The document discusses nephrotic syndrome and nephritic syndrome. It covers:
- Mechanisms of glomerular injury including proteinuria, hematuria, loss of filtration function, and hypertension.
- Causes of nephrotic syndrome including minimal change disease, membranous nephropathy, and focal segmental glomerulosclerosis which often involve podocyte dysfunction.
- Causes of nephritic syndrome include inflammatory diseases that break the glomerular basement membrane such as post-streptococcal glomerulonephritis.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be primary, caused by diseases of the kidney itself, or secondary, caused by systemic illnesses that affect the kidneys. The most common primary causes are minimal-change disease in children and membranous glomerulonephritis in adults. Secondary causes include diabetes, lupus, and infections. Treatment involves controlling edema with diuretics, treating underlying conditions, and using steroids, immunosuppressants, or ACE inhibitors depending on disease type and severity.
This document discusses several causes of hematuria in pediatrics including IgA nephropathy, Alport syndrome, acute poststreptococcal glomerulonephritis (APSGN), and hemolytic-uremic syndrome (HUS). IgA nephropathy is the most common chronic glomerular disease in children characterized by IgA deposits in the glomeruli. Alport syndrome is a hereditary nephritis caused by mutations in type IV collagen genes. APSGN occurs 1-2 weeks after a streptococcal infection and presents with gross hematuria, edema, and renal impairment. HUS is characterized by microangiopathic hemolytic anemia, thrombocytopenia,
Minimal change nephropathy and primary focal segmental glomerulosclerosis (FSGS) represent opposite ends of a spectrum of idiopathic nephrotic syndrome. Minimal change disease often responds well to corticosteroids, while FSGS typically shows little response and often progresses to renal failure. Membranous nephropathy is the most common cause of nephrotic syndrome in adults, with one-third of cases remitting spontaneously, one-third remaining nephrotic, and one-third progressing to renal failure. IgA nephropathy is the most common type of glomerulonephritis and can cause hematuria, proteinuria, hypertension, and end-
1. Acute post-streptococcal glomerulonephritis (APSGN) is a type of acute nephritic syndrome that occurs after a streptococcal infection.
2. It is characterized by edema, hematuria, proteinuria, and decreased kidney function.
3. The infection triggers an immune response where antibodies form complexes that deposit along the glomerular basement membrane, causing inflammation and kidney damage.
Nephrotic syndrome is defined by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is caused by damage to the glomerular basement membrane that increases pore size and protein leakage. Loss of protein like albumin leads to edema as serum oncotic pressure decreases. Steroids are first line treatment but some patients are steroid resistant. Kidney biopsy guides treatment, which may include immunosuppressants for steroid resistant forms. Complications include infection, hypercoagulability, and renal failure.
1) Glomerular diseases involve either nephrotic syndrome characterized by massive proteinuria or nephritic syndrome characterized by hematuria and inflammation.
2) Workup includes labs, urinalysis, protein quantification, serologies, and often kidney biopsy.
3) Common causes discussed include minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, acute poststreptococcal glomerulonephritis, and membranoproliferative glomerulonephritis.
Nephrotic syndrome is a kidney disorder characterized by protein in the urine, low albumin levels, edema, and high cholesterol. It can be caused by primary kidney diseases or secondary to other systemic illnesses. The main primary causes are minimal-change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Treatment involves corticosteroids, diuretics, ACE inhibitors, and managing symptoms and complications like infection and hyperlipidemia. Long-term monitoring is also important.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be primary, caused by diseases of the kidney itself, or secondary, caused by systemic illnesses that affect the kidneys. The most common primary causes are minimal-change disease in children and membranous glomerulonephritis in adults. Secondary causes include diabetes, lupus, and infections. Treatment involves controlling edema with diuretics, treating underlying conditions, and using steroids, immunosuppressants, or ACE inhibitors depending on disease type and severity.
This document discusses several causes of hematuria in pediatrics including IgA nephropathy, Alport syndrome, acute poststreptococcal glomerulonephritis (APSGN), and hemolytic-uremic syndrome (HUS). IgA nephropathy is the most common chronic glomerular disease in children characterized by IgA deposits in the glomeruli. Alport syndrome is a hereditary nephritis caused by mutations in type IV collagen genes. APSGN occurs 1-2 weeks after a streptococcal infection and presents with gross hematuria, edema, and renal impairment. HUS is characterized by microangiopathic hemolytic anemia, thrombocytopenia,
Minimal change nephropathy and primary focal segmental glomerulosclerosis (FSGS) represent opposite ends of a spectrum of idiopathic nephrotic syndrome. Minimal change disease often responds well to corticosteroids, while FSGS typically shows little response and often progresses to renal failure. Membranous nephropathy is the most common cause of nephrotic syndrome in adults, with one-third of cases remitting spontaneously, one-third remaining nephrotic, and one-third progressing to renal failure. IgA nephropathy is the most common type of glomerulonephritis and can cause hematuria, proteinuria, hypertension, and end-
1. Acute post-streptococcal glomerulonephritis (APSGN) is a type of acute nephritic syndrome that occurs after a streptococcal infection.
