The document discusses acute kidney injury (AKI), defining it, outlining causes and types including prerenal, intrinsic renal and postrenal, describing evaluation through investigations and clinical assessment, prevention and management recommendations including dialysis interventions, and complications of AKI.
This document discusses acute kidney injury (AKI), including its definition, causes, diagnostic approach, and management. It describes renal autoregulation and how various vasoconstrictors and vasodilators maintain renal blood flow. Prerenal, intrinsic, and postrenal causes of AKI are outlined. The diagnostic approach involves assessing history, physical exam, labs, and imaging to determine the etiology. Urine sediment analysis can provide clues about the underlying renal process. Management involves treating the underlying cause and preventing further injury.
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
Acute Kidney Injury (AKI) is a common complication, affecting 5-7% of hospital admissions and 30% of intensive care unit patients. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Biomarkers like cystatin C and kidney injury molecule 1 can help detect AKI earlier than creatinine. Treatment involves fluid resuscitation, eliminating nephrotoxins, and renal replacement therapy for complications like electrolyte imbalances or uremia. Outcomes depend on the underlying cause, with pre-renal and post-renal AKI having a better prognosis than intrinsic renal injury.
Acute kidney injury (AKI) is a common condition characterized by a sudden decline in kidney function. It affects 5-7% of hospital admissions and 30% of intensive care unit admissions. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Treatment focuses on optimizing fluid status and hemodynamics, removing nephrotoxins if possible, and initiating renal replacement therapy as needed based on the underlying cause and severity of AKI.
Cardiorenal syndrome (CRS) refers to conditions where acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. CRS is classified into 5 subtypes depending on whether cardiac or renal dysfunction occurs first, and whether it is acute or chronic. Type 1 involves acute cardiac dysfunction leading to acute kidney injury. Type 2 involves chronic cardiac dysfunction resulting in worsening chronic kidney disease. Type 3 involves acute kidney injury leading to cardiac issues. Type 4 involves chronic kidney disease contributing to cardiac problems. Type 5 involves systemic conditions affecting both organs. Early diagnosis and treatment tailored to the CRS subtype is important for improving outcomes.
This document provides an overview of chronic kidney disease (CKD) including definitions, epidemiology, pathophysiology, risk factors, and genetics. Some key points include:
- CKD is defined as kidney damage or glomerular filtration rate <60 mL/min/1.73m2 for ≥3 months.
- It affects 14-15% of US adults and prevalence increases with age. The leading causes are hypertension and diabetes.
- As CKD progresses, surviving nephrons undergo hypertrophy which can lead to sclerosis and loss of filtration surface area over time. Tubulointerstitial fibrosis also contributes to declining kidney function.
- The renin-angiotensin-
This document discusses acute kidney injury (AKI), including its definition, causes, diagnostic approach, and management. It describes renal autoregulation and how various vasoconstrictors and vasodilators maintain renal blood flow. Prerenal, intrinsic, and postrenal causes of AKI are outlined. The diagnostic approach involves assessing history, physical exam, labs, and imaging to determine the etiology. Urine sediment analysis can provide clues about the underlying renal process. Management involves treating the underlying cause and preventing further injury.
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
Acute Kidney Injury (AKI) is a common complication, affecting 5-7% of hospital admissions and 30% of intensive care unit patients. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Biomarkers like cystatin C and kidney injury molecule 1 can help detect AKI earlier than creatinine. Treatment involves fluid resuscitation, eliminating nephrotoxins, and renal replacement therapy for complications like electrolyte imbalances or uremia. Outcomes depend on the underlying cause, with pre-renal and post-renal AKI having a better prognosis than intrinsic renal injury.
Acute kidney injury (AKI) is a common condition characterized by a sudden decline in kidney function. It affects 5-7% of hospital admissions and 30% of intensive care unit admissions. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Treatment focuses on optimizing fluid status and hemodynamics, removing nephrotoxins if possible, and initiating renal replacement therapy as needed based on the underlying cause and severity of AKI.
Cardiorenal syndrome (CRS) refers to conditions where acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. CRS is classified into 5 subtypes depending on whether cardiac or renal dysfunction occurs first, and whether it is acute or chronic. Type 1 involves acute cardiac dysfunction leading to acute kidney injury. Type 2 involves chronic cardiac dysfunction resulting in worsening chronic kidney disease. Type 3 involves acute kidney injury leading to cardiac issues. Type 4 involves chronic kidney disease contributing to cardiac problems. Type 5 involves systemic conditions affecting both organs. Early diagnosis and treatment tailored to the CRS subtype is important for improving outcomes.
This document provides an overview of chronic kidney disease (CKD) including definitions, epidemiology, pathophysiology, risk factors, and genetics. Some key points include:
- CKD is defined as kidney damage or glomerular filtration rate <60 mL/min/1.73m2 for ≥3 months.
- It affects 14-15% of US adults and prevalence increases with age. The leading causes are hypertension and diabetes.
- As CKD progresses, surviving nephrons undergo hypertrophy which can lead to sclerosis and loss of filtration surface area over time. Tubulointerstitial fibrosis also contributes to declining kidney function.
- The renin-angiotensin-
Acute kidney injury (AKI) is common in hospitalized patients, occurring in 5-7% of hospitalized patients and up to 30% of ICU patients. Common causes include decreased renal perfusion due to factors like sepsis, surgery, heart or liver failure, nephrotoxic medications, or urinary tract obstruction. The definition of AKI involves an increase in serum creatinine of ≥0.3 mg/dL within 48 hours or ≥1.5 times baseline within 7 days. Management involves identifying and treating the underlying cause, maintaining fluid and electrolyte balance, and initiating renal replacement therapy in severe cases to prevent complications.
Approach to the Patient with Renal DiseasePatrick Carter
This document provides an overview of renal disease for medical students. It defines key terms related to renal function and urine findings. It describes tools for detecting renal disease including history, physical exam, urinalysis, and bloodwork. It discusses uremic syndrome and its effects on multiple organ systems. It differentiates between acute and chronic renal failure, nephritic and nephrotic syndrome based on causes, labs, and physical findings. The goal is to review approaches for evaluating and classifying patients with possible renal disease.
