The document discusses acute renal failure (ARF), including its definition, classification into pre-renal, renal and post-renal types, and common causes. It describes the pathophysiology of pre-renal azotemia and acute tubular necrosis (ATN). Diagnostic tools for ARF including urinary sediment examination, urine indices, and radiologic imaging are also summarized.
This document provides information on hematuria (blood in the urine) including causes, evaluation, diagnosis, and management. It discusses glomerular and non-glomerular causes of hematuria and lists various renal diseases that can cause hematuria such as IgA nephropathy, Alport syndrome, thin basement membrane disease, and membranoproliferative glomerulonephritis. The evaluation of hematuria involves urine analysis, urine culture, renal function tests, imaging studies, and sometimes renal biopsy. Management depends on the underlying cause and may include antibiotics, diuretics, immunosuppressive therapy, dialysis, or surgery.
HELLO FRIENDS HERE CAUSES OF HEMATURIA IS HERE MANAGEMENT IN NEXT PRESENTATION ...YOU CAN SEE AND SUBSCRIBE OVER YOU TUBE ...LEARN UROLOGY IS CHANNEL NAME
FOLLOW THE YOU TUBE CHANNEL FOR FUTURE UROLOGY VIDEO
https://www.youtube.com/channel/UCINcUe475Y3c3BvXHvZ8wEw
This document provides information on the clinical management of a patient presenting with jaundice. It begins by defining jaundice and explaining bilirubin metabolism. Jaundice is classified by the type of circulating bilirubin (conjugated or unconjugated) and site of the problem (prehepatic, hepatocellular, or cholestatic/obstructive). The causes, clinical manifestations, appropriate laboratory tests, and imaging studies are described for each type of jaundice to aid in diagnosis and management. A thorough history, physical exam, and targeted lab and imaging workup are recommended to determine the underlying etiology causing a patient's jaundice.
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.
History taking upper gastro intestinal bleedingAbino David
This document provides guidance on evaluating and managing a patient presenting with upper gastrointestinal bleeding. It outlines the differences between upper and lower GI bleeding and describes the relevant history, examination findings, and Rockall score for risk stratification. Key points include distinguishing symptoms of hematemesis versus hematochezia, assessing blood loss based on vital signs and volume, examining for stigmata of liver disease, and endoscopy to determine the source of bleeding and prognosis.
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.
This document discusses hematuria (blood in the urine) and obstructive uropathy (blockage of urine flow in the urinary tract). It covers evaluating hematuria through urinalysis, imaging tests, and cystoscopy. Common causes of hematuria include infections, stones, tumors, and glomerulonephritis. Obstructive uropathy can be congenital or acquired and cause changes to the urethra, bladder, ureters, and kidneys over time. Relieving the obstruction through surgery, stents, or nephrostomy is the main treatment approach.
This document discusses the approach to hematuria in children. It begins by defining hematuria and describing different types. It then outlines the most common etiologies of glomerular and non-glomerular hematuria. The document emphasizes taking a thorough history and physical exam. It recommends investigations including urine analysis, culture and microscopy, blood tests, imaging and potentially renal biopsy. Based on the cause, management may include reassurance, antibiotics, supportive care, monitoring, correcting complications, surgery or dialysis. The document provides a helpful algorithm for evaluating and managing hematuria in children.
This document provides information on hematuria (blood in the urine) including causes, evaluation, diagnosis, and management. It discusses glomerular and non-glomerular causes of hematuria and lists various renal diseases that can cause hematuria such as IgA nephropathy, Alport syndrome, thin basement membrane disease, and membranoproliferative glomerulonephritis. The evaluation of hematuria involves urine analysis, urine culture, renal function tests, imaging studies, and sometimes renal biopsy. Management depends on the underlying cause and may include antibiotics, diuretics, immunosuppressive therapy, dialysis, or surgery.
HELLO FRIENDS HERE CAUSES OF HEMATURIA IS HERE MANAGEMENT IN NEXT PRESENTATION ...YOU CAN SEE AND SUBSCRIBE OVER YOU TUBE ...LEARN UROLOGY IS CHANNEL NAME
FOLLOW THE YOU TUBE CHANNEL FOR FUTURE UROLOGY VIDEO
https://www.youtube.com/channel/UCINcUe475Y3c3BvXHvZ8wEw
This document provides information on the clinical management of a patient presenting with jaundice. It begins by defining jaundice and explaining bilirubin metabolism. Jaundice is classified by the type of circulating bilirubin (conjugated or unconjugated) and site of the problem (prehepatic, hepatocellular, or cholestatic/obstructive). The causes, clinical manifestations, appropriate laboratory tests, and imaging studies are described for each type of jaundice to aid in diagnosis and management. A thorough history, physical exam, and targeted lab and imaging workup are recommended to determine the underlying etiology causing a patient's jaundice.
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.
History taking upper gastro intestinal bleedingAbino David
This document provides guidance on evaluating and managing a patient presenting with upper gastrointestinal bleeding. It outlines the differences between upper and lower GI bleeding and describes the relevant history, examination findings, and Rockall score for risk stratification. Key points include distinguishing symptoms of hematemesis versus hematochezia, assessing blood loss based on vital signs and volume, examining for stigmata of liver disease, and endoscopy to determine the source of bleeding and prognosis.
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.
This document discusses hematuria (blood in the urine) and obstructive uropathy (blockage of urine flow in the urinary tract). It covers evaluating hematuria through urinalysis, imaging tests, and cystoscopy. Common causes of hematuria include infections, stones, tumors, and glomerulonephritis. Obstructive uropathy can be congenital or acquired and cause changes to the urethra, bladder, ureters, and kidneys over time. Relieving the obstruction through surgery, stents, or nephrostomy is the main treatment approach.
This document discusses the approach to hematuria in children. It begins by defining hematuria and describing different types. It then outlines the most common etiologies of glomerular and non-glomerular hematuria. The document emphasizes taking a thorough history and physical exam. It recommends investigations including urine analysis, culture and microscopy, blood tests, imaging and potentially renal biopsy. Based on the cause, management may include reassurance, antibiotics, supportive care, monitoring, correcting complications, surgery or dialysis. The document provides a helpful algorithm for evaluating and managing hematuria in children.
Hematuria refers to the presence of blood in the urine. A diagnosis requires red blood cells to be present in urine samples obtained at least a week apart. Hematuria can be classified as microscopic or macroscopic, intermittent or persistent, and by its location in the urinary tract. Potential causes include glomerular disease, tumors, infections, vascular abnormalities, stones and trauma. Evaluation involves urinalysis, urine culture, imaging tests like ultrasound and CT urography, and cystoscopy depending on risk factors. Treatment focuses on the underlying cause if identified, while asymptomatic microscopic hematuria often requires monitoring without intervention.
Anemia Indian scenario In Chronic Kidney Disease Patients Dr Ashutosh Ojha
this is a comprehensive presentation in Post Doctoral Certificate in Nephrology training program. At Gauhati Medical College Hospital ,Dept Of Nephrology.
This document discusses guidelines for hemodialysis prescription. It provides details on various aspects of the dialysis prescription including modality, frequency, duration, dose, dialysate composition and temperature. It emphasizes the importance of achieving adequate dialysis as defined by fluid removal, normalized electrolytes and minerals, adequate dialysis dose and absence of symptoms. The criteria for optimal dialysis are more stringent and include normalization of blood pressure and minerals without medications, absence of symptoms during and between treatments, no interference with daily life and near-normal life expectancy.
