2) Adding 5 codes (586.1-586.5) to stage CKD by severity of glomerular filtration rate reduction
3) Adding a 5th digit to CKD codes to indicate presence of proteinuria or albuminuria
4) Instructing use of CKD codes along with disease-specific codes (e.g. diabetes, glomerulonephritis) to identify et
This document proposes revisions to ICD-9-CM codes for chronic kidney disease (CKD) to improve identification and classification of CKD stages and related risk factors. The proposed changes include: 1) Distinguishing CKD from end-stage renal disease and dialysis vs. transplant status, 2) Classifying CKD severity into 5 stages based on glomerular filtration rate, 3) Indicating presence or absence of proteinuria for each CKD stage, and 4) Coding CKD etiology and related comorbidities. The goals are to better assess patient risk, determine treatment needs, examine health care utilization and costs, and advance CKD research.
1. Chronic kidney disease (CKD) is defined as kidney damage or decreased kidney function lasting at least 3 months. It is staged based on glomerular filtration rate (GFR) from normal kidney function to kidney failure.
2. The most common causes of CKD are diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. As CKD progresses, patients experience complications such as anemia, bone disease, cardiovascular disease, and metabolic acidosis.
3. Management of CKD focuses on slowing progression, treating complications, and preparing for renal replacement therapy if kidney failure occurs. Key interventions include blood pressure control, diabetes management, treatment of anemia, and dietary modifications.
This document discusses chronic kidney disease (CKD), including its definition as structural or functional abnormalities of the kidneys for over 3 months, stages of progression from normal kidney function to kidney failure, prevalence, clinical practice guidelines for diagnosis and management, classification based on etiology and diagnosis, and remaining treatment options for end-stage renal disease.
1. Chronic kidney disease (CKD) affects 1 in 10 people in the UK and is often unrecognized as it commonly occurs alongside other conditions like cardiovascular disease or diabetes.
2. CKD is defined as abnormalities of the kidneys persisting for over 3 months, determined by markers of kidney damage or a glomerular filtration rate (GFR) of under 60 ml/min/1.73m^2.
3. People with CKD should be monitored for progression and referred to a nephrologist if their GFR declines rapidly or they have advanced CKD with a GFR under 30 ml/min/1.73m^2.
Uremia refers to the pathological manifestations that result from severe azotemia or high levels of urea in the blood due to kidney failure. The onset of uremia symptoms can vary depending on how quickly kidney function is lost. Both uremia and the uremic syndrome describe a very high plasma urea concentration caused by renal failure. As kidney function declines in chronic kidney disease, patients may experience fluid and electrolyte abnormalities, endocrine and metabolic issues, neurological problems, cardiovascular and pulmonary issues, dermatological changes, gastrointestinal disturbances, and hematological and immunological abnormalities. Many of these complications improve with dialysis treatment, while some persist even with optimal therapy.
Important Roles for Primary Care Providers in Treating Chronic Kidney DiseaseJames Rose
The document discusses the roles of primary care providers and patients in addressing chronic kidney disease, noting that 31 million Americans have CKD but 90% do not know it, and outlines key risk factors, stages of CKD progression, importance of early detection through regular testing of creatinine and eGFR levels, and strategies for protecting kidney health including controlling comorbid conditions and lifestyle factors. The presentation was given by representatives from The Kidney Trust and National Kidney Foundation to promote better management of CKD.
This document provides an overview of chronic kidney disease (CKD). It begins by defining CKD and different stages of kidney disease severity. Major risk factors for CKD progression include diabetes and hypertension. Early detection and treatment can slow CKD progression and improve outcomes. Treatment focuses on controlling blood pressure and glucose, with ACE inhibitors/ARBs shown to protect kidney function. Lifestyle changes like diet and exercise are also important for management.