This document discusses cardiorenal syndrome (CRS), defined as when acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. It describes 5 types of CRS based on whether cardiac or renal dysfunction occurs acutely or chronically. Type 1 involves acute cardiac failure worsening renal function, while Type 2 involves chronic congestive heart failure causing chronic renal dysfunction. Biomarkers like NGAL can aid early diagnosis of CRS Type 1. Management involves diuretics, inotropes, vasodilators, and blocking the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs.
Chronic Kidney Disease, CKD, Nephrology, Dee Evardone
This document provides an overview of chronic kidney disease (CKD). It defines CKD as the presence of kidney damage or decreased kidney function for three or more months. Key points include:
- CKD is defined based on evidence of kidney damage through structural abnormalities found on biopsy, imaging, or urine tests, or decreased glomerular filtration rate (GFR) below 60 mL/min/1.73m2.
- Common causes of CKD include diabetes, hypertension, glomerulonephritis, cystic kidney diseases, and vascular diseases.
- The document outlines clinical and laboratory manifestations of CKD and approaches to evaluating and managing patients with CKD.
This document discusses vaccination in patients with chronic kidney disease (CKD). It outlines how CKD affects both the innate and adaptive immune systems, leading to impaired immunity. It describes alterations in end-stage renal disease that impair response to vaccines. Guidelines recommend vaccines for hepatitis B, pneumococcus, and influenza for CKD patients, with some vaccines requiring higher doses or more doses. Methods to potentially improve vaccine efficacy include use of immunomodulators like interleukin-2 administered with vaccines.
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
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
Dialysis disequilibrium syndrome (DDS) is characterized by neurological symptoms that occur during or after dialysis as a result of a rapid shift in osmoles like urea. It is caused by a transient osmotic gradient between plasma and brain cells as urea is swiftly removed by dialysis, causing water to shift into neurons and produce cerebral edema. Risk factors include the first dialysis treatment or high pre-dialysis BUN. Symptoms range from mild like headache to severe like seizures. Prevention focuses on limiting urea removal during initial sessions by using lower blood and dialysate flows with sodium modeling. Treatment is usually supportive and symptoms resolve within 24 hours.
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 presents a seminar on acute kidney injury (AKI) in children. It defines AKI and describes the RIFLE and AKIN criteria for classifying it. Common causes of pediatric AKI include pre-renal issues like dehydration, intrinsic renal problems like acute tubular necrosis, and post-renal obstruction. Clinical features depend on the etiology. Management involves treating life-threatening complications, fluid/electrolyte balance, nutrition support, and addressing the underlying disorder. Outcomes vary according to cause but have improved with advanced care; prevention emphasizes hydration and avoiding nephrotoxins.
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
Define Chronic Renal Failure.
Mention the main causes of Chronic Renal Failure.
Know the signs and symptoms of renal failure.
Know the treatment options of CRF
Know new definition of CKD
Acute renal failure is a clinical syndrome where sudden deterioration of renal function results in the kidneys' inability to maintain fluid and electrolyte homeostasis. It has various etiologies like pre-renal, intrinsic renal, and post-renal factors. Management involves treating the underlying cause, fluid resuscitation, controlling electrolyte abnormalities, and starting dialysis for refractory volume overload, hyperkalemia, acidosis, or neurological symptoms. The healthcare team works to stabilize the patient and prevent long-term kidney damage.
This document discusses renal failure in patients with cirrhosis. It defines hepatorenal syndrome (HRS) as a type of renal failure seen in cirrhosis without intrinsic kidney abnormalities. HRS is classified into types 1-4 depending on severity and timeline of onset. Type 1 has the worst prognosis with median survival of 1-2 weeks. Treatment involves vasoconstrictors like terlipressin combined with albumin for volume expansion. For refractory ascites, large volume paracentesis with albumin is first line, while TIPS may be considered. Renal replacement therapy alone does not improve outcomes in HRS but may be used as a bridge to liver transplantation, which is the definitive treatment for HRS
Anemia is a common complication of chronic kidney disease that can cause fatigue. While the kidneys normally produce erythropoietin to stimulate red blood cell production, CKD patients have relative erythropoietin deficiency. This leads to anemia which, if left untreated, can negatively impact quality of life and cardiovascular health. Erythropoiesis-stimulating agents and iron supplementation are used to treat anemia in CKD, though the appropriate hemoglobin target level remains an area of ongoing research and debate given risks identified with higher targets in some studies.
This document discusses acute kidney injury (AKI). It begins with the anatomy and function of the kidney, explaining that the nephron is the functional unit that produces urine. It then discusses definitions of AKI and acute renal failure (ARF), noting they are not synonymous, with AKI encompassing a spectrum of injury. Common causes of AKI are also summarized, including decreased renal perfusion, intrinsic renal disease, and urinary tract obstruction. Stages of AKI severity are described using the RIFLE criteria of Risk, Injury and Failure. Incidence of AKI in intensive care unit patients is estimated between 5-20% with high mortality.
This document provides an overview of glomerulonephritis (GN), including definitions, descriptions of normal glomerular structures, examples of light and electron microscopy images showing abnormalities in GN, classifications of GN as primary or secondary, mechanisms of glomerular injury, clinical manifestations, approaches to diagnosis, and discussions of specific types of GN such as IgA nephropathy, rapidly progressive GN, and Goodpasture's syndrome. Key information covered includes the pathology and clinical patterns of focal nephritic, diffuse nephritic, and nephrotic GN, as well as general workup and management considerations for glomerular disease.
Acute kidney injury (AKI) is common in hospitalized patients, occurring in 5-7% of hospitalized patients and up to 30% of ICU patients. Common causes include decreased renal perfusion due to factors like sepsis, surgery, heart or liver failure, nephrotoxic medications, or urinary tract obstruction. The definition of AKI involves an increase in serum creatinine of ≥0.3 mg/dL within 48 hours or ≥1.5 times baseline within 7 days. Management involves identifying and treating the underlying cause, maintaining fluid and electrolyte balance, and initiating renal replacement therapy in severe cases to prevent complications.