This document discusses upper urinary tract calculi (kidney stones). It notes that kidney stones are common in Pakistan and are caused by many factors. The document describes the types of stones, risk factors like diet and climate, and the multi-step process of stone formation. It outlines evaluations for stones and treatments options ranging from conservative management to procedures like ESWL, ureteroscopy, and surgery depending on the stone size, location, and other factors.
This document provides information on inserting tunneled dialysis catheters. It discusses the preferred insertion sites being the right internal jugular vein. Potential acute complications during insertion include arterial puncture, pneumothorax, hemothorax, and air embolism. Subacute complications after insertion include suboptimal flow due to malposition, kinking, clots or fibrin sheath formation. Tunnel tract infection is also discussed as a complication requiring antibiotic treatment and catheter removal. The document provides guidance on preventing and managing these potential complications.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Sickle cell nephropathy (SCN) is presence of sickled erythrocytes in the renal medulla that result in decreased medullary blood flow, ischemia, microinfarcts and papillary necrosis in the kidneys
A very simple yet comprehensive presentation to understand the concept of CRRT and its implementation in Intensive Care Unit. Intended for the very beginners in ICU. After going through the presentation you will be able to say "Now I know it!"
This presentation comprises of congenital anomalies of kidney and urinary tract made concise and in depth for PG preparation. It contains all important topics of the regarding subject covered in detail.
These slides describe the pathophysiology and the management of patients with liver cirrhosis and portal hypertension. The slides are at the level of post-graduate students
This document discusses the treatment of renal stones in children. It covers types of renal stones, medical management including treating pain and preventing future stone formation. Surgical and endoscopic procedures for stone removal are also discussed. Prevention focuses on adequate hydration and dietary modifications based on the stone composition. The prognosis depends on factors like nephrocalcinosis, treatment adherence, number of infections and procedures required. Close collaboration between urologists and nephrologists is important for managing these young patients.
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.
This document summarizes the pathogenesis and management of acute renal failure. It discusses the causes and stages of pre-renal, intrinsic renal, and post-renal acute kidney injury. Key factors in preventing acute renal failure in surgical patients include adequate hydration, maintaining renal perfusion pressure, avoiding nephrotoxins, and aggressive treatment of complications such as hyperkalemia. Treatment may involve renal replacement therapies like hemodialysis when criteria for initiation are met.
1) Hepatic hemangiomas are benign liver tumors consisting of blood-filled cavities lined by endothelial cells.
2) They are usually asymptomatic but can sometimes cause pain, nausea, or other digestive symptoms. Complications include bleeding, infection, or mass effect.
3) Diagnosis is usually made using ultrasound, CT, or MRI which show characteristic patterns of enhancement. Treatment is usually conservative but resection may be considered for large or symptomatic hemangiomas.
This document discusses renal replacement therapy options for patients with kidney failure, including dialysis and transplantation. It provides details on the two main types of dialysis: peritoneal dialysis, which uses the peritoneal membrane as a filter, and hemodialysis, which uses an artificial kidney to filter blood outside the body. Kidney transplantation is also covered, noting it requires patients first be on dialysis and listing the surgical procedure and common complications.
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.
This document discusses the management of anemia in chronic kidney disease (CKD). It begins by defining anemia and its causes in CKD, which include reduced erythropoietin production and decreased red blood cell survival due to kidney failure. Left untreated, anemia in CKD can lead to deterioration in cardiac function, impaired cognition, and increased fatigue and mortality risk. The main therapeutic options for treating anemia in CKD are red blood cell transfusions, androgens, and erythropoiesis-stimulating agents (ESAs). ESAs such as epoetin alfa and darbepoetin alfa are now the standard treatment as they reduce transfusion needs and risks while helping to mobilize
Liver cirrhosis is a chronic, progressive disease characterized by diffuse damage to liver cells and the formation of scar tissue. As healthy liver tissue is replaced by scar tissue, the liver loses its normal structure and function. Common causes include chronic hepatitis from alcohol, viruses, and other toxins. Late stage cirrhosis results in liver failure and life-threatening complications such as internal bleeding, infection, and hepatic encephalopathy.
This document discusses the evaluation of hematuria. It defines hematuria as the presence of red blood cells in urine and classifies it as gross or microscopic based on visibility. Microscopic hematuria is defined as >3 RBCs/HPF on urine sediment analysis from two samples. The document outlines the workup for hematuria, including history, physical exam, urine analysis, investigations like cystoscopy based on findings, and distinguishing between glomerular and non-glomerular causes. Causes of hematuria include renal and urologic malignancies, infections, stones, vascular diseases, and medications. Morphology of RBCs on microscopy helps localize the source of bleeding.
The document provides guidance on proper urine sample collection and analysis. It emphasizes analyzing urine as soon as possible, within 30 minutes ideally. If longer storage is needed, the urine must be refrigerated and brought to room temperature before examination. Physical, biochemical, and microscopic tests are described to examine properties like color, specific gravity, glucose, ketones, blood, and sediment such as casts, crystals, and cells. Proper collection and handling is important to accurately detect abnormalities.
Hematuria refers to the presence of blood in the urine. A diagnosis requires red blood cells to be present in urine samples obtained at least a week apart. Hematuria can be classified as microscopic or macroscopic, intermittent or persistent, and by its location in the urinary tract. Potential causes include glomerular disease, tumors, infections, vascular abnormalities, stones and trauma. Evaluation involves urinalysis, urine culture, imaging tests like ultrasound and CT urography, and cystoscopy depending on risk factors. Treatment focuses on the underlying cause if identified, while asymptomatic microscopic hematuria often requires monitoring without intervention.
Anemia Indian scenario In Chronic Kidney Disease Patients Dr Ashutosh Ojha
this is a comprehensive presentation in Post Doctoral Certificate in Nephrology training program. At Gauhati Medical College Hospital ,Dept Of Nephrology.
This document discusses guidelines for hemodialysis prescription. It provides details on various aspects of the dialysis prescription including modality, frequency, duration, dose, dialysate composition and temperature. It emphasizes the importance of achieving adequate dialysis as defined by fluid removal, normalized electrolytes and minerals, adequate dialysis dose and absence of symptoms. The criteria for optimal dialysis are more stringent and include normalization of blood pressure and minerals without medications, absence of symptoms during and between treatments, no interference with daily life and near-normal life expectancy.
This document discusses upper urinary tract calculi (kidney stones). It notes that kidney stones are common in Pakistan and are caused by many factors. The document describes the types of stones, risk factors like diet and climate, and the multi-step process of stone formation. It outlines evaluations for stones and treatments options ranging from conservative management to procedures like ESWL, ureteroscopy, and surgery depending on the stone size, location, and other factors.
