This document discusses acute kidney injury (AKI). It provides definitions of AKI from various clinical practice guidelines. AKI can be prerenal, intrinsic, or postrenal based on its etiology. Common causes are listed. Diagnosis involves medical history, physical exam, lab tests of blood and urine. Staging systems like RIFLE and KDIGO use changes in serum creatinine and urine output to stage AKI severity. Prevention focuses on identifying at-risk patients and implementing strategies like intravenous fluids. Treatment aims to support kidney function through fluid management, electrolyte monitoring, and potentially renal replacement therapy like hemodialysis.
Dilutional hyponatremia is common in cirrhosis patients with ascites, occurring in 30-60% of cases. It involves reduced ability to excrete water due to impaired kidney function and excess arginine vasopressin. Fluid restriction can prevent worsening hyponatremia but not increase sodium levels. New drugs that block vasopressin's effects, called V2 receptor antagonists, increase water excretion and serum sodium without electrolyte or blood pressure changes. Studies in animals and healthy humans show promise for V2 antagonists in treating hyponatremia in cirrhosis patients.
1) Telmisartan has the longest half-life, largest volume of distribution, highest lipophilicity, and lowest renal excretion of clinically available ARBs, resulting in the longest duration of action.
2) Telmisartan binds insurmountably to the AT1 receptor and has a much longer dissociation half-life compared to losartan, providing tighter, more sustained blockade of the RAS.
3) Telmisartan is the preferred ARB for patients with renal impairment due to its renal excretion profile and superior blood pressure lowering in renal disease compared to other ARBs like losartan.
Diabetic cardiomyopathy is characterized by abnormal myocardial structure and function in patients with diabetes but without other known causes of heart disease. It is caused by prolonged hyperglycemia and metabolic alterations that result in changes like fibrosis and impaired relaxation and filling of the heart. Diagnosis involves echocardiography and tissue Doppler imaging to detect early diastolic dysfunction. Treatment focuses on strict glycemic control as well as medications like ACE inhibitors, ARBs, beta-blockers, and statins to counter the effects of diabetes on the heart.
This document summarizes recent evidence on cardiovascular disease risk factors and lipid management. Key points include:
- Lowering LDL cholesterol and other apoB-containing lipoproteins reduces cardiovascular risk in a linear, dose-dependent manner with no lower limit.
- HDL cholesterol raising therapies have not been shown to reduce cardiovascular risk beyond modest reductions in apoB.
- Triglycerides associate with risk, but this is mediated by changes in non-HDL cholesterol and apoB levels rather than triglyceride levels alone.
- Calculated and direct LDL cholesterol measurements provide similar risk information in most cases, but direct measurement may be needed in some patients with high triglycerides or metabolic conditions.
This document provides information on acute kidney injury (AKI) including its definition, classification, clinical features, management, and prevention. It defines AKI according to the KDIGO guidelines and discusses pediatric RIFLE criteria. It covers creatinine as a marker of AKI severity, novel biomarkers, epidemiology, etiologies, pathophysiology, investigations, treatment including management of complications, and prevention of AKI. The key aspects are early recognition and fluid resuscitation of pre-renal causes, monitoring of fluid balance and electrolytes, and avoiding nephrotoxic medications.
Tolvaptan is an oral selective vasopressin V2 receptor antagonist used for the treatment of hyponatremia. [1] It produces significant aquaresis and increases serum sodium levels without affecting electrolyte levels. [2] Clinical trials showed tolvaptan effectively corrected hyponatremia in heart failure and cirrhosis patients. [3] In acute decompensated heart failure, tolvaptan provided relief of symptoms without affecting mortality, renal function, or electrolyte levels long-term. [3] The most common side effects are thirst, dry mouth, and polyuria. [4]
The document discusses the benefits of angiotensin receptor blockers (ARBs) in treating chronic kidney disease, specifically in patients with type 2 diabetes. It summarizes the results of the RENAAL clinical trial which found that losartan reduced the risk of doubling of serum creatinine, end-stage renal disease, and other kidney-related outcomes in patients with type 2 diabetes and nephropathy by 16-28% compared to placebo. The trial demonstrated that losartan provided renoprotective effects beyond blood pressure control alone in this high-risk population.
Drug induced Kidney Injury in the ICU. Presentation by Dr Sandra Kane Gill , President Society of Critical Care Medicine (SCCM) , USA at the Egyptian Critical care Summit 2022 conference , organized by the Egyptian College of Critical care Physicians (ECCCP) , Egypt
Dilutional hyponatremia is common in cirrhosis patients with ascites, occurring in 30-60% of cases. It involves reduced ability to excrete water due to impaired kidney function and excess arginine vasopressin. Fluid restriction can prevent worsening hyponatremia but not increase sodium levels. New drugs that block vasopressin's effects, called V2 receptor antagonists, increase water excretion and serum sodium without electrolyte or blood pressure changes. Studies in animals and healthy humans show promise for V2 antagonists in treating hyponatremia in cirrhosis patients.
1) Telmisartan has the longest half-life, largest volume of distribution, highest lipophilicity, and lowest renal excretion of clinically available ARBs, resulting in the longest duration of action.
2) Telmisartan binds insurmountably to the AT1 receptor and has a much longer dissociation half-life compared to losartan, providing tighter, more sustained blockade of the RAS.
3) Telmisartan is the preferred ARB for patients with renal impairment due to its renal excretion profile and superior blood pressure lowering in renal disease compared to other ARBs like losartan.
Diabetic cardiomyopathy is characterized by abnormal myocardial structure and function in patients with diabetes but without other known causes of heart disease. It is caused by prolonged hyperglycemia and metabolic alterations that result in changes like fibrosis and impaired relaxation and filling of the heart. Diagnosis involves echocardiography and tissue Doppler imaging to detect early diastolic dysfunction. Treatment focuses on strict glycemic control as well as medications like ACE inhibitors, ARBs, beta-blockers, and statins to counter the effects of diabetes on the heart.
This document summarizes recent evidence on cardiovascular disease risk factors and lipid management. Key points include:
- Lowering LDL cholesterol and other apoB-containing lipoproteins reduces cardiovascular risk in a linear, dose-dependent manner with no lower limit.
- HDL cholesterol raising therapies have not been shown to reduce cardiovascular risk beyond modest reductions in apoB.
- Triglycerides associate with risk, but this is mediated by changes in non-HDL cholesterol and apoB levels rather than triglyceride levels alone.
- Calculated and direct LDL cholesterol measurements provide similar risk information in most cases, but direct measurement may be needed in some patients with high triglycerides or metabolic conditions.