Approach to the Patient with Renal DiseasePatrick Carter
This document provides an overview of renal disease for medical students. It defines key terms related to renal function and urine findings. It describes tools for detecting renal disease including history, physical exam, urinalysis, and bloodwork. It discusses uremic syndrome and its effects on multiple organ systems. It differentiates between acute and chronic renal failure, nephritic and nephrotic syndrome based on causes, labs, and physical findings. The goal is to review approaches for evaluating and classifying patients with possible renal disease.
This document discusses cardiorenal syndrome (CRS), defined as when acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. It describes 5 types of CRS based on whether cardiac or renal dysfunction occurs acutely or chronically. Type 1 involves acute cardiac failure worsening renal function, while Type 2 involves chronic congestive heart failure causing chronic renal dysfunction. Biomarkers like NGAL can aid early diagnosis of CRS Type 1. Management involves diuretics, inotropes, vasodilators, and blocking the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs.
Chronic Kidney Disease, CKD, Nephrology, Dee Evardone
This document provides an overview of chronic kidney disease (CKD). It defines CKD as the presence of kidney damage or decreased kidney function for three or more months. Key points include:
- CKD is defined based on evidence of kidney damage through structural abnormalities found on biopsy, imaging, or urine tests, or decreased glomerular filtration rate (GFR) below 60 mL/min/1.73m2.
- Common causes of CKD include diabetes, hypertension, glomerulonephritis, cystic kidney diseases, and vascular diseases.
- The document outlines clinical and laboratory manifestations of CKD and approaches to evaluating and managing patients with CKD.
This document discusses vaccination in patients with chronic kidney disease (CKD). It outlines how CKD affects both the innate and adaptive immune systems, leading to impaired immunity. It describes alterations in end-stage renal disease that impair response to vaccines. Guidelines recommend vaccines for hepatitis B, pneumococcus, and influenza for CKD patients, with some vaccines requiring higher doses or more doses. Methods to potentially improve vaccine efficacy include use of immunomodulators like interleukin-2 administered with vaccines.
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
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
Dialysis disequilibrium syndrome (DDS) is characterized by neurological symptoms that occur during or after dialysis as a result of a rapid shift in osmoles like urea. It is caused by a transient osmotic gradient between plasma and brain cells as urea is swiftly removed by dialysis, causing water to shift into neurons and produce cerebral edema. Risk factors include the first dialysis treatment or high pre-dialysis BUN. Symptoms range from mild like headache to severe like seizures. Prevention focuses on limiting urea removal during initial sessions by using lower blood and dialysate flows with sodium modeling. Treatment is usually supportive and symptoms resolve within 24 hours.
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 presents a seminar on acute kidney injury (AKI) in children. It defines AKI and describes the RIFLE and AKIN criteria for classifying it. Common causes of pediatric AKI include pre-renal issues like dehydration, intrinsic renal problems like acute tubular necrosis, and post-renal obstruction. Clinical features depend on the etiology. Management involves treating life-threatening complications, fluid/electrolyte balance, nutrition support, and addressing the underlying disorder. Outcomes vary according to cause but have improved with advanced care; prevention emphasizes hydration and avoiding nephrotoxins.
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
Define Chronic Renal Failure.
Mention the main causes of Chronic Renal Failure.
Know the signs and symptoms of renal failure.
Know the treatment options of CRF
Know new definition of CKD
Acute renal failure is a clinical syndrome where sudden deterioration of renal function results in the kidneys' inability to maintain fluid and electrolyte homeostasis. It has various etiologies like pre-renal, intrinsic renal, and post-renal factors. Management involves treating the underlying cause, fluid resuscitation, controlling electrolyte abnormalities, and starting dialysis for refractory volume overload, hyperkalemia, acidosis, or neurological symptoms. The healthcare team works to stabilize the patient and prevent long-term kidney damage.
This document discusses renal failure in patients with cirrhosis. It defines hepatorenal syndrome (HRS) as a type of renal failure seen in cirrhosis without intrinsic kidney abnormalities. HRS is classified into types 1-4 depending on severity and timeline of onset. Type 1 has the worst prognosis with median survival of 1-2 weeks. Treatment involves vasoconstrictors like terlipressin combined with albumin for volume expansion. For refractory ascites, large volume paracentesis with albumin is first line, while TIPS may be considered. Renal replacement therapy alone does not improve outcomes in HRS but may be used as a bridge to liver transplantation, which is the definitive treatment for HRS
Anemia is a common complication of chronic kidney disease that can cause fatigue. While the kidneys normally produce erythropoietin to stimulate red blood cell production, CKD patients have relative erythropoietin deficiency. This leads to anemia which, if left untreated, can negatively impact quality of life and cardiovascular health. Erythropoiesis-stimulating agents and iron supplementation are used to treat anemia in CKD, though the appropriate hemoglobin target level remains an area of ongoing research and debate given risks identified with higher targets in some studies.
This document discusses acute kidney injury (AKI). It begins with the anatomy and function of the kidney, explaining that the nephron is the functional unit that produces urine. It then discusses definitions of AKI and acute renal failure (ARF), noting they are not synonymous, with AKI encompassing a spectrum of injury. Common causes of AKI are also summarized, including decreased renal perfusion, intrinsic renal disease, and urinary tract obstruction. Stages of AKI severity are described using the RIFLE criteria of Risk, Injury and Failure. Incidence of AKI in intensive care unit patients is estimated between 5-20% with high mortality.
This document provides an overview of glomerulonephritis (GN), including definitions, descriptions of normal glomerular structures, examples of light and electron microscopy images showing abnormalities in GN, classifications of GN as primary or secondary, mechanisms of glomerular injury, clinical manifestations, approaches to diagnosis, and discussions of specific types of GN such as IgA nephropathy, rapidly progressive GN, and Goodpasture's syndrome. Key information covered includes the pathology and clinical patterns of focal nephritic, diffuse nephritic, and nephrotic GN, as well as general workup and management considerations for glomerular disease.