Chronic kidney disease is defined by decreased kidney function or kidney damage lasting at least 3 months. It is caused by conditions that damage the kidneys such as diabetes and hypertension. Symptoms are often vague but can include fatigue, nausea, and decreased appetite. Complications include anemia, heart disease, bone disease, and nerve problems. Treatment focuses on controlling blood pressure and other risk factors as well as managing complications through diet, medication, dialysis or transplantation.
Uremia refers to the pathological manifestations that occur with severe azotemia or kidney failure. Symptoms of uremia develop as kidney function declines and waste products accumulate in the blood. Chronic kidney disease is defined as kidney damage or decreased kidney function lasting at least 3 months. It is staged based on glomerular filtration rate. Common complications in later stages include fluid and electrolyte abnormalities like hyperkalemia and metabolic acidosis, endocrine disorders like mineral bone disease, and neurological and cardiovascular issues. Dialysis can improve some manifestations of uremia but others may persist or progress despite treatment.
No, the combination of an ACE inhibitor and an ARB is not generally recommended for patients with diabetes and CKD. Some key points:
- There is no evidence that combining an ACEi with an ARB provides additional renal protection compared to monotherapy in patients with diabetes and CKD.
- Combining the two classes of drugs increases the risk of hyperkalemia and acute kidney injury without proven additional benefit over monotherapy.
- Current guidelines recommend using either an ACEi or an ARB as first-line therapy for albuminuria, but do not recommend combining the two classes of drugs.
So in summary, while ACEis and ARBs are both reasonable first-line options, combining
Mineral and Bone Disorder in Chronic Kidney Diseasedrsampadasinha
This document summarizes chronic kidney disease-mineral and bone disorder (CKD-MBD), including its definition, pathogenesis, diagnosis, and management recommendations. Specifically:
- CKD-MBD is defined as a systemic disorder involving abnormalities in calcium, phosphorus, vitamin D, PTH, and bone. It can cause skeletal and extraskeletal complications.
- As kidney function declines, abnormalities in mineral metabolism develop, leading to high or low bone turnover diseases. Phosphate retention, low calcitriol, and parathyroid gland changes drive secondary hyperparathyroidism.
- Diagnosis involves monitoring mineral levels and PTH. Bone biopsy determines the type of renal osteodystrophy
Chronic kidney disease and esrd(end stage renal diseaseZeelNaik2
CKD and ESRD.
Chronic Kidney Disease.
End-Stage Renal Disease.
CKD is a progressive loss of function over several months to years, characterized by gradual replacement of normal kidney architecture with interstitial fibrosis.
CKD is defined as either of the following conditions for a minimum of 3 months: GFR less than 60 ml/min/1.73 m2, or old damage to the kidneys with or without a decrease in GFR.
The prevalence of CKD increases with age and is greater in females.
CKD is a disease when GFR falls below 60 ml/min/1.73 m2 over at least 3 months.
CKD is a broad term that includes subtle decreases in kidney function that develop over a minimum of 3 months.
In contrast acute kidney injury refers to any deterioration in kidney function that happens in less than 3 months.
1) The document discusses the approach to chronic kidney disease (CKD). It defines CKD and outlines its stages based on glomerular filtration rate and albuminuria levels.
2) Risk factors for CKD mentioned include diabetes, hypertension, family history of kidney disease, use of certain medications, and prior acute kidney injury. The pathogenesis of CKD involves initial injury followed by adaptive hyperfiltration and long-term damage to remaining nephrons.
3) Evaluation of patients with suspected CKD involves obtaining a history, physical exam, lab tests including serum creatinine and urine analysis, and imaging like renal ultrasound. A kidney biopsy may be done if disease-specific therapy is still possible.
This document provides guidelines for the detection, prevention and management of kidney disease in people with diabetes. It aims to standardize screening approaches and improve diagnosis and management to reduce progression to end-stage renal disease. Key points covered include definitions of microalbuminuria and nephropathy, prevalence of chronic kidney disease in diabetes populations, screening recommendations including annual urine testing for albumin/protein starting at age 12, and the relationship between reduced kidney function and mortality risk. The goal is a collaborative approach between primary care, diabetes specialists and nephrology to manage renal complications of diabetes.