This document provides information on acute kidney injury (AKI) including its definition, classification, clinical features, management, and prevention. It defines AKI according to the KDIGO guidelines and discusses pediatric RIFLE criteria. It covers creatinine as a marker of AKI severity, novel biomarkers, epidemiology, etiologies, pathophysiology, investigations, treatment including management of complications, and prevention of AKI. The key aspects are early recognition and fluid resuscitation of pre-renal causes, monitoring of fluid balance and electrolytes, and avoiding nephrotoxic medications.
Tolvaptan is an oral selective vasopressin V2 receptor antagonist used for the treatment of hyponatremia. [1] It produces significant aquaresis and increases serum sodium levels without affecting electrolyte levels. [2] Clinical trials showed tolvaptan effectively corrected hyponatremia in heart failure and cirrhosis patients. [3] In acute decompensated heart failure, tolvaptan provided relief of symptoms without affecting mortality, renal function, or electrolyte levels long-term. [3] The most common side effects are thirst, dry mouth, and polyuria. [4]
The document discusses the benefits of angiotensin receptor blockers (ARBs) in treating chronic kidney disease, specifically in patients with type 2 diabetes. It summarizes the results of the RENAAL clinical trial which found that losartan reduced the risk of doubling of serum creatinine, end-stage renal disease, and other kidney-related outcomes in patients with type 2 diabetes and nephropathy by 16-28% compared to placebo. The trial demonstrated that losartan provided renoprotective effects beyond blood pressure control alone in this high-risk population.
Drug induced Kidney Injury in the ICU. Presentation by Dr Sandra Kane Gill , President Society of Critical Care Medicine (SCCM) , USA at the Egyptian Critical care Summit 2022 conference , organized by the Egyptian College of Critical care Physicians (ECCCP) , Egypt
Fixed dose combination products – rationality, status in india, development i...Dr Sukanta sen
The development of FDCs is becoming increasingly
important from a public health perspective.
•They are being used in the treatment of a wide range of
conditions and are particularly useful in the management of
human immunodeficiency virus/acquired immunodeficiency
syndrome (HIV/AIDS), malaria and tuberculosis, which are
considered to be the foremost infectious disease threats in the world today.
This document summarizes recent advances in understanding and treating hepatorenal syndrome (HRS). It defines HRS as a form of kidney injury seen in patients with cirrhosis and liver failure, characterized by impaired kidney function without structural kidney changes. The document reviews definitions of acute kidney injury in cirrhosis, types of HRS, biomarkers for diagnosis, pathophysiology involving reduced renal blood flow, and approaches to prevention, medical treatment including vasoconstrictors, and renal replacement therapies like renal transplantation for HRS.
This document discusses therapeutic drug monitoring of digoxin. Digoxin is a cardiac glycoside derived from Digitalis lanata and Digitalis purpurea. It has a steroidal structure with three digitoxose units bound by a glycosidic linkage. Digoxin is indicated for heart failure and atrial fibrillation with a dose of 0.125-0.25 mg tablets or 0.1-0.25 mg/mL injections. Therapeutic drug monitoring of digoxin is important due to its narrow therapeutic index and variability in patient response. Radioimmunoassay is commonly used to measure digoxin levels via competitive binding of labeled and unlabeled antigen to antibodies.
CPG: Prevention and Treatment of Venous Thromboembolism (VTE)Khairunnisa Zamri
This document provides guidelines for the prevention and treatment of venous thromboembolism (VTE). It defines VTE as deep vein thrombosis and pulmonary embolism. It discusses the epidemiology, causes, risk factors, pathophysiology and various methods for prophylaxis and treatment of VTE, including pharmacological agents such as low molecular weight heparins, fondaparinux, vitamin K antagonists, and new oral anticoagulants. It also covers topics such as risk assessment, timing of prophylaxis, duration of treatment and switching between different anticoagulation agents.
Burden and Control of Alcoholic Liver Cirrhosis in India Rizwan S A
1) Alcoholic liver disease ranges from steatosis (fatty liver) in 30% of heavy drinkers to cirrhosis in 10%.
2) In India, the annual death rate from alcoholic liver cirrhosis is 24 per 100,000 population, and 30% of all liver cirrhosis cases are attributable to alcohol abuse. Alcohol use is prevalent in 30% of adult men and 5% of adult women.
3) Prevention strategies include primary prevention through policies aimed at restricting alcohol production, pricing and marketing, as well as secondary prevention through screening of patients for risky drinking behaviors and providing advice to limit intake to less than 200ml per day for more than 14 years.
This document provides an overview of canagliflozin, an SGLT2 inhibitor used to treat type 2 diabetes. It discusses the pathogenesis of type 2 diabetes, progressive beta cell dysfunction, and the kidney's role in glucose regulation. It then reviews canagliflozin's mechanism of action as an SGLT2 inhibitor, increasing urinary glucose excretion and reducing blood glucose levels. The document summarizes canagliflozin's clinical trials, pharmacokinetics, efficacy, safety profile, and effects on renal function and lipids.
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 study investigated the effects of adding eplerenone to evidence-based heart failure therapies in patients with mild systolic heart failure symptoms. The study randomized 2,737 patients to receive either eplerenone or placebo. The primary outcome of death from cardiovascular causes or hospitalization for heart failure occurred in 18.3% of the eplerenone group compared to 25.9% of the placebo group, demonstrating that eplerenone reduced risks. The trial was stopped early due to these benefits after a median follow up of 21 months. Eplerenone was found to provide cardiovascular protection in patients with heart failure compared to placebo.
This document discusses atrial fibrillation (AF), the most common cardiac arrhythmia. It covers the ECG features of AF, risk factors, mechanisms, classification, evaluation, and management. Regarding management, the summary focuses on rate control using beta blockers, calcium channel blockers, or digoxin. It also touches on rhythm control strategies like electrical or pharmacological cardioversion. Anticoagulation is emphasized based on stroke risk according to the CHA2DS2-VASc score. The overall approach involves assessing stability, pursuing rate or rhythm control depending on symptoms, evaluating for anticoagulation need, and arranging follow-up.
Dapagliflozin is an SGLT2 inhibitor that has shown benefits in managing type 2 diabetes and reducing cardiovascular outcomes. The document summarizes results from several key studies on dapagliflozin. The DECLARE-TIMI trial showed that dapagliflozin reduced the risk of cardiovascular death or hospitalization for heart failure compared to placebo in patients with type 2 diabetes with high cardiovascular risk. The DAPA-HF trial found that dapagliflozin reduced the risks of worsening heart failure or cardiovascular death compared to placebo in patients with heart failure regardless of diabetes status. Dapagliflozin also improved outcomes related to heart failure in the DEFINE-HF trial.