This document discusses acute kidney injury (AKI), including its definition, classification systems, causes, diagnosis, treatment including renal replacement therapy modalities, and management. It provides an overview of AKI and recommendations from clinical practice guidelines for its diagnosis and treatment. Key points include defining AKI as an acute decrease in kidney function and glomerular filtration rate, the RIFLE and AKIN classification systems, common causes of AKI including sepsis and nephrotoxins, the timing of nephrology consultation, and the use of renal replacement therapies like continuous renal replacement therapy for critically ill patients with AKI.
Among patients taking warfarin who experienced INR levels above 3.0 (overanticoagulation), 20.5% developed presumptive warfarin-related nephropathy (WRN) defined as a rise in creatinine of 0.3 mg/dL or more within a week. The risk was higher among patients with chronic kidney disease (CKD), 33% of whom developed WRN, compared to 16.5% of patients without CKD. WRN was associated with higher mortality even after controlling for covariates. A prospective study is needed to further understand risk factors and consequences of WRN.
This document discusses contrast-induced acute kidney injury (CI-AKI). It begins with definitions of CI-AKI and compares older and newer criteria for defining it. It then discusses the pathophysiology of CI-AKI, including how risk factors like chronic kidney disease and diabetes can make the kidneys more vulnerable to injury from iodinated contrast media. It also outlines strategies for preventing CI-AKI, such as using smaller doses of contrast, intravenous rather than intra-arterial administration, iso-osmolar rather than low-osmolar contrast agents, and volume expansion. Meta-analyses are discussed that did not find clear evidence that iso-osmolar contrast is more effective at preventing CI-AK
The document discusses acute kidney injury (AKI), formerly called acute renal failure (ARF). It defines AKI as a sudden decrease in glomerular filtration rate (GFR) over hours to days. Serum creatinine is commonly used to assess renal function but is not an ideal marker as it rises after GFR drops and is affected by non-renal factors. The causes and types of AKI are described including pre-renal, renal (intrinsic), and post-renal. Acute tubular necrosis (ATN) is the most common cause of intrinsic AKI. Management involves identifying and correcting underlying causes, monitoring fluid balance, and treating complications like hyperkalemia. Dialysis is indicated for refractory
This document summarizes acute kidney injury (AKI), including causes, risk factors, diagnosis, management, and treatment options like renal replacement therapy. It emphasizes early detection of AKI to prevent further injury, and notes that fluid overload and late initiation of dialysis are associated with higher mortality. Management involves identifying and avoiding nephrotoxic agents, maintaining fluid balance, and considering renal replacement therapy with peritoneal dialysis, hemodialysis, or continuous renal replacement therapy depending on the clinical situation and local expertise. The goal is to recognize patients at risk and improve AKI care worldwide so that no one dies of preventable AKI by 2025.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure. It provides definitions of AKI, outlines criteria for diagnosis including RIFLE and AKIN classifications, and discusses etiologies such as pre-renal causes, acute tubular necrosis, interstitial nephritis, and glomerulonephritis. Risk factors, presentations, evaluations, and biomarkers for AKI are presented. Prevention and management of AKI in hepatic dysfunction and hepatorenal syndrome are also covered.
Acute kidney injury and chronic kidney disease in childrenSameekshya Pradhan
Acute kidney injury (AKI) and chronic kidney disease can affect children. AKI is defined as a rapid deterioration of renal function over hours to days. It has various etiologies including pre-renal, renal, and post-renal causes. Management involves treating life-threatening complications, maintaining fluid/electrolyte balance, supportive care, and dialysis. Chronic kidney disease develops over months to years and requires long-term management to delay progression.
This document provides an overview of renal replacement therapies used in critical care settings. It discusses some of the key questions around when and how to use these therapies for acute kidney injury (AKI) patients. While there is no definitive evidence that answers all the questions, the literature suggests starting renal replacement therapy early according to RIFLE criteria and aiming for a minimum dose of 35 ml/kg/hr. Choice of therapy mode (intermittent vs continuous) may not be as important as ensuring adequate dosing. Further research is still needed to fully understand how to optimize outcomes for AKI patients requiring renal replacement therapy.
Acute kidney injury (AKI), previously called acute renal failure, is a reversible increase in blood creatinine and nitrogenous waste products due to the kidney's inability to regulate fluids and electrolytes. AKI is classified using RIFLE and AKIN criteria and can have pre-renal, intrinsic renal, or post-renal causes. Common causes in children include sepsis, cardiac surgery, organ transplantation, hemolytic uremic syndrome, and acute glomerulonephritis. Diagnosis involves physical exam, lab tests of kidney function and urine analysis, and imaging studies may be needed to identify obstruction. Kidney biopsy may be required to determine etiology or prognosis when cause is unknown.
This document provides an overview of acute renal failure in children. It defines acute renal failure, discusses causes (pre-renal, intrinsic renal, post-renal), pathogenesis, laboratory findings, biomarkers, management including fluid resuscitation, diuretics, electrolyte abnormalities, nutrition, and indications for dialysis. Management is aimed at treating the underlying cause and maintaining fluid, electrolyte and acid-base balance until renal function recovers.
Acute renal failure (ARF), also known as acute kidney injury (AKI), can have various causes including pre-renal, renal, and post-renal factors. The definition includes an abrupt decline in kidney function over 48 hours seen through rises in creatinine or decreases in urine output. Evaluation involves assessing volume status, obtaining urine and blood tests, and ultrasound. Treatment focuses on identifying and treating the underlying cause, providing supportive care like fluid management, and potentially initiating renal replacement therapy for complications such as fluid overload or electrolyte imbalances. Prognosis depends on the severity and underlying etiology of the AKI.
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), formerly known as acute renal failure. It defines AKI and provides causes and characteristics of pre-renal, renal, and post-renal AKI. Pre-renal AKI is caused by decreased renal perfusion due to issues like volume depletion or heart failure. Renal AKI can be caused by issues affecting the glomeruli, interstitium, or tubules, such as acute tubular necrosis. Post-renal AKI is due to urinary tract obstruction. The document outlines evaluation of AKI including history, exam, urine and serum tests, imaging, and novel biomarkers. It also discusses complications of AKI and general management strategies.