This document provides information on inserting tunneled dialysis catheters. It discusses the preferred insertion sites being the right internal jugular vein. Potential acute complications during insertion include arterial puncture, pneumothorax, hemothorax, and air embolism. Subacute complications after insertion include suboptimal flow due to malposition, kinking, clots or fibrin sheath formation. Tunnel tract infection is also discussed as a complication requiring antibiotic treatment and catheter removal. The document provides guidance on preventing and managing these potential complications.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Sickle cell nephropathy (SCN) is presence of sickled erythrocytes in the renal medulla that result in decreased medullary blood flow, ischemia, microinfarcts and papillary necrosis in the kidneys
A very simple yet comprehensive presentation to understand the concept of CRRT and its implementation in Intensive Care Unit. Intended for the very beginners in ICU. After going through the presentation you will be able to say "Now I know it!"
This presentation comprises of congenital anomalies of kidney and urinary tract made concise and in depth for PG preparation. It contains all important topics of the regarding subject covered in detail.
These slides describe the pathophysiology and the management of patients with liver cirrhosis and portal hypertension. The slides are at the level of post-graduate students
This document discusses the treatment of renal stones in children. It covers types of renal stones, medical management including treating pain and preventing future stone formation. Surgical and endoscopic procedures for stone removal are also discussed. Prevention focuses on adequate hydration and dietary modifications based on the stone composition. The prognosis depends on factors like nephrocalcinosis, treatment adherence, number of infections and procedures required. Close collaboration between urologists and nephrologists is important for managing these young patients.
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.
This document summarizes the pathogenesis and management of acute renal failure. It discusses the causes and stages of pre-renal, intrinsic renal, and post-renal acute kidney injury. Key factors in preventing acute renal failure in surgical patients include adequate hydration, maintaining renal perfusion pressure, avoiding nephrotoxins, and aggressive treatment of complications such as hyperkalemia. Treatment may involve renal replacement therapies like hemodialysis when criteria for initiation are met.
1) Hepatic hemangiomas are benign liver tumors consisting of blood-filled cavities lined by endothelial cells.
2) They are usually asymptomatic but can sometimes cause pain, nausea, or other digestive symptoms. Complications include bleeding, infection, or mass effect.
3) Diagnosis is usually made using ultrasound, CT, or MRI which show characteristic patterns of enhancement. Treatment is usually conservative but resection may be considered for large or symptomatic hemangiomas.
This document discusses renal replacement therapy options for patients with kidney failure, including dialysis and transplantation. It provides details on the two main types of dialysis: peritoneal dialysis, which uses the peritoneal membrane as a filter, and hemodialysis, which uses an artificial kidney to filter blood outside the body. Kidney transplantation is also covered, noting it requires patients first be on dialysis and listing the surgical procedure and common complications.
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.
This document discusses the management of anemia in chronic kidney disease (CKD). It begins by defining anemia and its causes in CKD, which include reduced erythropoietin production and decreased red blood cell survival due to kidney failure. Left untreated, anemia in CKD can lead to deterioration in cardiac function, impaired cognition, and increased fatigue and mortality risk. The main therapeutic options for treating anemia in CKD are red blood cell transfusions, androgens, and erythropoiesis-stimulating agents (ESAs). ESAs such as epoetin alfa and darbepoetin alfa are now the standard treatment as they reduce transfusion needs and risks while helping to mobilize
Liver cirrhosis is a chronic, progressive disease characterized by diffuse damage to liver cells and the formation of scar tissue. As healthy liver tissue is replaced by scar tissue, the liver loses its normal structure and function. Common causes include chronic hepatitis from alcohol, viruses, and other toxins. Late stage cirrhosis results in liver failure and life-threatening complications such as internal bleeding, infection, and hepatic encephalopathy.
This document discusses the evaluation of hematuria. It defines hematuria as the presence of red blood cells in urine and classifies it as gross or microscopic based on visibility. Microscopic hematuria is defined as >3 RBCs/HPF on urine sediment analysis from two samples. The document outlines the workup for hematuria, including history, physical exam, urine analysis, investigations like cystoscopy based on findings, and distinguishing between glomerular and non-glomerular causes. Causes of hematuria include renal and urologic malignancies, infections, stones, vascular diseases, and medications. Morphology of RBCs on microscopy helps localize the source of bleeding.
The document provides guidance on proper urine sample collection and analysis. It emphasizes analyzing urine as soon as possible, within 30 minutes ideally. If longer storage is needed, the urine must be refrigerated and brought to room temperature before examination. Physical, biochemical, and microscopic tests are described to examine properties like color, specific gravity, glucose, ketones, blood, and sediment such as casts, crystals, and cells. Proper collection and handling is important to accurately detect abnormalities.
Dokumen tersebut membahas tentang fluida dinamis yang mencakup rumus-rumus dasar seperti debit, persamaan kontinuitas, hukum Bernoulli, dan contoh soal-soalnya beserta pembahasannya seperti tentang debit, kecepatan aliran pada pipa, gaya angkat pada sayap pesawat, dan lain sebagainya.
This document summarizes key topics about chronic kidney disease (CKD), including definitions, classification stages based on glomerular filtration rate (GFR), clinical consequences such as increased cardiovascular risk, and treatment goals like blood pressure and proteinuria control. It discusses markers of renal function like serum creatinine and estimated GFR, as well as complications of CKD like anemia and how they are treated. Target hemoglobin levels with erythropoietin therapy and outcomes of hemodialysis are also summarized.
This document provides an overview of renal pathology. It begins by outlining the topics to be covered, including organizing renal pathology, symptoms of renal pathology, kidney failure (acute vs chronic), sites of renal pathology in the glomeruli, tubules, interstitium and collecting system, and biochemical abnormalities. It then delves into each topic, defining and describing acute and chronic kidney failure, their causes and clinical phases. It also details the pathogenesis and histology of different types of glomerulonephritis and discusses pathology in the tubules, interstitium and collecting system. Throughout, it emphasizes the most common causes and clinical presentations of renal diseases.
Acute renal failure (ARF) is defined as a rapid reduction in kidney function resulting in build-up of waste products. It can be prerenal (functional), renal (structural), or postrenal (obstruction). Common causes include decreased blood flow, nephrotoxins, and urinary tract obstruction. Patients may present with edema, electrolyte abnormalities, and uremic symptoms. Diagnosis involves urine and blood tests. Treatment focuses on treating the underlying cause, fluid management, and sometimes dialysis.
This document summarizes renal pathology and glomerular diseases. It discusses how diseases can affect the glomeruli, tubules, interstitium and vasculature. The glomeruli are described as a network of capillaries lined by endothelial cells, the glomerular basement membrane, and podocytes. Immunological and toxic mechanisms can cause glomerular injury. Membranous glomerulopathy is described as the most common cause of nephrotic syndrome in adults, characterized by thickening of the glomerular capillary wall.
This document discusses acute renal failure (ARF) and its causes, definitions, and classifications. It describes the key components of the nephron and how ARF results from a reduction in glomerular filtration rate (GFR). ARF can be classified as pre-renal, renal, or post-renal based on its underlying cause and pathophysiology. The most common type of renal ARF is acute tubular necrosis (ATN), which results from intrinsic injury to the renal tubules.
13 Evaluation And Management Of Acute Renal FailureDang Thanh Tuan
The document discusses evaluation and management of acute renal failure (ARF). It defines ARF as a rapid decline in kidney function over hours to weeks. ARF can be prerenal, intrinsic renal, or postrenal. Prerenal ARF is caused by reduced blood flow to the kidneys and is often reversible. Intrinsic renal ARF involves direct kidney damage from conditions like acute tubular necrosis. Postrenal ARF occurs when urine outflow is blocked. Management involves treating underlying causes, preventing further injury, managing complications conservatively, and initiating renal replacement therapy if needed.