There are two distinct goals of drug therapy in CHF.
Relief of congestion/ low cardiac output symptoms and restoration of cardiac performance.
Ionotropic agents, Vasodilators, Diuretics, BETA Blockers.
Arrest/reversal of disease progression and prolongation of survival.
ACE inhibitors, ARBs, Beta Blockers, Aldosterone Antagonists.
Creatinine clearance: When Does It Matter?PASaskatchewan
This document provides information on estimating kidney function and adjusting drug dosing in patients with chronic kidney disease (CKD). It describes the differences between creatinine clearance (CrCl), estimated glomerular filtration rate (eGFR), and their respective formulas (Cockcroft-Gault and MDRD/CKD-EPI). While both CrCl and eGFR can be used to estimate kidney function and guide drug dosing, CrCl may be preferred in the elderly and for drugs with a narrow therapeutic index. The document reviews drug classes that commonly require dosage adjustments in CKD and provides an example case of adjusting anticoagulation therapy in a patient with CKD.
Diabetic cardiomyopathy refers to myocardial disease in diabetic subjects that cannot be ascribed to hypertension, coronary artery disease (CAD), or any other known cardiac disease. Key aspects discussed include the high prevalence of heart failure in diabetic patients, pathophysiological changes such as hypertrophy and fibrosis, and risk factors like hyperglycemia and hypertension. Management involves tight control of blood pressure and blood glucose, as well as medications like angiotensin-converting enzyme inhibitors, beta blockers, and aldosterone receptor antagonists which have been shown to improve outcomes. Aggressive modification of cardiovascular risk factors is important in the management of diabetic cardiomyopathy.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/AtiaKPIdzAQ
Arabic Language version of this lecture is available at:
https://youtu.be/2cwyPcRDGEY
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
This document summarizes the Simplicity HTN-2 and Simplicity HTN-3 clinical trials that evaluated the effectiveness of renal denervation for treating resistant hypertension. The Simplicity HTN-2 trial found that renal denervation significantly reduced blood pressure in patients with resistant hypertension compared to a control group. However, the larger Simplicity HTN-3 trial, which was blinded and sham-controlled, did not find a significant reduction in blood pressure between the renal denervation and sham groups at 6 months.
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
Diabetic nephropathy is a leading cause of end-stage renal disease worldwide. Strict control of blood glucose, blood pressure, angiotensin system inhibitors, and other risk factors can help prevent or slow the progression of kidney damage. The stages include early hyperfiltration, development of microalbuminuria, progression to macroalbuminuria and renal failure. Management focuses on glycemic control, blood pressure reduction, angiotensin blockade, cholesterol control, and management of anemia and cardiovascular risk factors to preserve kidney function for as long as possible.
The document discusses the proposal to change the name of non-alcoholic fatty liver disease (NAFLD) to metabolic associated fatty liver disease (MAFLD). It notes that NAFLD's name does not accurately capture the metabolic nature of the disease. The name change was proposed by an international panel of experts and aims to reduce stigmatization and increase consideration of the disease. If adopted, MAFLD would be used instead of NAFLD to describe fatty liver disease associated with metabolic dysfunction. The document supports the name change as a way to properly frame the growing epidemic of this liver disease.
This document provides an overview of acute kidney injury (AKI), including its definition, prevalence, diagnosis, pathophysiology, biomarkers, and staging criteria according to RIFLE, AKIN, and KDIGO. It discusses the need for biomarkers to detect AKI early before increases in serum creatinine. Commonly used biomarkers mentioned include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), and cystatin C. The pathophysiology of AKI involves alterations in renal perfusion, tubular dysfunction and cell death, intrat
This document defines acute kidney injury (AKI) and describes its staging, risk factors, types, epidemiology, etiology, clinical presentation, diagnosis, and management. AKI is defined as a rapid decrease in kidney function shown by changes in serum creatinine, BUN, and urine output. It stages AKI severity based on changes in serum creatinine and urine output. Common causes of AKI include reduced renal perfusion, intrinsic kidney damage, and urinary obstruction. Treatment involves fluid hydration, electrolyte management, avoiding nephrotoxins, and considering diuretics or renal replacement therapy in severe cases.
Fixed dose combination products – rationality, status in india, development i...Dr Sukanta sen
The development of FDCs is becoming increasingly
important from a public health perspective.
•They are being used in the treatment of a wide range of
conditions and are particularly useful in the management of
human immunodeficiency virus/acquired immunodeficiency
syndrome (HIV/AIDS), malaria and tuberculosis, which are
considered to be the foremost infectious disease threats in the world today.
This document summarizes recent advances in understanding and treating hepatorenal syndrome (HRS). It defines HRS as a form of kidney injury seen in patients with cirrhosis and liver failure, characterized by impaired kidney function without structural kidney changes. The document reviews definitions of acute kidney injury in cirrhosis, types of HRS, biomarkers for diagnosis, pathophysiology involving reduced renal blood flow, and approaches to prevention, medical treatment including vasoconstrictors, and renal replacement therapies like renal transplantation for HRS.
This document discusses therapeutic drug monitoring of digoxin. Digoxin is a cardiac glycoside derived from Digitalis lanata and Digitalis purpurea. It has a steroidal structure with three digitoxose units bound by a glycosidic linkage. Digoxin is indicated for heart failure and atrial fibrillation with a dose of 0.125-0.25 mg tablets or 0.1-0.25 mg/mL injections. Therapeutic drug monitoring of digoxin is important due to its narrow therapeutic index and variability in patient response. Radioimmunoassay is commonly used to measure digoxin levels via competitive binding of labeled and unlabeled antigen to antibodies.
CPG: Prevention and Treatment of Venous Thromboembolism (VTE)Khairunnisa Zamri
This document provides guidelines for the prevention and treatment of venous thromboembolism (VTE). It defines VTE as deep vein thrombosis and pulmonary embolism. It discusses the epidemiology, causes, risk factors, pathophysiology and various methods for prophylaxis and treatment of VTE, including pharmacological agents such as low molecular weight heparins, fondaparinux, vitamin K antagonists, and new oral anticoagulants. It also covers topics such as risk assessment, timing of prophylaxis, duration of treatment and switching between different anticoagulation agents.
Burden and Control of Alcoholic Liver Cirrhosis in India Rizwan S A
1) Alcoholic liver disease ranges from steatosis (fatty liver) in 30% of heavy drinkers to cirrhosis in 10%.
2) In India, the annual death rate from alcoholic liver cirrhosis is 24 per 100,000 population, and 30% of all liver cirrhosis cases are attributable to alcohol abuse. Alcohol use is prevalent in 30% of adult men and 5% of adult women.