1) Acute kidney injury (AKI) is common, affecting up to 7-50% of ICU patients. It can be caused by prerenal, intrinsic renal, or postrenal factors.
2) The AKIN criteria is commonly used to stage AKI based on changes in serum creatinine and urine output. Stage 1 AKI involves a mild increase in creatinine or decrease in urine output.
3) Intrinsic renal AKI includes acute tubular necrosis, acute interstitial nephritis, and glomerulonephritis. These can be differentiated based on urine and microscopy findings as well as clinical context.
This document discusses acute kidney injury (AKI), providing definitions, causes, evaluation, and treatment. It notes that AKI is a sudden reduction in kidney function that can be caused by pre-renal issues like low blood volume, renal issues affecting the kidneys directly, or post-renal obstruction. Common causes include sepsis, hypotension, nephrotoxins, and acute tubular necrosis. Evaluation involves history, exam, labs including electrolytes and urine analysis, and sometimes renal ultrasound or biopsy. Treatment depends on the underlying cause but generally involves fluid resuscitation, removing nephrotoxins, treating infections, and potentially renal replacement therapy. Prognosis depends on factors like age, illness duration, organ
22 - Acute and chronic kidney failure.pptxStewardBwalya1
Most medical students graduate without knowing the diagnosis and management of acute and chronic kidney failure. Renal units requires you to have a thorough knowledge. So this presentation will assist you to have such knowledge
This document provides an overview of acute renal failure (ARF), also known as acute kidney injury (AKI). It defines ARF, discusses epidemiology and etiology. For etiology, it distinguishes between pre-renal, renal, and post-renal causes of ARF and lists examples for each. It describes the clinical features, diagnosis, and management of ARF, including treatment and indications for renal replacement therapy. ARF is generally reversible if the underlying cause is addressed promptly. Differentiating between pre-renal, renal and post-renal ARF involves considering history, physical exam findings, lab tests and urine analysis.
1. Acute kidney injury (AKI) is the sudden deterioration of renal function that can range from mild to severe. It is a global problem associated with high morbidity and mortality.
2. AKI is classified based on location of injury (pre-renal, intrinsic, post-renal), urine output, and severity of decline in renal function. Common causes include sepsis, nephrotoxins, and decreased renal perfusion.
3. Management involves treating the underlying cause, maintaining fluid/electrolyte balance, and potentially renal replacement therapy for complications like fluid overload or severe electrolyte imbalances. Outcomes depend on factors like age, cause, and need for dialysis.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure. It defines AKI as the rapid deterioration of renal function over hours to days, resulting in the failure of the kidneys to excrete waste and regulate fluids and electrolytes. AKI can be classified in different ways, including whether urine output is low or normal. Prerenal, renal, and postrenal causes of AKI are described. The epidemiology, etiology, diagnosis, and management of AKI are also outlined. Treatment involves supportive care through fluid management, electrolyte correction, and potentially renal replacement therapy in severe cases.
This document provides an overview of pharmacotherapy for renal disorders. It begins by outlining various renal disorders including acute renal failure, chronic renal failure, drug-induced renal disease, glomerulonephritis, nephrotic/nephritic syndromes, acid-base disorders, and disorders of fluid and electrolyte homeostasis. It then focuses on acute kidney injury (AKI), discussing definition, staging, risk factors, pathophysiology, clinical presentation, investigations, and management. Prevention and treatment of specific causes of AKI like contrast-induced nephropathy and nephrolithiasis are also covered.
Dr. Ahmed Elberry provides an overview of acute kidney injury (AKI) including its definition, classification systems, causes, mechanisms, and clinical manifestations. AKI can be caused by prerenal, renal, or postrenal factors and results in a abrupt decrease in kidney function over hours to days. Common causes include ischemia, infections, drugs like NSAIDs, contrast media, and aminoglycosides. Patients with AKI may experience oliguria, azotemia, fluid overload, and electrolyte abnormalities.
The document provides information about kidney structure and function, as well as kidney diseases. It discusses that the kidneys contain nephrons and filter blood to remove waste and regulate fluid levels. It describes acute kidney injury (AKI) as a sudden decline in kidney function, and chronic kidney disease (CKD) as long-term decreased function. For kidney failure, dialysis or transplantation is needed to replace lost kidney function.
Neonatal acute kidney injury (AKI) can result from prerenal, intrinsic renal, or postrenal causes. It is characterized by impaired kidney function and dysregulation of fluid, acid-base, electrolytes, and waste products. AKI is defined using modified KDIGO criteria of changes in serum creatinine and urine output. Prevention focuses on supporting circulation and avoiding nephrotoxins. Treatment involves careful fluid management, electrolyte replacement, and potentially renal replacement therapy. Outcomes depend on the severity and etiology of AKI, with prognosis generally worse than in adults.
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.
Acute kidney injury (AKI) is characterized by an abrupt reduction in kidney function evidenced by changes in serum creatinine, blood urea nitrogen, and urine output. It is classified based on risk, injury, and failure using criteria from RIFLE, AKIN, and KDIGO. The main causes of AKI are pre-renal from decreased perfusion, intrinsic renal from structural kidney damage, and post-renal from urinary obstruction. Treatment focuses on supportive care through fluid management and potentially renal replacement therapy to restore kidney function.
This document provides an overview of acute kidney injury (AKI). It defines AKI and discusses its causes, diagnosis, staging, management principles, and outcomes. The main points are:
- AKI is defined as a rapid reduction in kidney function over hours to days. Common causes include low blood flow, toxins, infections, and ischemia.
- Diagnosis involves blood and urine tests to assess kidney function and rule out other issues. Staging of AKI severity is based on changes in creatinine and urine output.
- Management focuses on treating the underlying cause, maintaining fluid/electrolyte balance, and potentially renal replacement therapy for severe cases. Outcomes depend on the cause and stage
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.