04 Differential Diagnosis Of Acute Renal Failureguest2379201
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, perinatal issues in newborns. It also covers intrinsic renal failure due to tubular diseases, interstitial diseases, glomerular diseases, vascula diseases, and nephrotoxins. Post-renal ARF due to urinary tract obstruction is also summarized. The document provides details on evaluation and laboratory findings that can help in differential diagnosis of ARF.
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, hemorrhage, and asphyxia in newborns. Intrinsic renal failure can be caused by tubular diseases, interstitial diseases, glomerular diseases, or vascula diseases. Acute tubular necrosis is described as the most common cause. Post-renal ARF can result from urinary tract obstruction. Laboratory findings that can aid in diagnosis are also summarized.
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure. It discusses prerenal, intrinsic renal, and postrenal causes of acute renal failure. Prerenal causes include volume depletion, advanced liver disease, congestive heart failure, and renal arterial disease. Intrinsic renal causes include tubular diseases, interstitial diseases, glomerular diseases, and vascula diseases. Postrenal causes involve urinary obstruction.
The document discusses acute kidney injury (AKI), defining it and outlining criteria for diagnosis. It covers the epidemiology of AKI, noting it occurs in 5-35% of hospitalized or ICU patients with mortality up to 75-90% in sepsis and 35-45% without. Common causes of AKI are discussed as well as diagnostic evaluations including lab tests, imaging, and biomarkers. Complications and specific types of AKI like acute tubular necrosis and contrast-induced nephropathy are summarized.
08 Al Ghonaim Approach To Acute Renal FailureDang Thanh Tuan
The document discusses acute renal failure (ARF), including its definition, epidemiology, etiology, diagnosis, and treatment. ARF can be pre-renal, renal, or post-renal in origin. The most common cause is acute tubular necrosis, often from hypotension, sepsis, or nephrotoxins. Diagnosis involves lab tests of kidney function and urinalysis. Treatment focuses on fluid management, avoiding nephrotoxins, and possibly dialysis.
08 Al Ghonaim Approach To Acute Renal Failureguest2379201
The document discusses acute renal failure (ARF), including its definition, epidemiology, etiology, diagnosis, and treatment. ARF can be pre-renal, renal, or post-renal in etiology. The most common cause is acute tubular necrosis, often from hypotension, sepsis, or nephrotoxins. Diagnosis involves lab tests of kidney function and urinalysis. Treatment focuses on fluid management, avoiding nephrotoxins, and possibly dialysis.
The document discusses acute renal failure (ARF), defining it as a sudden reduction in kidney function that results in waste accumulating in the blood. It classifies ARF by urine volume and lists the main causes as pre-renal, post-renal, and renal. Pre-renal causes include volume depletion and problems with blood flow. Post-renal causes involve urine outflow issues. Renal causes include tubular necrosis, interstitial nephritis, and glomerular disease. The document provides details on evaluating and managing ARF, including through fluid management, treating electrolyte abnormalities, and considering renal replacement therapy.
The document discusses acute renal failure (ARF), defining it as the loss of renal function over hours to days resulting in the accumulation of nitrogenous waste products in the blood. It classifies the etiologies of ARF into prerenal, intrinsic renal, and postrenal causes. Prerenal ARF is due to decreased effective blood volume leading to renal vasoconstriction, while postrenal ARF results from urinary tract obstruction. Intrinsic renal ARF includes acute tubular necrosis, acute interstitial nephritis, and glomerulonephritis. Clinical evaluation involves assessing for risk factors and distinguishing between the types of ARF to guide management and treatment.
The document discusses acute renal failure (ARF), defining it as the loss of renal function over hours to days resulting in the accumulation of nitrogenous waste products in the blood. It classifies the etiologies of ARF into prerenal, intrinsic renal, and postrenal causes. Prerenal ARF is due to decreased effective blood volume leading to renal vasoconstriction, while postrenal ARF results from urinary tract obstruction. Intrinsic renal ARF includes acute tubular necrosis, acute interstitial nephritis, and glomerulonephritis. Clinical evaluation involves assessing for risk factors and distinguishing between the types of ARF to guide treatment and management.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
The document discusses renal failure including definitions of acute renal failure (ARF), chronic renal failure (CRF), and end-stage renal disease (ESRD). It covers classifications and common causes of renal failure. Key points include that ARF can be pre-renal, renal, or post-renal in origin and has many potential causes. CRF is a slow, progressive loss of kidney function that is irreversible and can be caused by diabetes, hypertension, glomerulonephritis, and other conditions. Monitoring of renal function includes tests of serum creatinine and clearance rates.
1. Acute renal failure (ARF) is a rapid decline in kidney function over days to weeks leading to increased nitrogenous waste products in the blood. It occurs in 5% of hospitalized patients and up to 30% of ICU patients.
2. ARF can be pre-renal, renal, or post-renal. The most common causes are prerenal conditions that compromise renal blood flow like dehydration, and intrinsic renal disorders like acute tubular necrosis and interstitial nephritis.
3. Diagnosis is based on blood and urine tests showing increased creatinine and azotemia. Treatment focuses on fluid management, identifying and treating underlying causes, and potentially initiating dialysis
This document provides an overview of common renal disorders, including acute renal failure (ARF), chronic renal failure, nephrotic syndrome, nephrolithiasis, and renal tubular acidosis. ARF is characterized by a rapid decline in glomerular filtration rate and is divided into prerenal, intrinsic renal, and postrenal types. Chronic renal failure is usually caused by diabetes or glomerulonephritis and results in metabolic abnormalities and uremic syndrome. Nephrotic syndrome involves proteinuria, hypoalbuminemia, edema, and hyperlipidemia due to increased glomerular permeability. Nephrolithiasis is caused by supersaturation of urine leading to stone formation,
Acute renal failure (ARF) is a sudden decrease in kidney function that results in the buildup of waste products in the blood. It can be caused by decreased blood flow to the kidneys, direct kidney damage, or urinary tract obstruction. The most common type is prerenal ARF due to low blood volume or pressure. Symptoms include thirst, dizziness, and reduced urine output. Treatment focuses on correcting the underlying cause, managing fluid balance and dialysis if needed. ARF is usually reversible but can last weeks depending on the severity of the initial insult.
The document discusses renal failure, including acute kidney injury (AKI) and chronic kidney disease (CKD). It covers the epidemiology and burden of kidney disease globally and in India. It describes the anatomy and physiology of the kidney and nephron. It defines AKI and its stages, causes including prerenal, intrarenal and postrenal factors. Signs, symptoms, diagnosis and management of AKI are summarized. CKD is defined and its stages, signs and symptoms, and diagnosis are outlined. Risk factors for CKD are also mentioned.
This document discusses renal failure and renal parenchymal disease. It defines acute renal failure as a rapid deterioration in renal function characterized by azotemia and a decline in GFR, which may or may not be accompanied by oliguria. Chronic renal failure is defined as kidney damage or decreased function for 3 or more months resulting in a GFR of less than 60 mL/min/1.17m2. The causes of acute and chronic renal failure are discussed under prerenal, intrarenal and postrenal categories. Imaging findings of various renal parenchymal diseases on ultrasound, CT and MRI are also summarized. Morphological criteria to categorize different renal abnormalities based on ultrasound findings are provided.