2. It is characterized by edema, hematuria, proteinuria, and decreased kidney function.
3. The infection triggers an immune response where antibodies form complexes that deposit along the glomerular basement membrane, causing inflammation and kidney damage.
Nephrotic syndrome is defined by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is caused by damage to the glomerular basement membrane that increases pore size and protein leakage. Loss of protein like albumin leads to edema as serum oncotic pressure decreases. Steroids are first line treatment but some patients are steroid resistant. Kidney biopsy guides treatment, which may include immunosuppressants for steroid resistant forms. Complications include infection, hypercoagulability, and renal failure.
1) Glomerular diseases involve either nephrotic syndrome characterized by massive proteinuria or nephritic syndrome characterized by hematuria and inflammation.
2) Workup includes labs, urinalysis, protein quantification, serologies, and often kidney biopsy.
3) Common causes discussed include minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, acute poststreptococcal glomerulonephritis, and membranoproliferative glomerulonephritis.
Nephrotic syndrome is a kidney disorder characterized by protein in the urine, low albumin levels, edema, and high cholesterol. It can be caused by primary kidney diseases or secondary to other systemic illnesses. The main primary causes are minimal-change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Treatment involves corticosteroids, diuretics, ACE inhibitors, and managing symptoms and complications like infection and hyperlipidemia. Long-term monitoring is also important.
Acute Poststreptococcal Glomerulonephritis (APSGN) is caused by certain strains of Group A streptococci that infect the throat or skin. It presents with hematuria, edema, hypertension, and sometimes acute renal failure. The kidneys show enlarged glomeruli with immune complex deposition on the glomerular basement membrane. Treatment focuses on supportive care with bed rest, salt restriction, diuretics for hypertension or edema, and antibiotics to limit spread of infection. The condition usually resolves spontaneously within a few weeks.
This document provides information on nephrotic syndrome, including its epidemiology, classification, diagnosis, and treatments. It defines nephrotic syndrome as a condition where the kidneys leak large amounts of protein into the urine. The document discusses primary and secondary causes of nephrotic syndrome such as minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and diabetic nephropathy. Diagnosis involves urine tests and potentially a renal biopsy. Treatments focus on managing the underlying cause, reducing proteinuria and edema, and treating complications like hyperlipidemia.
Glomerulonephritis is characterized by inflammation of the glomerulus and small blood vessels of the kidney. It can be caused by various primary kidney diseases or systemic diseases. The main types are focal, diffuse, and segmental, depending on the glomerular involvement. Glomerulonephritis results in injury to the glomerular filtration barrier, increasing permeability and leading to loss of proteins in the urine. Presenting symptoms include edema, hypertension, hematuria, and renal impairment. Kidney biopsy is important for diagnosis and treatment planning. Management involves controlling symptoms, treating the underlying cause, and immunosuppression in some cases.
The document discusses proteinuria and hematuria in children. It covers the definition, causes, evaluation, and treatment of both conditions. Proteinuria can be caused by glomerular, tubular, or overflow mechanisms and is evaluated through urine dipsticks, 24-hour urine collection, and urine protein to creatinine ratio. Hematuria can be gross or microscopic and is seen in conditions like UTI, nephrolithiasis, glomerulonephritis, IgA nephropathy, and Alport syndrome. Evaluation of hematuria involves urinalysis, urine culture, imaging, and considering familial causes. Specific renal diseases like post-streptococcal glomerulonephritis
Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, hyperlipidemia, and edema. It results from increased permeability of the glomerular basement membrane. The majority of cases are primary or idiopathic nephrotic syndrome. Treatment involves corticosteroids, diet modifications to reduce proteinuria, and managing complications such as edema and infection risk. Nursing care focuses on fluid balance, nutrition, infection prevention, and family education and support.