Acute Kidney Injury epidemiology, pathophysiology and management based on current evidence. The presentation is suitable for internal medicine trainees and nephrology fellows.
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1. ACUTE KIDNEY INJURY
1
DR Jayakrishnan M P
PG Resident, Dept of Medicine
MGM Medical College, Indore
2. DEFINITION
• Increase in S.Cr by ≥ 0.3 mg/dl within 48 hours ; or
• Increase in S. Cr to ≥ 1.5 times baseline, which is
known and presumed to occur within the prior 7
days ; or
• Urine volume < 0.5 ml/kg/h for 6 hours
• AKI is not ATN, nor is it renal failure.
KDIGO guidelines 2012 2
5. Staging of AKI – AKIN Criteria(2007)
Stage Serum creatinine Urine output
1 1.5-1.9 times baseline or
≥ 0.3 mg/dl increase
< 0.5 ml/kg/h for 6-12
hours
2 2-2.9 times baseline < 0.5 ml/kg/h for ≥ 12
hours
3 3.0 times baseline or
Initiation of renal replacement
therapy or
In patients < 18 years, decrease
in eGFR to < 35 ml/ min per
1.73 m2
< 0.3 ml/kg/h for ≥ 24
hours or
Anuria for ≥ 12 hours
5
6. ETIOLOGY
Causes of Prerenal AKI(40-55%):
• Hemorrhage
• GI Loss – diarrhoea,vomiting,NG tube loss
• Renal loss – diuretics,DI
• Burns,Hyperthermia
• Nephrotic Syndrome,Cirrhosis
• Reduced CO: Cardiogenic shock,CHF, pericardial
diseases,vavular diseases.
• Systemic vasodilatation – Sepsis,Cirrhosis,Anaphylaxis,Drugs
• Renal Vasoconstriction – Early sepsis, HRS, Acute
hypercalcaemia,Drugs-NE,
vasopressin,NSAIDS,ACEIs,Calcineurin inhibitors, Iodinated
contrast agents
• Abdominal compartment syndrome.
BRENNER AND RECTORS - THE KIDNEY 9TH EDITION
6
11. Prerenal AKI
• Most common cause of AKI in the outpatient setting
– Look for patients with hemorrhage, GI and urinary fluid
loss,severe burns
– Decreased effective arterial blood volume ( CHF, Cirrhosis
or nephrotic syndrome).
– Drugs– NSAIDS,ACEIs,ARBs
– O/E: tachycardia,signs of dehydration ,orthostatic
hypotension,reduced JVP.
CLINICAL EVALUATION
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
11
12. Intrinsic kidney Diseases
• ATN - Acute Tubular Necrosis
– Usually occurs after an ischemic event or exposure to nephrotoxic
agents.
• AIN - Acute Interstitial Nephritis
– Classic presentation is fever, rash, eosinophilia and Cr bump 7-10 days
after drug exposure.
• CIN - Contrast Induced Nephropathy
– Increased Cr of 0.5mg/dl or 25% 48hrs after contrast administration.
• Others – Glomerular Disease, Pigmented Nephropathy,
Thrombotic Microangiopathy
CLINICAL EVALUATION
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
12
13. Postrenal diseases:
• H/O of pelvic tumors, irradiation, congential abnormalities,
kidney stones, genitourinary procedures or surgeries,spinal
cord injury,DM
• Nocturia,urinary frequency,urgency,hesistency,urinary
retension
• O/E Enlarged prostate on PR examination,Distended bladder
CLINICAL EVALUATION
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
13
14. INVESTIGATIONS
Urine Analysis:
• Specific gravity: > 1.01 -1.020 – Prerenal AKI
1.010(isosthenuria) - ATN
• Haematuria – glomerulonephritis,urologic disease,interstitial
nephritis,trauma,renal infarction,pigment nephropathy.
• Urine sediment analysis:
- Normal with hyaline casts- prerenal AKI
- Pigmented granular casts- ischaemic or nephrotoxic ATN
- RBC casts – acute glomerular disease
- WBC & nonpigmented granular casts –interstitial nephritis
- Broad granular casts – CKD
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn
14
15. INVESTIGATIONS
• Eosinophiluria – drug induced AIN
• Uric acid crystals – urate nephropathy
• Oxalate crystals – ethylene glycol toxicity
Proteinuria:
• < 1g/day – ischaemic and nephrotoxic ATN
• > 1g/day – glomerular diseases,multiple myeloma,drug
induced AIN.
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn15
16. • Urine biochemical parameters:
Diagnostic Index Prerenal AKI ATN
FENa <1% >2%
Urine Na <20 >40
U Cr/Pl Cr >40 <20
U urea N/Pl urea N >8 <3
Urine SG >1.018 1.010
Urine osmolality >500 300
Pl BUN/Cr >20 <10-15
Renal failure Index
Una/(UCr/Pl Cr)
<1 >1
Urine sediment Hyaline casts Muddy brown
granular casts 16
17. INVESTIGATIONS
Laboratory evaluation:
• BUN : S Cr - >20:1 - prerenal AKI
10:1 - intrinsic AKI
• Rhabdomyolysis –hyperkalemia,hyperuricemia
hyperphosphatemia,hypocalcemia,elevated CPK
• Tumor lysis syndrome/urate nephropathy –hyperkalemia,
hyperuricemia hyperphosphatemia,elevated uric acid,normal
CPK,Urine Uric acid/Cr ratio > 1
• Ethylene glycol poisoning – elevated serum anion gap and
osmolal gap
• Severe Anaemia – hemolysis,multiple myeloma,thrombotic
angiopathy
• Eosinophilia – Allergic interstitial nephritis
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn17
18. INVESTIGATIONS
• Radiologic Evaluation :
Xray KUB
Renal Ultrasonography
Noncontrast CT
MRI
• Renal biopsy: To assess the cause for intrinsic AKI after
excluding pre and post renal AKI.