This document discusses acute renal failure (ARF), including:
- ARF is common in hospitalized patients and associated with high morbidity and mortality. It is often multifactorial, with identifiable risk factors.
- The main causes of ARF are pre-renal azotemia, acute tubular necrosis, acute glomerulonephritis, and acute interstitial nephritis. Acute tubular necrosis is the most common intrinsic cause.
- Diagnosis involves laboratory evaluation of serum creatinine and BUN levels, urinalysis, and urine indices. Treatment is largely supportive to avoid further insults and correct underlying causes. Prevention focuses on maintaining euvolemia and avoiding nep
Acute renal failure (ARF) is a sudden reduction in kidney function that results in waste accumulating in the blood. It occurs in 5% of hospitalized patients and 35% of intensive care unit patients. ARF can be prerenal from decreased blood flow, renal from direct kidney damage, or postrenal from urinary tract obstruction. Causes include dehydration, heart issues, infections, kidney diseases, and nephrotoxic drugs. Symptoms include reduced urine output and waste buildup in the blood. Treatment focuses on fluid management, electrolyte control, and potentially dialysis. Prevention involves proper hydration and treating infections promptly.
1) Procedural sedation is used for many medical procedures and aims to provide analgesia, amnesia, and reduce anxiety while maintaining airway reflexes and spontaneous breathing.
2) While pulse oximetry became standard in the 1980s, capnography has emerged as the new gold standard for monitoring procedural sedation as it can detect respiratory issues that oximetry may miss.
3) Overlake Hospital implemented capnography monitoring for all procedural sedations after reviewing evidence and determining it was more effective for patient safety than relying on respiratory therapists to continuously monitor each procedure.
The evolution of pediatric mechanical ventilatorsDang Thanh Tuan
1. Mechanical ventilators have evolved from simple analog machines to sophisticated microprocessor-controlled devices with advanced modes of ventilation.
2. Early ventilators were open-loop controlled while modern ventilators use various closed-loop and dual-loop control schemes to better match ventilation to patient needs.
3. The newest generations of ventilators use proportional assist, automatic tube compensation, adaptive support ventilation, and other advanced modes that aim to provide more patient-synchronized support and facilitate weaning. However, further research is still needed to fully understand the outcomes of these newer ventilation strategies.
The document discusses various methods of patient monitoring during anesthesia, including their purposes, advantages, and limitations. It covers monitoring vital signs, standards for basic anesthesia monitoring according to the ASA, techniques like non-invasive blood pressure monitoring, ECG, pulse oximetry, capnography, and invasive arterial line monitoring. Key aspects emphasized are integrating multiple monitoring methods to evaluate oxygenation, ventilation, and circulation.
The document discusses the introduction and clinical applications of volumetric capnography (VCO2) at one hospital. It provides an agenda for the topics covered, which include VCO2 management, clinical applications, and data from the University of Tennessee Medical Center's experience using VCO2. Key applications discussed are ventilation management, monitoring changes in perfusion, optimization of positive end-expiratory pressure, and assisting with ventilator weaning trials. The University of Tennessee Medical Center saw decreases in length of mechanical ventilation, ventilator days, and re-intubation rates after implementing VCO2 monitoring.
18 basics of pediatric airway anatomy, physiology and managementDang Thanh Tuan
The document provides an overview of pediatric airway anatomy, physiology, and management. It discusses the differences between pediatric and adult airways, including a more rostral larynx, relatively larger tongue, angled vocal cords, differently shaped epiglottis, and funneled larynx in children. It also reviews normal airway management techniques like bag-mask ventilation and various airway devices, as well as complications from intubation. The goal is to protect, adequately ventilate, and oxygenate the pediatric airway.
The document discusses the use of capnography for non-intubated patients experiencing trouble breathing. It describes how capnography can help identify and monitor conditions like bronchospasm from asthma or COPD by examining patterns in exhaled carbon dioxide levels. Specific capnographic signatures are presented for different respiratory conditions including asthma attacks, COPD exacerbations, congestive heart failure, and hypoventilation states. Case studies demonstrate how capnography can track changes in a patient's condition before and after treatment.
Capnography can be used to summarize 3 key applications for intubated patients:
1) It can confirm correct endotracheal tube placement and detect displacement. Characteristic waveforms indicate proper vs displaced placement.
2) During CPR, it can assess the effectiveness of chest compressions by correlating end-tidal CO2 levels with cardiac output and blood flow.
3) It provides an early indicator of return of spontaneous circulation through a rapid rise in CO2 levels, earlier than other signs like pulse or blood pressure. It also aids the decision to cease resuscitation efforts based on CO2 levels.
Capnography measures exhaled carbon dioxide (CO2) to provide real-time monitoring of ventilation, unlike pulse oximetry which monitors oxygen saturation in the blood and is slower to detect changes. A normal capnographic waveform has four phases: 1) dead space, 2) ascending, 3) alveolar plateau, and 4) descending. The end-tidal CO2 value reflects the highest CO2 concentration in exhaled air and typically ranges from 35-45mmHg. Capnography can immediately detect conditions that impact ventilation such as hypoventilation, hyperventilation, and bronchospasm based on changes to the waveform shape, frequency, and CO2 values.
This document provides an overview of capnography, which is a technology that objectively measures ventilation by detecting exhaled carbon dioxide. It can be used for both intubated and non-intubated patients to continuously monitor ventilation and the patient's ABCs. The document reviews the history of capnography, from its initial use in operating rooms to new portable technologies suitable for emergency medical services. It also outlines the clinical applications of capnography such as verifying endotracheal tube placement and monitoring treatment effectiveness.
Dr. Ajmal Eusuf discusses the importance and benefits of capnography monitoring in the ICU. Capnography can be used to confirm proper endotracheal tube placement, monitor ventilation, and detect various respiratory issues. While capnography is standard practice in operating rooms and recommended by guidelines, only about half of UK ICUs currently use it as a mandatory monitoring tool. Adopting capnography as routine bedside monitoring in the ICU would help compliance with protocols and better patient care, especially for critically ill patients who are sicker than those in operating rooms.
The document discusses two options for capnography monitoring from ZOLL - the CAPNOSTAT 3 mainstream CO2 sensor and the LoFlo sidestream CO2 module. It provides details on the benefits of each, such as the CAPNOSTAT sensor's accuracy and resistance to contaminants, and the LoFlo module's interchangeability and low 50ml/min sampling rate. The document emphasizes that both provide reliable, accurate CO2 monitoring and waveforms for assessing patient ventilation.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
The precise decrement in GFR that constitutes acute renal failure is ill-defined, and varies in different studies. Using absolute increments in the plasma creatinine concentration (P Cr ) is especially problematic (see next slide).
This slide depicts the inverse relationship between P Cr and GFR (measured by inulin clearance) in a large number of subjects with varying degrees of renal function. The hyperbolic relationship between P Cr and GFR complicates the use of absolute increments in P Cr (e.g., > 0.5 or 1.0 mg/dl) as yardsticks for defining acute renal failure.