3) Prevention strategies include primary prevention through policies aimed at restricting alcohol production, pricing and marketing, as well as secondary prevention through screening of patients for risky drinking behaviors and providing advice to limit intake to less than 200ml per day for more than 14 years.
This document provides an overview of canagliflozin, an SGLT2 inhibitor used to treat type 2 diabetes. It discusses the pathogenesis of type 2 diabetes, progressive beta cell dysfunction, and the kidney's role in glucose regulation. It then reviews canagliflozin's mechanism of action as an SGLT2 inhibitor, increasing urinary glucose excretion and reducing blood glucose levels. The document summarizes canagliflozin's clinical trials, pharmacokinetics, efficacy, safety profile, and effects on renal function and lipids.
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 study investigated the effects of adding eplerenone to evidence-based heart failure therapies in patients with mild systolic heart failure symptoms. The study randomized 2,737 patients to receive either eplerenone or placebo. The primary outcome of death from cardiovascular causes or hospitalization for heart failure occurred in 18.3% of the eplerenone group compared to 25.9% of the placebo group, demonstrating that eplerenone reduced risks. The trial was stopped early due to these benefits after a median follow up of 21 months. Eplerenone was found to provide cardiovascular protection in patients with heart failure compared to placebo.
This document discusses atrial fibrillation (AF), the most common cardiac arrhythmia. It covers the ECG features of AF, risk factors, mechanisms, classification, evaluation, and management. Regarding management, the summary focuses on rate control using beta blockers, calcium channel blockers, or digoxin. It also touches on rhythm control strategies like electrical or pharmacological cardioversion. Anticoagulation is emphasized based on stroke risk according to the CHA2DS2-VASc score. The overall approach involves assessing stability, pursuing rate or rhythm control depending on symptoms, evaluating for anticoagulation need, and arranging follow-up.
Dapagliflozin is an SGLT2 inhibitor that has shown benefits in managing type 2 diabetes and reducing cardiovascular outcomes. The document summarizes results from several key studies on dapagliflozin. The DECLARE-TIMI trial showed that dapagliflozin reduced the risk of cardiovascular death or hospitalization for heart failure compared to placebo in patients with type 2 diabetes with high cardiovascular risk. The DAPA-HF trial found that dapagliflozin reduced the risks of worsening heart failure or cardiovascular death compared to placebo in patients with heart failure regardless of diabetes status. Dapagliflozin also improved outcomes related to heart failure in the DEFINE-HF trial.
There are two distinct goals of drug therapy in CHF.
Relief of congestion/ low cardiac output symptoms and restoration of cardiac performance.
Ionotropic agents, Vasodilators, Diuretics, BETA Blockers.
Arrest/reversal of disease progression and prolongation of survival.
ACE inhibitors, ARBs, Beta Blockers, Aldosterone Antagonists.
Creatinine clearance: When Does It Matter?PASaskatchewan
This document provides information on estimating kidney function and adjusting drug dosing in patients with chronic kidney disease (CKD). It describes the differences between creatinine clearance (CrCl), estimated glomerular filtration rate (eGFR), and their respective formulas (Cockcroft-Gault and MDRD/CKD-EPI). While both CrCl and eGFR can be used to estimate kidney function and guide drug dosing, CrCl may be preferred in the elderly and for drugs with a narrow therapeutic index. The document reviews drug classes that commonly require dosage adjustments in CKD and provides an example case of adjusting anticoagulation therapy in a patient with CKD.
Diabetic cardiomyopathy refers to myocardial disease in diabetic subjects that cannot be ascribed to hypertension, coronary artery disease (CAD), or any other known cardiac disease. Key aspects discussed include the high prevalence of heart failure in diabetic patients, pathophysiological changes such as hypertrophy and fibrosis, and risk factors like hyperglycemia and hypertension. Management involves tight control of blood pressure and blood glucose, as well as medications like angiotensin-converting enzyme inhibitors, beta blockers, and aldosterone receptor antagonists which have been shown to improve outcomes. Aggressive modification of cardiovascular risk factors is important in the management of diabetic cardiomyopathy.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/AtiaKPIdzAQ
Arabic Language version of this lecture is available at:
https://youtu.be/2cwyPcRDGEY
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
This document summarizes the Simplicity HTN-2 and Simplicity HTN-3 clinical trials that evaluated the effectiveness of renal denervation for treating resistant hypertension. The Simplicity HTN-2 trial found that renal denervation significantly reduced blood pressure in patients with resistant hypertension compared to a control group. However, the larger Simplicity HTN-3 trial, which was blinded and sham-controlled, did not find a significant reduction in blood pressure between the renal denervation and sham groups at 6 months.
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
Diabetic nephropathy is a leading cause of end-stage renal disease worldwide. Strict control of blood glucose, blood pressure, angiotensin system inhibitors, and other risk factors can help prevent or slow the progression of kidney damage. The stages include early hyperfiltration, development of microalbuminuria, progression to macroalbuminuria and renal failure. Management focuses on glycemic control, blood pressure reduction, angiotensin blockade, cholesterol control, and management of anemia and cardiovascular risk factors to preserve kidney function for as long as possible.
The document discusses the proposal to change the name of non-alcoholic fatty liver disease (NAFLD) to metabolic associated fatty liver disease (MAFLD). It notes that NAFLD's name does not accurately capture the metabolic nature of the disease. The name change was proposed by an international panel of experts and aims to reduce stigmatization and increase consideration of the disease. If adopted, MAFLD would be used instead of NAFLD to describe fatty liver disease associated with metabolic dysfunction. The document supports the name change as a way to properly frame the growing epidemic of this liver disease.
This document provides an overview of acute kidney injury (AKI), including its definition, prevalence, diagnosis, pathophysiology, biomarkers, and staging criteria according to RIFLE, AKIN, and KDIGO. It discusses the need for biomarkers to detect AKI early before increases in serum creatinine. Commonly used biomarkers mentioned include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), and cystatin C. The pathophysiology of AKI involves alterations in renal perfusion, tubular dysfunction and cell death, intrat
This document defines acute kidney injury (AKI) and describes its staging, risk factors, types, epidemiology, etiology, clinical presentation, diagnosis, and management. AKI is defined as a rapid decrease in kidney function shown by changes in serum creatinine, BUN, and urine output. It stages AKI severity based on changes in serum creatinine and urine output. Common causes of AKI include reduced renal perfusion, intrinsic kidney damage, and urinary obstruction. Treatment involves fluid hydration, electrolyte management, avoiding nephrotoxins, and considering diuretics or renal replacement therapy in severe cases.