Chronic kidney disease (CKD) is a global public health problem with rising rates worldwide. CKD can be caused by conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and others. Progression of CKD can be monitored using glomerular filtration rate and proteinuria levels, with faster progression seen in diabetes. Complications of advanced CKD include uremia, malnutrition, fluid and electrolyte imbalances, and mineral bone disease. Non-dialytic management focuses on controlling hypertension, diabetes, and slowing progression.
This document discusses chronic kidney disease (CKD), including its definition, staging, epidemiology, causes, progression, complications, and non-dialytic management. CKD is defined based on kidney damage or decreased glomerular filtration rate below 60 mL/min/1.73m2 for over 3 months. Common causes include hypertension, diabetes, glomerulonephritis, and HIV. Progression is monitored using GFR and proteinuria levels, with faster progression seen in diabetes. Complications involve fluid/electrolyte disorders, bone disease, cardiovascular issues, and others. Non-dialytic management focuses on treating the underlying cause, controlling blood pressure and other risk factors, and preparing for renal replacement
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
Executive Directors Chat Leveraging AI for Diversity, Equity, and InclusionTechSoup
Let’s explore the intersection of technology and equity in the final session of our DEI series. Discover how AI tools, like ChatGPT, can be used to support and enhance your nonprofit's DEI initiatives. Participants will gain insights into practical AI applications and get tips for leveraging technology to advance their DEI goals.
How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
• The Committee on Ways and Means has been investigating several universities since November 15, 2023, when the Committee held a hearing entitled From Ivory Towers to Dark Corners: Investigating the Nexus Between Antisemitism, Tax-Exempt Universities, and Terror Financing. The Committee followed the hearing with letters to those institutions on January 10, 202
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
বাংলাদেশ অর্থনৈতিক সমীক্ষা (Economic Review) ২০২৪ UJS App.pdf
Att ckd oct04
1. Chronic Kidney Disease:
Proposed Revisions to the
ICD-9-CM Classification
Lesley Stevens MD
Tufts-New England Medical Center
National Kidney Foundation
2. Objectives
• Kidney Failure
• Stages of Chronic Kidney Disease
• Definition and Classification of CKD
• GFR
• Proteinuria
• Etiology
• Current use of ICD-9-CM codes for CKD
• Proposed changes to ICD-9-CM
4. Cardiovascular Mortality in the General
Population and in ESRD Treated by Dialysis
Annual mortality (%)
100
Dialysis
10
1
General population
0.1 Male
Female
0.01 Black
White
25–34 35–44 45–54 55–64 65–74 75–84 ≥85
Age (years)
5. Costs of Associated with Initiation of
Dialysis
St Peters, Khan, Ebben. Li, Xue, Pereira, Collins . Kidney Int. 200.
6. Stages in Progression of Chronic Kidney
Disease and Therapeutic Strategies
Complications
Complications
Increased
Increased Kidney
Kidney CKD
Normal Damage
Damage ↓ GFR
↓ GFR
risk failure
failure death
Screening CKD risk Diagnosis Estimate Replacement
for CKD reduction; & treatment; progression; by dialysis
risk factors Screening for Treat Treat & transplant
CKD comorbid complications;
conditions; Prepare for
Slow replacement
progression
7. Definition of CKD
Structural or functional abnormalities of
the kidneys for >3 months, as
manifested by either:
1. Kidney damage, with or without decreased
GFR, as defined by
• pathologic abnormalities
• markers of kidney damage, including
abnormalities in the composition of the blood or
urine or abnormalities in imaging tests
2. GFR <60 ml/min/1.73 m2, with or without
kidney damage
8. Prevalence of CKD and Estimated Number of
Adults with CKD in the US (NHANES 88-94)
Prevalence*
GFR
Stage Description N
(ml/min/1.73 m2) %
(1000s)
Kidney Damage with
1 ≥ 90 5,900 3.3
Normal or ↑ GFR
Kidney Damage with
2 60-89 5,300 3.0
Mild ↓ GFR
3 Moderate ↓ GFR 30-59 7,600 4.3
4 Severe ↓ GFR 15-29 400 0.2
5 Kidney Failure < 15 or Dialysis 300 0.1
*Stages 1-4 from NHANES III (1988-1994). Population of 177 million with age ≥20. Stage 5 from USRDS (1998), includes
approximately 230,000 patients treated by dialysis, and assuming 70,000 additional patients not on dialysis. GFR estimated
from serum creatinine using MDRD Study equation based on age, gender, race and calibration for serum creatinine. For
Stage 1 and 2, kidney damage estimated by spot albumin-to-creatinine ratio ≥17 mg/g in men or ≥25 mg/g in women in two
measurements.