To function properly, the kidney requires: (1) normal blood flow; functioning glomeruli and tubules to separate and process an ultafiltrate containing waste products from the blood; and (3) drainage and elimination of formed urine from the body. The sudden interruption of any of these processes will lead to Acute Renal Failure (ARF) . Disorders causing ARF are classified on the basis their primary site of interference with these processes. Conditions which interfere with blood delivery to the kidney are called Prerenal, and are most commonly functional (and potentially reversible) in nature (e.g., ECF volume contraction, congestive heart failure) but on occasion may be structural (e.g., renal artery stenosis). Diseases which cause intrinsic injury to the kidney proper (glomeruli, tubules, interstitium, small blood vessels) are grouped under Renal causes of ARF (e.g., acute glomerulonephritis, acute tubular necrosis, acute interstitial nephritis or small vessel vasculitis). Acute Tubular Necrosis is a distinctive clinicopathological syndrome in which the tubules are the primary site of injury. The terms ARF and ATN should not be used interchangeably. Finally, conditions which interfere with normal drainage and elimination of formed urine are classified as Postrenal (e.g., prostatic outlet obstruction, bilateral ureteral obstruction). Pre-renal ARF (also commonly referred to as “pre-renal azotemia”) and acute tubular necrosis (ATN) are the most common causes of acute renal failure in hospitalized patients.
Some combination of hypovolemia, hypotension and diminished renal perfusion is the most common cause of ARF in hospitalized patients. Identification of pre-renal (functional) ARF is important because it is generally reversible. Pre-renal ARF may evolve from blood loss, sodium depletion (due to diarrhea, excessive diuresis or congenital or acquired salt-wasting disorders), redistribution of plasma volume to a so-called “third space” (e.g., ascites in patients with hemorrhagic pancreatitis or hepatic cirrhosis), or reductions in effective arterial blood volume with consequent renal hypoperfusion (as in congestive heart failure, hepatic cirrhosis or nephrotic syndrome). In other situations, especially when for one reason or another renal perfusion is tenuous or already compromised, drugs which affect afferent and/or efferent arteriolar resistance (e.g., NSAIDs, ACE inhibitors) can precipitate pre-renal azotemia.
The determinants of renal blood flow (RBF) are summarized in this slide. In the absence of renal artery stenosis, renal arterial pressure (RAP) is the same as systemic mean arterial pressure (commonly referred to by nephrologists as “renal perfusion pressure”). Renal venous pressure (RVP) is usually, but not always, low and relatively constant. The glomerular afferent and efferent arterioles are the major sites of renal vascular resistance (R aff and R eff , respectively); changes in either will affect renal blood flow (RBF). In the “universal pressure;flow relationship”, F = flow; P = change in pressure; R = resistance. RBF = renal blood flow; RAP = renal arterial pressure; RVP = renal venous pressure; R aff = afferent arteriolar resistance; R eff = efferent arteriolar resistance
It is useful to think about glomerular capillary hydrostatic pressure (P GC ), and its primary role in determining GFR (blue arrow), in terms of the ratio of efferent to afferent arteriolar resistance (i.e., R eff /R aff ). Increases in R eff /R aff increase P GC and therefore tend to increase GFR. Similarly, decreases in R eff /R aff decrease P GC and therefore tend to decrease GFR.
The kidney is able to maintain a relatively constant glomerular filtration rate (GFR) and to a lesser extent renal blood flow (RBF) despite modest reductions in mean arterial pressure. This process, termed renal autoregulation , derives largely from hormonally-mediated adjustments in afferent and efferent arteriolar resistance. By increasing R eff /R aff angiotensin-II and prostaglandin-E maintain P GC and GFR at the expense of RBF. As a result, filtration fraction (GFR/RBF) and post-glomerular capillary oncotic pressure increase, which facilitates Na and water reabsorption from the adjacent proximal tubule. Angiotensin-II also directly increases proximal tubular Na reabsorption and by stimulating aldosterone synthesis and release increases Na reabsorption in more distal tubular segments as well. At the same time, volume-related antidiuretic hormone release leads to enhanced water and urea reabsortion in the collecting duct. Urine formed under these conditions is of reduced volume , highly concentrated , and contains scant amounts of sodium . These characteristics are the basis of tests (see later slides) for distinguishing pre-renal azotemia from acute tubular necrosis. Renal autoregulation breaks down as mean arterial pressure falls below about 80 mm Hg, at which point further adjustments in intra-renal hemodynamics are unable to maintain GFR and RBF in the face of a progressive reduction in renal perfusion pressure.
Ischemia has been recognized as a cause of acute renal failure since the 1940s. This form of ATN includes any pathophysiologic state in which volume depletion, impaired cardiac output, or vascular pooling results in renal hypoperfusion. The degree and duration of renal hypoperfusion (ischemia) necessary to cross from a readily reversible form of ARF (pre-renal) to a less reversible or irreversible form of ARF despite correction of the hypoperfusion (post- ischemic acute tubular necrosis) is highly variable. In addition to ischemia, there are a variety of endogenous and exogenous toxins that can lead to acute tubular necrosis.
Acute tubular necrosis showing focal loss of tubular epithelial cells (arrows) and partial occlusion of tubular lumens by cellular debris (D) (H&E stain). The histologic findings in ischemic acute tubular necrosis may be disproportionately small in comparison to the magnitude of renal dysfunction. Focal necrosis of single proximal tubular cells and clusters of cells is seen in the majority of cases of ATN. Portions of tubules not involved by necrosis commonly show effacement of the proximal tubule brush border. Other pathologic findings include flattening of the tubular epithelium and dilatation of the tubular lumina. Many of the flattened tubular cells exhibit signs of regeneration – i.e., mitoses and large hyperchromatic nuclei. Regenerative changes and foci of necrosis are often seen in the same biopsy specimen. Distal nephron segments are characteristically occluded by urinary casts of hyaline, granular, and pigmented varieties.
Another example of ischemic ATN (PAS stain).
Some of the more common nephrotoxins associated with acute tubular necrosis are listed on this slide.
Tubular epithelial degeneration and hyaline amphophilic casts (positive with immunologic stains for myoglobin) in a patient with rhabdomyolysis and myoglobinuric acute tubular necrosis.
The tubular epithelial cells show extensive cytoplasmic vacuolar change in a case of ethylene glycol poisoning.
Acute interstitial nephritis (AIN) is most often caused by drugs (in such cases it is often called “allergic intersitial nephritis”), although bacterial (including Legionella and leptospirosis) and viral infections may also be responsible. Sarcoidosis causes granulomatous interstitial nephritis. Although the number of drugs associated with AIN is large, relatively few have been reported to cause AIN with any frequency. AIN was initially reported with methicillin but this antibiotic is rarely used today. However, other beta-lactam antibiotics (penicillins and cephalosporins) remain a frequently reported cause of AIN. Of the quinolones, AIN has been most often seen with ciprofloxacin. NSAIDs can cause either AIN, nephrotic syndrome, or both. Although reported with cimetidine, AIN is extremely rare with other H 2 receptor blockers such as ranitidine. Sulfonamide-containing antibiotics (sulfamethoxazole in the trimethoprim-sulfamethaxazole combination) and diuretics derived from sulfonamides (thiazides, bumetamide, furosemide) can also cause AIN.