1) Acute kidney injury (AKI) is an abrupt decrease in kidney function over 7 days that results in a buildup of waste in the body. It can be caused by reduced blood flow to the kidneys or kidney damage.
2) AKI is common, affecting 1-25% of hospitalized patients depending on whether they are in the ICU or not. Mortality is high, reaching 50% for ICU patients with multiple organ failure.
3) AKI is staged based on changes in creatinine and urine output. Prevention focuses on identifying at-risk patients and avoiding insults like dehydration and nephrotoxic drugs. Treatment involves supportive care, reversing causes if possible, and
This document provides an overview of acute kidney injury (AKI), formerly known as acute renal failure. It discusses the definition, epidemiology, diagnostic criteria, etiology, pathophysiology, diagnostic evaluation, urine and blood findings, complications, supportive management including nutrition and monitoring, indications for hemodialysis, timing of dialysis initiation, and prognosis. AKI is characterized by sudden impairment of kidney function and retention of waste products. It commonly occurs in hospitalized patients, especially those in the intensive care unit. The most widely used diagnostic criteria are from KDIGO. Common causes include acute tubular necrosis, prerenal azotemia, and acute injury superimposed on chronic kidney disease. Supportive care focuses on fluid
Guideline, management of acute kidney injuryvita madmo
This document provides guidelines for the management of acute kidney injury (AKI). It defines AKI and outlines stages of severity based on the RIFLE, AKIN and KDIGO criteria. Management of AKI focuses on treating underlying causes, maintaining fluid and electrolyte balance, and considering renal replacement therapy for complications like fluid overload or severe azotemia. Dialysis modalities and anticoagulation options are discussed. The guidelines recommend supportive care including diet modification and avoiding nephrotoxic drugs.
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.
Tauhid Ahmed Bhuiyan, PharmD presented a document on drug-induced acute kidney injury. The document discussed the background, epidemiology and overview of acute kidney injury. It reviewed the pathogenic mechanisms and prevention strategies of drug-induced acute kidney injury. It also evaluated the implications of computerized clinical decision support systems for medication dosing in patients with renal insufficiency.
The document discusses renal impairment in anesthesia, including acute kidney injury (AKI) and chronic kidney disease (CKD). It covers the definition, causes, and staging of AKI and CKD. Pre-operative management of patients with renal impairment focuses on optimizing fluid, electrolyte and acid-base status. Intra-operatively, reduced doses of medications may be needed due to impaired drug clearance. Regional anesthesia offers advantages over general anesthesia when possible. Careful post-operative monitoring of fluid balance and renal function is also emphasized.
This document summarizes guidelines for timing renal replacement therapy (RRT) in acute kidney injury (AKI) and chronic kidney disease (CKD).
For AKI, it defines stages of injury and discusses definitions from KDIGO. It outlines indications for urgent vs elective RRT, including life-threatening conditions like fluid overload or hyperkalemia. While early RRT is controversial, recent trials found no clear benefit to early vs delayed initiation. Ongoing studies may provide more conclusive answers.
For CKD stage 5, it notes non-specific uremic symptoms as indications for dialysis along with declining nutritional status or refractory fluid/metabolic issues. Absolute indications include uremic per
Dr. Manan B. Shah presented on biomarkers for acute kidney injury. The presentation discussed the need for biomarkers to detect AKI earlier than serum creatinine, as creatinine levels typically rise only after 50% kidney function is lost. Several promising urinary biomarkers were described, including NGAL, KIM-1, IL-18, and cystatin C, which can indicate kidney injury earlier. The presentation proposed that a panel of biomarkers may help guide whether renal replacement therapy is needed for patients with AKI. Early detection and treatment of AKI using biomarkers could potentially improve outcomes by preventing or minimizing kidney injury.
This document provides an overview of acute kidney injury (AKI), including its classification, epidemiology, etiology, pathophysiology, patient assessment, and clinical presentation. It discusses the RIFLE, AKIN, and KDIGO classification systems for AKI and covers the major causes and mechanisms of pre-renal, intrinsic, and post-renal AKI. Patient assessment involves reviewing the medical history, medications, physical exam, and distinguishing signs of AKI from chronic kidney disease. Changes in urinary output can help indicate the underlying cause of AKI in hospitalized patients.
Acute kidney injury (AKI) is a deterioration of renal function over hours to days resulting in failure to excrete waste and maintain homeostasis. [1] There are over 35 AKI definitions showing its complexity. [2] It can be classified as oliguric/non-oliguric or prerenal, renal, postrenal. [3] Prerenal and acute tubular necrosis account for most hospital AKI cases. [4] Management involves diagnosis through tests and imaging, and treatment focusing on fluid balance, electrolytes, and potentially renal replacement therapy. [5] The prognosis remains poor especially in critically ill patients, as currently the condition can only be supported but not cured. [6
This document discusses acute kidney injury (AKI), including its definition, epidemiology, causes, diagnosis, and treatment approaches. It provides details on:
- AKI definitions including RIFLE and KDIGO criteria.
- Common causes of AKI including pre-renal, intrinsic renal, and post-renal etiologies.
- Diagnostic evaluation including blood and urine tests, imaging, and biomarkers.
- General treatment principles including fluid resuscitation, eliminating nephrotoxins, and initiating renal replacement therapy.
- Specific approaches for pre-renal, intrinsic renal, and post-renal AKI as well as infections, nephrotoxins, and complications.
This document defines acute kidney injury (AKI) and describes its classification, diagnosis, and management. AKI is an abrupt deterioration in kidney function that is usually reversible. It is classified using criteria like RIFLE, AKIN, and KDIGO that stage AKI based on changes in serum creatinine and urine output. Biomarkers like cystatin C and NGAL can help detect early AKI. Treatment involves fluid resuscitation, removing nephrotoxins, and initiating renal replacement therapy if needed. Outcomes depend on the underlying cause and range from complete recovery to end-stage renal disease.
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.
Acute kidney injury (AKI) is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.It's most common in those who are critically ill and already hospitalized.
This document discusses the diagnosis and management of acute kidney injury (AKI) in the intensive care unit (ICU). It defines AKI and outlines biomarkers that can help identify it earlier than creatinine. Common causes of AKI in the ICU include sepsis, major surgery, low cardiac output, and medications. The document reviews risk factors for developing AKI and strategies for preventing it, such as fluid management and avoiding nephrotoxins. It discusses general management of established AKI including nutrition, anticoagulation, and dialysis. The impact of renal replacement therapy on outcomes is also addressed.