9. Prevalence of Abnormalities at each level of GFR
*>140/90 or antihypertensive medication p-trend < 0.001 for each abnormality
10. Age-Standardized Rates of Death from Any Cause
(Panel A) and Cardiovascular Events (Panel B),
According to the Estimated GFR among 1,120,295
Ambulatory Adults
Go, A, et al. NEJM 351: 1296
11. Clinical Practice Guidelines for the Detection,
Evaluation and Management of CKD
Stage Description GFR Evaluation Management
At increased
Test for CKD Risk factor management
risk
Diagnosis
Kidney
Comorbid Specific therapy, based on diagnosis
damage with
1 >90 conditions Management of comorbid conditions
normal or ↑
CVD and CVD Treatment of CVD and CVD risk factors
GFR
risk factors
Kidney
Rate of
2 damage with 60-89 Slowing rate of loss of kidney function 1
progression
mild ↓ GFR
Moderate ↓
3 30-59 Complications Prevention and treatment of complications
GFR
Preparation for kidney replacement therapy
4 Severe ↓ GFR 15-29
Referral to Nephrologist
5 Kidney Failure <15 Kidney replacement therapy
1
Target blood pressure less than 130/80 mm Hg. Angiotension converting enzyme inhibitors
(ACEI) or angiotension receptor blocker (ARB) for diabetic or non-diabetic kidney disease with spot
urine total protein-to-creatinine ratio of greater than 200 mg/g.
12. Definition of ESRD vs Kidney Failure
• ESRD is a federal government defined
term that indicates chronic treatment by
dialysis or transplantation
• Kidney Failure: GFR < 15 ml/min/1.73
m2 or on dialysis.
13. Importance of Proteinuria in CKD
Interpretation Explanation
Marker of kidney Spot urine albumin-to-creatinine ratio >30 mg/g or
damage spot urine total protein-to-creatinine ratio >200 mg/g
for >3 months defines CKD
Clue to the type Spot urine total protein-to-creatinine ratio >500-
(diagnosis) of CKD 1000 mg/g suggests diabetic kidney disease,
glomerular diseases, or transplant glomerulopathy.
Risk factor for adverse Higher proteinuria predicts faster progression of
outcomes kidney disease and increased risk of CVD.
Effect modifier for Strict blood pressure control and ACE inhibitors are
interventions more effective in slowing kidney disease
progression in patients with higher baseline
proteinuria.
Hypothesized If validated, then lowering proteinuria would be a
surrogate outcomes goal of therapy.