Most patients with allergic intersitial nephritis have will have fever and in many cases this will be accompanied by a rash. However, the other “classic” findings listed on this slide are much more variable, and all one may see is fever and otherwise unexplained acute renal failure. In NSAID-induced allergic interstitial nephritis fever, rash and eosinophilia are typically absent and acute renal failure and nephrotic level proteinuria may be the only findings. Significant proteinuria is unusual in other forms of allergic interstitial nephritis. The sediment will usually show WBC (with a sterile culture), WBC casts, and RBCs. Previously eosinophiluria was regarded as highly specific for AIN, but experience has not borne this out.
Drug-induced allergic interstitial nephritis (H&E stain). Note the diffuse interstitial infiltrate, many red-staining eosinophils, and sparing of the glomerulus (on the left).
Cholesterol embolization may occur after a “sentinel” procedure (e.g., cardiac catherization) or be associated with slowly progressive renal failure over a period of months or years. Whatever the time course, it is generally irreversible. Cholesterol emboli usually lodge in vessels 100 to 200 microns in diameter, and are visualized as clear spaces where the cholesterol crystals have been dissolved by routine processing. The early response of platelets and occasional mononuclear cells is seen in the medium size artery occluded by acute cholesterol emboli in the left panel (Jones Silver stain). In later stages of organization the lumen may have more fibrous reorganization surrounding the cholesterol clefts, as shown in the right panel (PAS stain). Chlosterol embolization is an often unrecognized cause of acute renal failure which may be indistinguishable from the “bland” variety of allergic interstitial nephritis except by biopsy. In addition to ARF, other manifestations of the occlusion of small arteries by atheroembolic material include skin mottling (livedo reticularis), blue toes and distal digital infarcts with intact peripheral pulses. Transient eosinophilia, hypocomplementemia, and an elevated sedimentation rate are sometimes also seen.
In addition to ischemia, contrast media remains one of the most common forms of acute tubular necrosis. It’s reported prevalence varies depending on study design (retrospective or prospective), the criteria used to define ARF, and if general or high-risk populations are evaluated. The single most important risk factor is underlying renal insufficiency, which may not always be obvious even with routine laboratory studies.
The greater the degree of renal insufficiency, the greater the risk for contrast-induced ARF. Although diabetes is commonly listed as a risk factor, there is little increased risk for contrast ARF in diabetics with normal renal function. However, it does appear that diabetics with impaired renal function are at greater risk than non-diabetics with comparable degrees of renal insufficiency. Multiple myeloma is more of a historical risk factor for contrast ARF and was initially reported with early preparations of contrast media which had diminished solubility or enhanced precipitation with Tamm-Horsfall protein compared to modern day contrast media. Contrast media used in the 1970s and 1980s were negatively charged benzene rings and thus were coupled with cations such as sodium or meglumine. Thus, two molecules were required to deliver the iodine attached to each benzene ring, therefore increasing the osmolality of the contrast media. These early versions are referred to as ionic or high-osmolar media and are less commonly used today. Current contrast media are iodine containing benzene rings which are not charged and thus their osmolality is roughly half of the high-osmolar compounds. These compounds are referred to as non-ionic or low osmolar contrast media. In patients with underlying renal insufficiency especially those with diabetes (but not in patients with normal renal function), prospective studies have shown a reduced incidence of ARF with non-ionic compared to ionic contrast media. Although there is no ‘threshold’ dose of contrast media which if exceeded will significantly increase the risk of ARF, in general the greater the volume of contrast given the greater the risk for ARF.
For the majority of patients with contrast-induced ARF, onset as manifested by a rise in serum creatinine is seen within the first 24 hrs after contrast exposure. A small number of additional cases may require 48 hrs after exposure to become apparent. If ARF is not manifested by 48 hrs after exposure to contrast, it is very unlikely to occur. Fortunately for the majority of patients (~ 75%) with contrast ARF, the renal failure is mild, its duration is brief, most patients are non-oliguric, and dialysis is rarely needed. The urinary sediment may contain the “muddy-brown” pigmented casts and renal tubular cells typical of ATN (to be discussed later) or may be quite bland. Somewhat atypical for acute tubular necrosis, the fractional excretion of sodium is often low (also to be discussed later). Finally, in patients who are administered contrast media through an arterial vessel, contrast media ARF needs to be distinguished from atheroembolic (cholesterol) ARF.
Since the administration of contrast media is predictable, numerous prophylactic strategies have been proposed to prevent ARF. In general, radiologic procedures requiring parenteral contrast media administration should be avoided, especially in “high-risk” patients, when other imaging procedures (ultrasound, MRI, CT without contrast) are able to provide equivalent information. Current evidence suggests that the imaging agent gadolinium used in magnetic resonance imaging is not nephrotoxic. Prophylactic strategies are usually reserved for patients at “high-risk” for contrast ARF (i.e., have renal insufficiency). Hydration with 1/2 normal or normal saline remains the standard for prophylaxis. The optimal volume and duration of hydration have not been definitively determined but most protocols require 8-12 hrs of hydration before and after contrast exposure. The use of low-osmolar contrast media at the smallest possible volume is obviously important. N-acetylcysteine or the selective D-1 dopamine receptor agonist fenoldopam are currently popular prophylactic strategies, but large prospective randomized studies supporting their efficacy are lacking. Mannitol, furosemide and atrial natriuretic peptide appear ineffective.
The nature of the obstructing lesion, the site of the obstruction, the rapidity of onset, and the magnitude of the obstruction are all important determinants of the presentation of postrenal ARF. Since postrenal ARF is often reversible, it is essential that the clinician quickly recognize and correct the cause of obstruction. In addition to a careful history and physical examination and examination of the urinary sediment, renal ultrasound and spiral computed tomography are the diagnostic tools most helpful in detecting obstruction. Because of ‘compensatory’ increases in GFR in the contralateral non-obstructed kidney, unilateral ureteral obstruction does not usually result in a rise in the serum creatinine concentration.
A careful microscopic examination of the urine sediment, quantification of the urine volume, determination of urinary electrolytes, and a variety of radiologic studies are the tools the clinician uses in conjunction with a thorough history and physical examination to determine the cause of ARF in any given patient.
A carefully performed urinalysis is a critical tool in determining the cause of acute renal failure.
RBC casts when present are virtually diagnostic of glomerulonephritis or vasculitis. However, the absence of RBC casts does not exclude glomerulonephritis. In recent years RBC morphology has been used to distinguish the source of hematuria. Dysmorphic RBC strongly suggest glomerular bleeding. Examples of dysmorphism include a’punched-out’ central defect (‘doughnut -like’), diverticular projections from the cell rim (‘blebs’), and partially destroyed and fragmented RBC.
Two examples of red blood cell casts, typical of glomerular bleeding.
Monomorphic (non-dysmorphic) RBC suggest non-glomerular source of bleeding – i.e., bleeding from the calyces, pelvis, ureter(s), bladder, prostate or urethra. Dysmorphic red blood cells suggest glomerular injury.
Dysmorphic red blood cells are best viewed under phase-contrast microscopy (as in this example). Note the ‘blebs’ and punched-out centers (arrows).
Another example of dysmorphic RBC (viewed by scanning electron microscopy).
The presence of WBC alone or in association with WBC casts suggests either allergic interstitial nephritis or acute pyelonephritis. A urine culture can usually differentiate these two possibilities. Eosinophiluria is suggestive of allergic interstitial nephritis.