BRENNER AND RECTORS - THE KIDNEY 9TH Edtn18
19. Acute Kideny Injury
Prerenal
Uosm > 5000 mosm/kg
Una < 20meq/L
FEna < 1%
Microscopy - bland
Intrinsic Renal Diseases
Postrenal
Uosm: variable
Una: low early, high late
FEna: variable
Microscopy - bland
Ischemic / Toxic ATN
Uosm ~ 300 mosm/kg
Una > 40meq/L
FEna > 2%
Microscopy – dark pigment cast
Acute Interstitial Nephritis
Uosm: variable, ~300 mosm.kg
Una > 40 meq/L
FEna > 2%
Microscopy – leukocytes,
erythrocyts, leukocyte casts
Acute Glomerulonephritis
Uosm: variable (>400 in early GN)
Una: variable (<20meq/l in early GN)
FEna: variable, <1% in early GN
Microscopy – hematuria, proteinuria
Erythrocyte casts (dysmorphic)
19
20. COMPLICATIONS OF AKI
• Metabolic:Hyperkalemia,hyponatremia,hypocalcemia,hyperp
hosphatemia,hypermagnesemia,hyperuricemia,metabolic
acidosis.
• Cardiovascular: Pulmonary oedema, arrhythmia,
pericarditis,perricardial effusion,pulmonary
embolism,hypertension,MI.
• GI: Nausea,vomiting,malnutrition,haemorrhage.
• Neurologic: irritability,asterixis,seizures,mental status
changes.
• Haematologic: anaemia,bleeding.
• Infectious: pneumonia,septicemia,UTI
• Others: Hiccoughs,elevated PTH,Low total T3 and T4.
BRENNER AND RECTORS - THE KIDNEY 9TH
20
22. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Goals:
- To facilitate recovery of kidney function
- To prevent death
- To minimize the risk of CKD
• Patients be stratified& manage according to their
susceptibilities and exposure to reduce the risk of AKI.
• Test patients at increased risk for AKI with measurements of
SCr and urine output.
• Individualize frequency and duration of monitoring based on
patient risk and clinical course.
22
23. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Evaluate to determine the cause, with special attention to
reversible causes.
• Monitor with measurements of SCr and urine output to stage
the severity.
• Manage patients according to the stage and cause.
• Evaluate patients 3 months after AKI for resolution, new onset,
or worsening of pre-existing CKD.
23
24. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Prerenal AKI:
• Volume resuscitation
- Packed cell transfusion
- Crystalloids prefered than colloids
- Treat underlying cause
• Use of vasopressors in conjunction with fluids in patients with
vasomotor shock with, or at risk for AKI.
24
25. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• CHF:
- Cautious use of diuretics
- Ionotropes
- Vasodilators to reduce afterload
- Mechanical support – intra aortic balloon pumps,ventricular
assist devices.
• Liver failure and HRS:
- Intravenous Albumin
- Drugs: Terlipressin, Norepinephrine, Octreotide+Midodrine
- Peritoneovenous shunts,Portosystemic shunts
26. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Avoid using diuretics to prevent or treat AKI, except in the
management of volume overload.
• Avoid using low-dose dopamine to prevent or treat AKI.
• Avoid using fenoldopam/ atrial natriuretic peptide (ANP)/
recombinant human (rh)IGF-1 to prevent or treat AKI.
26
27. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Intrinsic AKI :
• Sepsis :
- haemodynamic targets: MAP>65mmHg,CVP-10-12mmHg,
Urine O/P-.5ml/kg/hr, central venous O2 saturation >70%
- Use crystalloid solutions, RBC transfusion, Vasopressors
- Intensive insulin therapy- Target glucose level 110- 149mg/dl
• Correct intravascular volume depletion
• Avoid nephrotoxic medications
28. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Aminoglycosides :
• Avoid unless no suitable, less nephrotoxic, therapeutic
alternatives are available.
• Single daily doses are prefered.
• Monitor drug levels if multiple daily dosing is used for more than
24 hours or single-daily dosing for more than 48 hours.
• Use topical or local applications than i.v. application, when
feasible and suitable.
28
29. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
• Use lipid formulations of amphotericin B .
• In the treatment of systemic mycoses or parasitic infections,
azole antifungal agents and/or the echinocandins are
prefered.
29
30. Contrast medium induced AKI:
• Screening(S Cr,r/f questionnaire,Urine protein)
• Use iso osmolar or low osmolar iodinated contrast media
• Use lowest possible dose
• Isotonic saline or sodium bicarbonate
- 1 ml/kg/hr for 12 hours before and after procedure
- OP settings – 3ml/kg/hr for 1hr before procedure f/b 1-
1.5ml/kg/hr for 6hrs after the procedure.
• Oral N Acetyl cysteine 600 BD to 1200mg BD
• Avoid Diuretics,Theophylline, Dopamine,
Fenoldopam,CCBs,Mannitol, Prophylatic haemodialysis.
32. • Use of Dopamine ,Fenoldopam,Natriuretic peptides,Mannitol
are not recommended.
• Avoid Loop diuretics for prevention and management of AKI
except in case of fluid overload.
Postrenal AKI:
• PCN, Ureteric stents
• Correction of underlying cause
33. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Indications for RRT
Absolute :
- Volume overload unresponsive to diuretic therapy
- Refractory hyperkalemia
- Persistent metabolic acidosis
- Overt uremic symptoms – Encephalopathy, Pericarditis,
Uremic bleeding diathesis.
Relative:
- Progressive azotemia without uraemic manifestations
- Persistent oliguria
33
35. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Initiate RRT emergently when life-threatening changes in
fluid, electrolyte, and acid-base balance exist.
• Consider the broader clinical context, the presence of
conditions that can be modified with RRT, and trends of
laboratory tests—rather than single BUN and creatinine
thresholds alone.
• Discontinue RRTwhen it is no longer required, either because
intrinsic kidney function has recovered to the point that it is
adequate to meet patient needs, or because RRT is no longer
consistent with the goals of care.
• Avoid using diuretics to enhance kidney function recovery, or
to reduce the duration or frequency of RRT.
35
36. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
Anticoagulation:
• In a patient with AKI requiring RRT, base the decision to use
anticoagulation for RRT on assessment of the patient’s
potential risks and benefits from anticoagulation.