and target for
interventions
14. Albuminuria as a Risk Factor for CVD in
PREVEND
Hillege HL et al. Circulation 2002: 106: 1777-1782
15. Progression of Kidney Disease related to
level of proteinuria and blood pressure
lowering in MDRD Study
Petersen. Annals of Internal Medicine. 1995
16. Clinical Practice Guidelines for
Management of Hypertension in CKD
Type of Kidney Disease Blood Pressure Preferred Agents Other Agents
Target for CKD, with or to Reduce CVD Risk
(mm Hg) without and Reach Blood
Hypertension Pressure Target
Diabetic Kidney Disease
ACE inhibitor Diuretic preferred,
Nondiabetic Kidney or ARB then BB or CCB
Disease with Urine Total
Protein-to-Creatinine
Ratio ≥200 mg/g <130/80
Nondiabetic Kidney Diuretic preferred,
Disease with Spot Urine then ACE inhibitor,
Total Protein-to-Creatinine ARB, BB or CCB
ratio <200 mg/g None preferred
Kidney Disease in Kidney CCB, diuretic, BB,
Transplant Recipient ACE inhibitor, ARB
17. Classification of CKD by Diagnosis
• Diabetic Kidney Disease
• Glomerular diseases (autoimmune diseases,
systemic infections, drugs, neoplasia)
• Vascular diseases (renal artery disease,
hypertension, microangiopathy)
• Tubulointerstitial diseases (urinary tract infection,
stones, obstruction, drug toxicity)
• Cystic diseases (polycystic kidney disease)
• Diseases in the transplant (Allograft nephropathy,
drug toxicity, recurrent diseases, transplant
glomerulopathy)
18. Current use of ICD-9-CM codes for
Kidney Disease
• ICD-9-CM codes for kidney disease were
used in 1% of all patients.
GFR Sensitivity Specificity
30-59 6 97
< 30 39 96
* GFR in ml/min/1.72 m2
19. Current use of ‘585’ (chronic renal
failure) in 277, 262 adults visiting an
outpatient commercial clinical
laboratory
GFR (ml/min/1.73 m2)*
>90 60-89 30-59 15-29 <15
No 585 code** 13 60 27 3 <1
585 code 10 62 23 2 <1
* GFR in ml/min/1.72 m2
**Row Percentages
20. Proposed Classification: ESRD code
585 End Stage Renal Disease;
on dialysis
585.1 End Stage Renal Disease;
transplanted
Use additional code to identify
chronic kidney disease (586.1-586.9)
21. Proposed Classification: CKD code
586.1 Stage I CKD: Kidney damage with normal or
increased glomerular filtration rate (GFR), greater than
or equal to 90 ml/min/1.73m2
586.2 Stage II CKD: Kidney damage with mild decrease in
GFR 60-89 ml/min/1.73m2
586.3 Stage III CKD: Kidney damage with moderate
decrease in GFR 30-59 ml/min/1.73m 2
586.4 Stage IV CKD: Kidney damage with severe decrease
in GFR 15-29 ml/min/1.73m2
586.5 Stage V CKD: Kidney damage with GFR of less than
15 ml/min/1.73m2 Kidney failure with GFR less than 15
ml/min/1.73m2 and not on dialysis
Note: Codes apply only to patients diagnosed kidney disease > 3 mo
22. Proposed Classification:
CKD code 5th digit
• Each 586 (CKD) code requires a 5th digit
to indicate evidence of proteinuria or
albuminuria
– 586.X0 for those without evidence of proteinuria or
albuminuria
– 586.X1 for those with evidence of proteinuria or
albuminuria
23. Proposed Classification: Etiology
• Instructions to code for CKD stage
along with disease specific codes
250.4 Diabetes with renal manifestations
Use additional code to identify manifestation, as:
Add chronic kidney disease (585.1-585.9)
582.81 Chronic glomerulonephritis in diseases
classified elsewhere: amyloidosis, SLE
Use additional code to identify manifestation, as:
Add chronic kidney disease (585.1-585.9)
24. Benefits of Revised ICD-9-CM codes
1. Distinguish between ESRD and CKD; between dialysis
and transplantation
2. Assess risk for adverse outcomes, expected
complications and comorbid disease by the combination
of severity of CKD (stages), proteinuria and diagnosis
3. Determine which patients require specific treatments
based on severity of CKD, and in particular proteinuria
4. Examine of health care utilization and costs. Assess
rural and urban settings and racial disparities
5. Assess quality of care delivered
6. Progress toward achievement of Healthy People 2010
goals
7. Allow CMS and USRDS to develop specific research
files to investigators to enhance our knowledge of CKD
by the major risk groups