White bood cells are sometimes called “glitter” cells because of the Brownian motion of the neutrophilic particles.
Note the clear cell outlines and granular cytoplasm.
If the urine demonstrates pigmented granular (“muddy-brown”) casts and/or renal tubular epithelial (RTE) cells in large numbers or in casts, acute tubular necrosis should be strongly considered.
Pigmented granular (“muddy brown”) casts are characteristic of acute tubular necrosis. Although the exact pathogenesis of cast formation is not known, the major component is Tamm-Horsfall glycoprotein, a strongly anionic macromolecule secreted by the ascending thick limb of Henle. Hyaline and waxy casts are also prominent in this particular urinary sediment.
The volume of urine excreted over a 24 hour period is often helpful in narrowing the differential diagnosis of ARF. Anuria is defined by some authors as the virtual absence of urine while others apply the term for daily urine volumes less than 100 ml. Prolonged anuria is uncommon in ATN but sometimes can be seen in the early stages of ATN if hypotension or volume depletion leads to intense salt and water reabsorption.
Oliguria is defined by a urine volume between 100 and 500 ml/24h*. The two most common causes of oliguria in hospitalized patients are prerenal azotemia (ECF volume depletion, for example) and ATN. Non-oliguric ARF (sometimes called “polyuric” ARF) is most commonly due to ATN, but partial urinary outflow obstruction must also be considered. *Normal individuals can concentrate their urine to a maximum of about 1200 mOsm/L. To remain in solute balance on an average diet requires the daily elimination of about 600 mOsm of electrolytes. Thus, under physiologic conditions, the daily solute load could be eliminated in about 500 ml of urine.
Prior to the article by Anderson (reference below), it was believed that most cases of ATN were oliguric. Today, we know that ATN can present with oliguria or non-oliguria and that both presentations are common. Any cause of ATN can present with nonoliguria ; non-oliguria is more likely with nephrotoxic causes of ATN such as aminoglycosides, contrast media, cis-platinum, and amphotericin. The increased incidence of non-oliguric ATN during the past 25 years is most likely due to the increased usage of nephrotoxins, more frequent chemical testing, and more aggressive use of fluids, potent diuretics, and vasodilators in the management of ATN. The reduced mortality of non-oliguric compared to oliguric ATN is probably not because of the increased urine volume but rather due to a lower associated mortality of the conditions causing non-oliguric compared to oliguric ATN. (Data from Anderson et al: Non-oliguric Acute Renal Failure. New Engl J Med 296:134, 1977.)
As discussed, the main differential in the oliguric patient with acute renal failure is between pre-renal azotemia (PR) and acute tubular necrosis (ATN). Although a careful history and physical examination coupled with a careful urinalysis will often distinguish between these two conditions, the use of urinary electrolytes provides further information. The basis of the urinary electrolytes is the different tubular responses to salt and water conservation. Tubular function with pre-renal azotemia is normal allowing maximum tubular sodium and water reabsorption resulting in a concentrated urine that is low in sodium. In acute tubular necrosis, tubular dysfunction leads to sodium wasting and an inability to concentrate the urine. The ratio of urine to plasma creatinine concentrations (U/P) Cr has also been proposed as a discriminating marker. In pre-renal ARF, U Cr is high due to water reabsorption without Cr reabsorption and P Cr is usually only mildly increased resulting in a high (U/P) Cr ratio. In ATN, the U Cr is lower due to an inbility to concentrate the urine and the P Cr is increased in prpoprtion to the degree of renal failure so the U/P cr is generally lower than that seen in pre-renal azotemia. Unfortunately, as shown in the slide, there is considerable overlap (“grey zone”) in all these indices. The so-called “renal failure index” [RFI = U Na /(U/P) Cr ] and the more commonly employed fractional excretion of Na [FE Na = 100(U Na X P Cr ) / (P Na X U Cr )], which combine different “single” indices, provide better discrimination. Recent data have demonstrated that the fractional excretion of sodium (FE Na ) , which expresses the fraction of filtered sodium that escapes reabsorption and eventually appears in the urine, is a more discriminating test to distinguish between pre-renal azotemia and oliguric ATN. FE Na > 1 % strongly suggests ATN while FE Na < 1 % suggests pre-renal azotemia. However, the FE Na is not infallible, and there are a number of exceptions where pre-renal azotemia can be associated with FE Na values greater than 1 % - e.g., recent diuretic use or pre-renal azotemia superimposed on chronic renal insufficiency. In a similar manner, many instances of ATN will have FE Na < 1 % - e.g., early phase of contrast-induced ATN, rhabdomyolysis or septic ATN. Thus, the clinician should utilize the FE Na in conjunction with the overall clinical picture and other lab tests and should not be ‘wedded’ to a particular FE Na result when other data suggest a different cause for ARF.
Intravenous pyelogram showing bilateral hydronephrosis and hydroureter (arrow) due to ureterovesical obstruction. Radiologic studies such as the IVP ( intravenous pyelogram; also called an excretory urogram) or routine CAT scans which require intraveous contrast media are now rarely performed as the initial screening tests to see if post-renal (i.e., obstructive) ARF is present. As discussed earlier, the risk of ATN from contrast media is greatly enhanced in the presence of a reduced GFR, which is the case in patients with ARF. In addition, contrast media is eliminated by glomerular filtration – thus, in the presence of reduced GFR from obstruction, delayed films (several hours) after injection are often required before enough contrast has been filtered and fills the pelvocalyceal system. Current radiologic methods to screen for obstruction use renal ultrasounds or in some cases helical or spiral CAT scans without IV contrast.
The normal kidney is approximately 10 cm in its longitudinal length and 5-6 cm in its transverse diameter. The relatively echo-free renal parenchyma surrounds a central section of tightly compacted echodensities caused by the urothelium of the pelvis and calyces. Hydronephrosis is detected by ultrasonography as an enlarged echo-free area that spreads apart the normal central echodensities. As the obstruction persists and worsens, dilated calyces appear as echo-free fluid pouches extending from the periphery of the expanded echo-free pelvis. In the setting of obstruction, the renal ultrasound has been demonstrated to have a sensitivity of approximately 98% and a specificity of 75%. This high sensitivity makes the renal ultrasound an excellent screening test to look for obstruction. Reasons for false negative exams in addition to performing the study immediately after obstruction include dehydration, extreme obesity, bowel gas or retroperitoneal fibrosis. The lower specificity and higher false positive rate is due to the difficulty in distinguishing a normal extra-renal pelvis from mild hydronephrosis.
This longitudinal ultrasound shows a kidney with moderate hydronephrosis. The dilation of the collecting system extends from the renal pelvis to the calyces. The parenchyma is relatively normal in thickness. Dilatation of the collecting system is detectable by ultrasonography within 24 hrs of urinary outflow obstruction. Thus, it is possible (but very unusual) that patients evaluated within only a couple hours of the onset of obstruction may still have normal renal ultrasounds.
Abdominal CAT scan with contrast demonstrates right hydronephrosis and hydroureter as a consequence of ureteral obstruction. CAT scans can often demonstrate hyodronephrosis even without intravenous contrast. However, CAT scans are much more expensive than renal ultrasounds and should be used for screening purposes only if the renal ultrasound cannot be performed for technical reasons (e.g., extreme obesity).