Acte kidney injury-advances in diagnosis & management.Suneth Weerarathna
This document discusses advances in the diagnosis and management of acute kidney injury (AKI). It begins with objectives and outlines of topics including AKI definitions, classification systems, biomarkers for early detection, and management strategies. Novel biomarkers such as Kim-1, NGAL, and cystatin C allow detection of AKI earlier than serum creatinine. While renal replacement therapy is important for established AKI, prevention and treatment of underlying causes are priorities. Overall, awareness of AKI is increasing worldwide and standardized criteria along with new diagnostics and therapies can lead to better outcomes.
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.
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AKI- Pharmacotherapy Handbook 2021 .pdf
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74
Acute Kidney Injury
• Acute kidney injury (AKI) is a clinical syndrome generally defined by an abrupt
reduction in kidney function as evidenced by changes in serum creatinine (Scr),
blood urea nitrogen (BUN), and urine output.
• RIFLE (Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Renal Dis-
ease), AKIN (Acute Kidney Injury Network), and the Kidney Disease: Improving
Global Outcomes (KDIGO) clinical practice guidelines are three criteria-based
classification systems developed to define and stage AKI in different patient popula-
tions (Table 74-1).
• All three staging systems have been validated across different patient popula-
tions, and their staging correlates closely with hospital mortality, cost, and length
of stay.
• Scr and urine output are the main diagnostic criteria for each staging system.
PATHOPHYSIOLOGY
• AKI can be categorized as prerenal (resulting from decreased renal perfusion in the
setting of undamaged parenchymal tissue), intrinsic (resulting from structural dam-
age to the kidney, most commonly the tubule from an ischemic or toxic insult), and
postrenal (resulting from obstruction of urine flow downstream from the kidney)
(Figure 74-1).
CLINICAL PRESENTATION
• Patient presentation varies widely and depends on the underlying cause. Early rec-
ognition and cause identification are critical, as they directly affect the outcome of
AKI. Outpatients often are not in acute distress; hospitalized patients may develop
AKI after a catastrophic event.
• Symptoms in the outpatient setting include acute change in urinary habits, sud-
den weight gain, or severe abdominal or flank pain. Signs include edema, colored
or foamy urine, and, in volume-depleted patients, postural hypotension, decreased
jugular venous pressure, and dry mucous membranes.
DIAGNOSIS
• Thorough medical and medication histories, physical examination, assessment of
laboratory values, and, if needed, imaging studies are important in the diagnosis
of AKI.
• Scr cannot be used alone to diagnose AKI because it is insensitive to rapid changes in
glomerular filtration rate (GFR). Scr lag behind the GFR’s decline by 1-2 days, leading
to a significant overestimation of GFR in the early stages of AKI and a potential delay
in diagnosis of the syndrome. The use of BUN in AKI is very limited because urea
production and renal clearance are heavily influenced by extrarenal factors such as
critical illness, volume status, protein intake, and medications.
• Urine output measured over a specified period of time allows for short-term assess-
ment of renal function, but its utility is limited to cases in which it is significantly
decreased.
• In addition to BUN and Scr, selected blood and urine tests, and urinary sediment are
used to differentiate the cause of AKI and guide patient management (Tables 74-2
and 74-3).
• Simultaneous measurement of urine and serum electrolytes and calculation of the
fractional excretion of sodium (FENa
) can help determine the etiology of AKI (see
Table 74-2).
CH74.indd 864 20-11-2020 13:02:30
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Acute Kidney Injury | CHAPTER 74
• The FENa
is one of the better diagnostic parameters to differentiate the cause of AKI
and is calculated as:
F 100)
E U Scr U S
Na Na Cr Na
= × × ×
( /( )
where UNa
= urine sodium, Scr = serum creatinine, UCr
= urine creatinine, and SNa
= serum sodium.
• A number of new serum and urinary biomarkers have been investigated to detect and
predict the clinical outcomes of AKI, including tissue inhibitor of metalloproteinases
2 (TIMP-2) and insulin-like growth factor binding protein 7 (IGFBP7).
TABLE 74-1 RIFLE, AKIN, and KDIGO Classification Schemes for AKIa
RIFLE Category Scr and GFRb
Criteria
Urine Output
Criteria
Risk Scr increase to 1.5-fold or GFR decrease
>25% from baseline
<0.5 mL/kg/hr
for ≥6 hr
Injury Scr increase to 2-fold or GFR decrease
>50% from baseline
<0.5 mL/kg/hr for
≥12 hr
Failure Scr increase to 3-fold or GFR decrease
>75% from baseline, or Scr ≥4 mg/dL
(354 μmol/L) with an acute increase of
at least 0.5 mg/dL (44 μmol/L)
Anuria for ≥12 hr
Loss Complete loss of function (RRT) for >4 weeks
ESKD RRT >3 months
AKIN Criteria Scr Criteria
Urine Output
Criteria
Stage 1 Scr increase ≥0.3 mg/dL (27 μmol/L)
or 1.5- to 2-fold from baseline
<0.5 mL/kg/hr
for ≥6 hr
Stage 2 Scr increase >2- to 3-fold from baseline <0.5 mL/kg/hr for
≥12 hr
Stage 3 Scr increase >3-fold from baseline, or Scr ≥4
mg/dL (354 μmol/L) with an acute increase
of at least 0.5 mg/dL (44 μmol/L), or need
for RRT
<0.3 mL/kg/hr for
≥24 hr or anuria
for ≥12 hr
KDIGO Criteria Scr Criteria
Urine Output
Criteria
Stage 1 Scr increase ≥0.3 mg/dL (27 μmol/L)
or 1.5–1.9 times from baseline
<0.5 mL/kg/hr for
6–12 hr
Stage 2 Scr increase 2–2.9 times from baseline <0.5 mL/kg/hr for
≥12 hr
Stage 3 Scr increase three times from baseline, or Scr
≥4 mg/dL (354 μmol/L), or need for RRT, or
eGFRc
<35 mL/min/1.73 m2
(0.34 mL/sec/
m2
) in patients <18 years
Anuria for ≥12 hr
a
For all staging systems, the criterion that leads to worst possible diagnosis should be used.
b
GFR calculated using the Modification of Diet in Renal Disease (MDRD) equation.
c
GFR calculated using the Schwartz formula.
AKI, acute kidney injury; AKIN, Acute Kidney Injury Network; ESKD, end-stage kidney disease; eGFR,
estimated glomerular filtration rate; h, hours; KDIGO, Kidney Disease: Improving Global Outcomes;
RIFLE, Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Kidney Disease; RRT, renal
replacement therapy; Scr, serum creatinine.