• Anticoagulation during RRT in AKI is recommended if a
patient does not have an increased bleeding risk or impaired
coagulation and is not already receiving systemic
anticoagulation.
36
37. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• For patients without an increased bleeding risk or impaired
coagulation and not already receiving effective systemic
anticoagulation:
- In intermittent RRT, use either UF or LMW heparin.
- In CRRT, use regional citrate anticoagulation rather than
heparin in patients who do not have CIs for citrate.
- In patients with contraindications for citrate, use either UF
or LMW heparin.
37
38. • For patients with increased bleeding risk who are not receiving
anticoagulation:
- Regional citrate anticoagulation can be used, rather than no
anticoagulation, during CRRT .
- Avoid regional heparinization during CRRT .
• In patients with heparin-induced thrombocytopenia (HIT), direct
thrombin inhibitors (argatroban) or Factor Xa inhibitors
(danaparoid or fondaparinux) are recommended rather than
other or no anticoagulation during RRT.
38
39. • Initiate RRT via an uncuffed nontunneled dialysis catheter,
rather than a tunneled catheter.
• Vein for insertion of a dialysis catheter:
- Right jugular vein > femoral vein > left jugular vein
- Last choice: subclavian vein(dominant side).
- use USG guidance for dialysis catheter insertion.
• Take a CXR promptly after placement and before first use of
an IJV or subclavian dialysis catheter.
39
40. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Avoid topical antibiotics over the skin insertion site of a
nontunneled dialysis catheter.
• Avoid using antibiotic locks for prevention of catheter-related
infections of nontunneled dialysis catheters.
• Use dialyzers with a biocompatible membrane for IHD and
CRRT .
• Use continuous and intermittent RRT as complementary
therapy.
• Use CRRT for hemodynamically unstable patients.
• Use CRRT for AKI patients with acute brain injury or
increased ICP or generalized brain edema.
40
41. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Use bicarbonate as a buffer in dialysate and replacement fluid
for RRT in patients with AKI and circulatory shock/ liver failure
and/ lactic acidemia.
• Dialysis fluids and replacement fluids in patients with AKI, at a
minimum, should comply with American Association of
Medical Instrumentation (AAMI) standards regarding
contamination with bacteria and endotoxins.
41
42. DIALYSIS INTERVENTIONS FOR THE
MANAGEMENT OF AKI
• Provide RRT to achieve the goals of electrolyte, acid-base,
solute, and fluid balance that will meet the patient’s needs.
• A Kt/V of 3.9 per week is recommended when using
intermittent or extended RRT in AKI.
• An effluent volume of 20–25 ml/kg/h is recommended for
CRRT in AKI.
42
43. Supportive management of AKI
• Intravascular volume overload :
- Salt and water restriction,diuretics,Ultrafiltration
• Hyponatremia :
- Restriction of oral and iv free water
• Hyperkalemia:
- Dietary restriction
- Discontinue K+ supplements/K+ sparing diuretics
- K+ binding resins, Loop diuretics
- Glucose(50 ml 50%)+ Regular Insulin 10-15U IV
- Sodium bicarbonate
- Calcium gluconate
- RRT
44. Supportive management of AKI
• Metabolic Acidosis :
- Restriction of dietary protein
- Sodium bicarbonate, RRT
• Hyperphosphatemia :
- Diet restriction,
- PO4- binding agents(Ca carbonate,ca acetate,Sevelamer)
• Hypocalcemia :
- Calcium Carbonate
Hypermagnesemia :
- Discontinuation of Mg containing Antacids
45. PREVENTION AND MANAGEMENT OF AKI –
RECOMMENDATIONS KDIGO GUIDELINES 2012
Nutrition :
• Total energy intake of 20–30 kcal/kg/d any stage of AKI.
• Avoid restriction of protein intake.
- 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients
without need for dialysis.
- 1.0–1.5 g/kg/d in patients with AKI on RRT
- up to a maximum of 1.7 g/kg/d in patients on CRRT and
in hypercatabolic patients.
• Enteral route is prefered for nutrition.
45
46. Supportive management of AKI
• Drug dosage :
- Adjustment of all dosages for GFR and renal replacement
modality.
47. AKI Stage
Discontinue all nephrotoxic agents when possible
Ensure volume status and perfusion pressure
Consider functional hemodynamic monitoring
Monitor serum creatinine and urine output
Avoid hyperglycemia
Consider alternative to radiocontrast procedures
Non invasive diagnostic work up
Consider invasive diagnostic work up
Check for changes in drug dosing
Consider renal replacement therapy
Consider icu admission
Avoid subclavian catheters if possible
High Risk Stage 1 Stage 2 Stage 3
47
48. • Identify AKI early on
– Monitor serum Cr for at risk patients
– Make sure I/Os are recorded correctly
• Diagnose as Prerenal, Intrinsic or Postrenal
– Detailed history
– Order routine labs including UA, Uosm, Ucr, Una
(Urine Urea if on diuretics)
– Imaging studies as necessary
• Begin appropriate treatment
– Stop offending agent
– Fluids if appropriate
– Relieve obstruction
– Renal dosing of medicines
Take Home Points
48
Audience Participation:
Why do you get an elevated BUN-creatinine ratio?
In patients with prerenal azotemia, both BUN and Creatinine can increase, but BUN often increases disproportionately more than creatinine. In the setting of decreased effective blood volume, slow flow through the tubules allows more time for BUN to be reabsorbed and creatinine to be secreted. In other words, BUN clearance goes down lower than Cr.
If you don’t identify Prerenal Azotemia, it will progress to ATN
Other types of disease to consider are:
Pigmented Nephropathy from hemoglobin or myoglobin
Thrombotic Microangiopathy- TTP/HUS
And the whole topic of glomerular disease
The whole talk can be given from this slide, so take time to go over each box
Audience Participation:
Sodium is not a good marker of kidney function in patients on diurectics. What test should you use?
- FeUrea (replace sodium with urea in the equation above). FeUrea<35% suggests prerenal AKI