This document provides an overview of hematuria and glomerular causes of hematuria. It defines macroscopic and microscopic hematuria and discusses various glomerular diseases that can cause hematuria including IgA nephropathy, Alport syndrome, thin basement membrane disease, post-infectious glomerulonephritis, and Henoch–Schönlein purpura. It describes the clinical presentations, pathologies, diagnoses, and treatments of these conditions. Key investigations for glomerular hematuria are outlined.
Glomerular diseases account for a significant proportion of acute and chronic kidney disease and can have various causes including immune system problems, inherited conditions, and protein deposition in the glomeruli. The response of the glomerulus depends on the type of injury and may cause blood or protein in the urine, as well as high blood pressure or impaired kidney function. Diagnosis involves urine and blood tests to examine for blood, protein, and kidney function. Common glomerular diseases include minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy.
Based on the information provided, the most likely diagnosis is idiopathic nephrotic syndrome. Some key points:
- The child is 5 years old, which is a common age for nephrotic syndrome to present.
- There is generalized body swelling (edema), hypoalbuminemia (serum albumin 17), heavy proteinuria (4+ on urine dipstick), and hyperlipidemia (cholesterol 12), meeting the criteria for nephrotic syndrome.
- No obvious underlying cause is identified, so it is likely primary/idiopathic in nature.
The main possible etiologies/causes of nephrotic syndrome include minimal change disease, focal segment
Glomerulonephritis is inflammation of the glomeruli in the kidneys. It can be acute or chronic. Acute glomerulonephritis usually develops after a streptococcal infection and causes rapid damage to the glomeruli, reducing kidney function. Chronic glomerulonephritis develops gradually over years and can lead to irreversible kidney damage and failure if left untreated. The document discusses the causes, pathophysiology, clinical manifestations, diagnosis, and management of both acute and chronic glomerulonephritis.
2. Glomerulonephritis & hypertension in children 01.04.15 lecture.pptxIvwananjisikombe1
Acute glomerulonephritis (AGN) is characterized by edema, hematuria, proteinuria, and hypertension resulting from inflammation of the glomeruli. It is commonly caused by a prior streptococcal infection. The inflammation damages renal tissue through immune complex deposition and cellular proliferation. Treatment focuses on controlling blood pressure and fluid balance. Medical management includes diuretics, ACE inhibitors, calcium channel blockers, and other antihypertensives. Outcomes are generally good if the inflammatory process is self-limited, but progressive kidney damage can occur if inflammation persists long-term.
This document discusses generalized edema, proteinuria, nephrotic syndrome, and nephritic syndrome. It defines the conditions and describes their signs, symptoms, causes, investigations, treatment, prognosis, and complications. Nephrotic syndrome is characterized by heavy proteinuria, low serum albumin, edema, and high cholesterol. The most common cause is minimal change disease. Nephritic syndrome indicates glomerular inflammation with hematuria, hypertension, edema and mild proteinuria. Common causes include post-streptococcal glomerulonephritis and IgA nephropathy. Corticosteroids are first-line treatment for nephrotic syndrome while nephritic syndrome is usually managed supportively.
1. Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Common causes include minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy.
2. Patients with nephrotic syndrome are at increased risk of thromboembolic complications such as deep vein thrombosis and pulmonary embolism due to hypercoagulability. They also face higher risks of acute kidney injury, infections, anemia, and protein malnutrition.
3. Prophylactic anticoagulation is often used to prevent thromboembolic events, with treatment choices dependent on albumin levels and bleeding risk. Managing underlying infections
This document provides information about nephrotic syndrome including its definition, causes, signs and symptoms, investigations, management, and complications. Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be caused by primary/idiopathic conditions like minimal change disease or secondary causes such as SLE, diabetes, or drugs. Management involves dietary modifications, diuretics, steroid therapy, and immunosuppressive drugs depending on disease severity and response to treatment. Complications include thrombosis, peritonitis, and hypovolemia which require prompt intervention.
This document provides information on rapidly progressive renal failure (RPRF), including its definition, causes, investigations, diagnosis, and treatment. Key points:
- RPRF is characterized by progressive renal failure over weeks that is not due to acute kidney injury or chronic kidney disease. The kidney biopsy often shows lesions in the glomerular, tubulointerstitial, or vascular compartments.
- Common causes of RPRF include crescentic glomerulonephritis (seen in 54% of cases), acute interstitial nephritis (18%), and IgA nephropathy (15%).