CH74.indd 865 20-11-2020 13:02:35
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Acute Kidney Injury | CHAPTER 74
PREVENTION
• Goals of Prevention: The goals are to screen and identify patients at risk; monitor high-risk
patients until the risk subsides; and implement prevention strategies when appropriate.
GENERAL APPROACH TO PREVENTION
Nonpharmacologic Therapy
• Intravenous fluids are routinely used in the prevention of AKI. KDIGO guidelines
recommend isotonic crystalloids over colloids for intravascular volume expansion.
Balanced solutions may offer some benefit compared to normal saline solutions.
• Fluids are the mainstay of therapy for prevention of contrast-induced acute kidney
injury (CI-AKI), a common cause of acute tubular necrosis in the inpatient setting.
• KDIGO guidelines recommend either sodium bicarbonate or isotonic saline infu-
sions in high-risk individuals receiving radiocontrast media. A common sodium
bicarbonate regimen is 154 mEq/L (mmol/L) infused at 3 mL/kg/hr for 1 hour before
the procedure and at 1 mL/kg/hr for 6 hours after the procedure. One frequently cited
normal saline regimen is 1 mL/kg/hr for 12 hours pre- and post-procedure.
• Oral ingestion of a specific amount of water pre- and post-procedure is best reserved
for outpatients with either normal or mildly impaired renal function undergoing
elective procedures.
Pharmacologic Therapy
• Inadequate evidence exists to support use of ascorbic acid, an antioxidant, in the
treatment or prevention of CI-AKI. The landmark PRESERVE trial demonstrated no
benefit of N-acetylcysteine in the prevention of CI-AKI.
• Both hyper- and hypoglycemia are associated with adverse patient outcomes. Guide-
lines from the American Diabetes Association and Surviving Sepsis Campaign rec-
ommend a glycemic target range of 140–180 mg/dL (7.8–10 mmol/L) and less than
180 mg/dL (10 mmol/L), respectively, in critically ill patients.
TREATMENT OF ACUTE KIDNEY INJURY
• Goals of Treatment: Short-term goals include minimizing the degree of insult to the
kidney, reducing extrarenal complications, and expediting recovery of renal function.
Restoration of renal function to pre-AKI baseline is the ultimate goal.
TABLE 74-2 Diagnostic Parameters for Differentiating Causes of AKIa
Laboratory Test Prerenal AKI Intrinsic AKI Postrenal AKI
Urine sediment Hyaline casts, may be
normal
Granular casts,
cellular debris
Cellular debris
Urinary RBC None 2–4+ Variable
Urinary WBC None 2–4+ 1+
Urine Na (mEq/L or
mmol/L)
<20 >40 >40
FENa
(%) <1 >2 Variable
Urine specific
gravity
>1.018 <1.012 Variable
a
Common laboratory tests are used to classify the cause of AKI. Functional AKI, which is not
included in this table, would have laboratory values similar to those seen in prerenal AKI. The
laboratory results listed under intrinsic AKI are those seen in acute tubular necrosis, the most
common cause of intrinsic AKI.
AKI, acute kidney injury; FENa
, fractional excretion of sodium; RBC, red blood cell; Scr, serum
creatinine; WBC, white blood cell.
CH74.indd 867 20-11-2020 13:02:37
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SECTION 14 | Renal Disorders
GENERAL APPROACH TO TREATMENT
• There is no specific treatment that can reverse AKI or hasten its recovery. Support-
ive measures that focus on hemodynamics, fluid balance, acid–base balance, and
electrolyte homeostasis are the mainstays of therapy.
NONPHARMACOLOGIC THERAPY
• Fluid therapy is used to maintain or restore intravascular volume to assure adequate
renal perfusion. Use IV fluids judiciously to prevent volume depletion and/or fluid
overload which adversely affect kidney function and increase mortality.
• Serum electrolytes should be monitored daily. Hyperkalemia is the most common
and serious electrolyte abnormality in AKI. Hypernatremia and fluid retention
commonly occur, requiring calculation of daily sodium intake, including sodium
contained in commonly administered antibiotics.
• Phosphorus and magnesium should be monitored, especially in patients with signifi-
cant tissue destruction due to increased amounts of released phosphorus; neither is
efficiently removed by dialysis.
TABLE 74-3 Urinary Findings as a Guide to the Etiology of Acute Kidney Injury
Type of Urinary
Evaluation Presence of Suggestive of
Urinalysis Leukocyte esterases Urinary tract infection
Nitrites Urinary tract infection
Protein
Mild (<0.5 g/day) Tubular damage
Moderate (0.5–3
g/day)
Glomerulonephritis, pyelonephritis, tubular
damage
Large (>3 g/day) Glomerulonephritis, nephrotic syndrome
Hemoglobin Glomerulonephritis, pyelonephritis, renal
infarction, renal tumors, kidney stones
Myoglobin Rhabdomyolysis-associated tubular
necrosis
Urobilinogen Hemolysis-associated tubular necrosis
Urine sediment Microorganisms Urinary tract infection
Cells Red blood cells Glomerulonephritis, urinary tract infection,
renal infarction, papillary necrosis, renal
tumors, kidney stones
White blood cells Urinary tract infection, interstitial nephritis
Eosinophils Drug-induced interstitial nephritis, renal
transplant rejection
Epithelial cells Tubular necrosis
Casts Granular casts Tubular necrosis
Hyaline casts Prerenal azotemia
White blood cell casts Urinary tract infection, interstitial nephritis
Red blood cell casts Glomerulonephritis, renal infarct, lupus
nephritis, vasculitis
Crystals Urate Postrenal obstruction
Calcium phosphate Postrenal obstruction
CH74.indd 868 20-11-2020 13:02:37
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Acute Kidney Injury | CHAPTER 74
• Nutritional management of critically ill patients with AKI is complex due to multiple
mechanisms for metabolic derangements. Nutritional requirements are altered by
stress, inflammation, and injury that lead to hypermetabolic and hypercatabolic
states.
• In severe AKI, renal replacement therapy (RRT), such as hemodialysis and peritoneal
dialysis, is used to treat fluid overload, electrolyte disturbances (eg, hyperkalemia),
acid–base imbalances, uremic complications, and pulmonary edema. See Table 74-4
for indications for RRT in AKI. Intermittent and continuous (CRRT) options have
different advantages (and disadvantages); the choice usually depends on physician
preference and resources available. No difference in mortality or dialysis dependence
has been shown; however, CRRT is generally preferred in hemodynamically unstable
patients.
• Intermittent hemodialysis (IHD) is the most frequently used RRT and has the
advantage of widespread availability and the convenience of lasting only 3–4 hours.
Disadvantages include difficult venous dialysis access in hypotensive patients and
hypotension due to rapid removal of large amounts of fluid.
• Several CRRT variants have been developed including continuous venovenous hemo-
filtration (CVVH), continuous venovenous hemodialysis (CVVHD), and continuous
venovenous hemodiafiltration (CVVHDF) which differ in fluid clearance and solute
removal. CRRT gradually removes solute, resulting in better tolerability by critically
ill patients. Disadvantages include limited availability of equipment, need for inten-
sive nursing care, and the need to individualize IV replacement, dialysate fluids, and
drug therapy adjustments.
• Circuit clotting and filter patency limit CRRT performance requiring anticoagula-
tion. The KDIGO Work Group recommends regional citrate as the preferred anti-
coagulant. This requires infusion of parenteral calcium which may limit feasibility
of regional citrate when the supply of parenteral calcium is limited. The specific
approach to anticoagulation is patient specific; if the patient requires systemic antico-
agulation for an underlying comorbidity (eg, atrial fibrillation, artificial heart valve)
no additional anticoagulation for RRT is needed.
PHARMACOLOGIC THERAPY
• Loop diuretics effectively reduce fluid overload but can worsen AKI. Equipotent
doses of loop diuretics (furosemide, bumetanide, torsemide, and ethacrynic acid)
have similar efficacy. KDIGO guidelines recommend limiting the use of loop diuret-
ics to the management of fluid overload and avoiding their use for the sole purpose
of prevention or treatment of AKI. Continuous infusions of loop diuretics appear
to overcome diuretic resistance and to have fewer adverse effects than intermittent
boluses but require more extensive and frequent monitoring.
TABLE 74-4 Common Indications for Renal ReplacementTherapy
Indication for RRT Clinical Setting
A: acid–base abnormalities Metabolic acidosis (especially if pH <7.2)
E: electrolyte imbalance Severe hyperkalemia and/or hypermagnesemia
I: intoxications Salicylates, lithium, methanol, ethylene glycol,
theophylline, phenobarbital
O: fluid overload Fluid overload (especially pulmonary edema unresponsive
to diuretics)
U: uremia Uremia or associated complications (neuropathy,
encephalopathy, pericarditis)
CH74.indd 869 20-11-2020 13:02:37
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SECTION 14 | Renal Disorders
• Strategies are available to overcome diuretic resistance (Table 74-5). Combination
therapy of loop diuretics plus a diuretic from a different pharmacologic class such
as diuretics that work at the distal convoluted tubule (thiazides) or the collecting
duct (amiloride, triamterene, and spironolactone) may have a synergistic effect.
Metolazone is commonly used with a loop diuretic because, unlike other thiazides, it
produces effective diuresis at GFR less than 20 mL/min (0.33 mL/sec).
Drug-Dosing Considerations
• Drug therapy optimization in AKI is a challenge. Confounding variables include
residual drug clearance, fluid accumulation, and use of RRTs.
• Pharmacotherapy decisions should take into consideration the four distinct phases of
AKI: initiation, extension, maintenance, and recovery phase. This requires frequent
monitoring and adjustment of drug dosing to optimize therapy as kidney function
stabilizes.
• Volume of distribution for water soluble drugs is significantly increased due to
edema. Use of dosing guidelines for chronic kidney disease (CKD) does not reflect
the clearance and volume of distribution in critically ill AKI patients.
• Patients with AKI may have a higher residual nonrenal clearance than those with
CKD with similar creatinine clearances; this complicates drug therapy individualiza-
tion, especially with RRTs.
• The mode of CRRT determines rate of drug removal, further complicating indi-
vidualization of drug therapy. Rates of ultrafiltration, blood flow, and dialysate flow
influence drug clearance during CRRT.
TABLE 74-5 Common Causes of Diuretic Resistance in Patients with Acute Kidney Injury
Causes of Diuretic Resistance Potential Therapeutic Solutions
Excessive sodium intake (sources may
be dietary, IV fluids, and drugs)
Remove sodium from nutritional sources and
medications
Inadequate diuretic dose or
inappropriate regimen
Increase dose, increase frequency, use continuous
infusion, or add thiazide
Reduced oral bioavailability (usually
furosemide)
Use parenteral therapy, switch to oral torsemide
or bumetanide
Nephrotic syndrome (loop diuretic
protein binding in tubule lumen)
Increase dose, add thiazide
Reduced renal blood flow
Drugs (NSAIDs, ACEIs, vasodilators) Discontinue these drugs if possible
Intravascular depletion Intravascular volume expansion
Increased sodium resorption
Distal nephron hypertrophy Add thiazide, sodium restriction
Postdiuretic sodium retention Dietary sodium restriction, use continuous
infusion
Heart failure Assess effective circulatory volume, increase dose,
increase frequency, use continuous infusion
Cirrhosis Assess effective circulatory volume, consider
paracentesis
Acute tubular necrosis Increase diuretic dose, diuretic combination
therapy
ACEIs, angiotensin-converting enzyme inhibitors; NSAIDs, nonsteroidal anti-inflammatory drugs.
CH74.indd 870 20-11-2020 13:02:38
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Acute Kidney Injury | CHAPTER 74
EVALUATION OF THERAPEUTIC OUTCOMES
• Vigilant monitoring of patient status is essential (Table 74-6).
• Perform therapeutic drug monitoring for drugs that have a narrow therapeutic index
if results can be obtained in a timely manner.
See Chapter 60, Acute Kidney Injury, authored by Jenana Halilovic Maker, Lauren Roller,
and William Dager, for a more detailed discussion of this topic.
TABLE 74-6 Key Monitoring Parameters for Patients with Established Acute Kidney Injury
Parameter Frequency
Fluid intake and output Daily
Patient weight Daily
Hemodynamics (eg, blood pressure, heart rate, mean
arterial pressure.)
Hourly/Every shift
Blood chemistries
Sodium, potassium, chloride, bicarbonate, calcium,
phosphate, magnesium
Daily
Blood urea nitrogen/serum creatinine Daily
Drugs and their dosing regimens Daily
Nutritional regimen Daily
Blood glucose Daily (minimum)
Therapeutic drug monitoring of renally cleared drugs
(eg, vancomycin aminoglycosides)
Highly variable, about three times
weekly
Times of administered doses Daily
Doses relative to administration of renal replacement
therapy
Daily
Urinalysis, urinary output
Calculate measured creatinine clearance Every time measured urine
collection performed
Calculate fractional excretion of sodium Every time measured urine
collection performed
Plans for renal replacement therapy Daily
CH74.indd 871 20-11-2020 13:02:38