- Diagnosis involves ruling out other causes through history, physical exam, labs, and
A 7-year-old boy was admitted with facial puffiness, passing smoky urine, and decreased urine output for 1 week. Examination showed pallor, high blood pressure, and a skin lesion on his elbow. Tests found protein and red blood cells in his urine, and raised blood urea. An ultrasound showed enlarged pale kidneys. The document discusses nephrotic syndrome, including its definition, causes, presentation, diagnosis, management, and nursing care. Nephrotic syndrome results from kidney damage that allows protein to leak into the urine, lowering blood protein levels and causing edema. Management focuses on fluid control, diuretics, ACE inhibitors, and sometimes steroids to preserve kidney function.
Primary glomerular diseases include various forms of glomerulonephritis and nephrotic syndrome. Acute glomerulonephritis is defined by the sudden onset of hematuria, proteinuria, and red blood cell casts. It is caused by an immunological reaction, often due to a streptococcal infection, that results in inflammation and proliferation in the glomerulus. Symptoms include edema, hypertension, and decreased kidney function. Treatment involves a low sodium diet, fluid restriction, antibiotics, corticosteroids, diuretics, and dialysis if needed. With treatment, most cases of acute glomerulonephritis resolve though some may progress to chronic kidney disease.
Nephrotic syndrome affects 1-3 per 100,000 children below age 16. It is most commonly caused by minimal change disease in children, responding to corticosteroid therapy in 80% of cases. A kidney biopsy is generally not required initially as most children will respond to corticosteroids. For steroid-sensitive nephrotic syndrome, treatment involves prednisone for 12 weeks including 4-6 weeks daily followed by alternate-day dosing for 2-5 months. Frequently relapsing or steroid-dependent cases may be treated with corticosteroid-sparing agents such as cyclophosphamide, levamisole, or calcineurin inhibitors.
The document discusses nephritic syndrome and its causes. It provides details on:
1. Acute post-streptococcal glomerulonephritis (APSGN), a classical illness resulting from prior streptococcal infection that presents with hematuria, edema, and hypertension.
2. Hemolytic uremic syndrome (HUS), mostly affecting children under 4, that follows gastroenteritis and presents with anemia, hematuria, edema, oliguria, and hypertension.
3. Differentiating features between nephrotic and nephritic syndrome based on onset, edema, blood pressure, proteinuria, and hematuria.
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.
Acute Poststreptococcal Glomerulonephritis (APSGN) is caused by certain strains of Group A streptococci that infect the throat or skin. It presents with hematuria, edema, hypertension, and sometimes acute renal failure. The kidneys show enlarged glomeruli with immune complex deposition on the glomerular basement membrane. Treatment focuses on supportive care with bed rest, salt restriction, diuretics for hypertension or edema, and antibiotics to limit spread of infection. The condition usually resolves spontaneously within a few weeks.
This document provides information on nephrotic syndrome, including its epidemiology, classification, diagnosis, and treatments. It defines nephrotic syndrome as a condition where the kidneys leak large amounts of protein into the urine. The document discusses primary and secondary causes of nephrotic syndrome such as minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and diabetic nephropathy. Diagnosis involves urine tests and potentially a renal biopsy. Treatments focus on managing the underlying cause, reducing proteinuria and edema, and treating complications like hyperlipidemia.
Glomerulonephritis is characterized by inflammation of the glomerulus and small blood vessels of the kidney. It can be caused by various primary kidney diseases or systemic diseases. The main types are focal, diffuse, and segmental, depending on the glomerular involvement. Glomerulonephritis results in injury to the glomerular filtration barrier, increasing permeability and leading to loss of proteins in the urine. Presenting symptoms include edema, hypertension, hematuria, and renal impairment. Kidney biopsy is important for diagnosis and treatment planning. Management involves controlling symptoms, treating the underlying cause, and immunosuppression in some cases.
The document discusses proteinuria and hematuria in children. It covers the definition, causes, evaluation, and treatment of both conditions. Proteinuria can be caused by glomerular, tubular, or overflow mechanisms and is evaluated through urine dipsticks, 24-hour urine collection, and urine protein to creatinine ratio. Hematuria can be gross or microscopic and is seen in conditions like UTI, nephrolithiasis, glomerulonephritis, IgA nephropathy, and Alport syndrome. Evaluation of hematuria involves urinalysis, urine culture, imaging, and considering familial causes. Specific renal diseases like post-streptococcal glomerulonephritis
Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, hyperlipidemia, and edema. It results from increased permeability of the glomerular basement membrane. The majority of cases are primary or idiopathic nephrotic syndrome. Treatment involves corticosteroids, diet modifications to reduce proteinuria, and managing complications such as edema and infection risk. Nursing care focuses on fluid balance, nutrition, infection prevention, and family education and support.
This document provides an overview of hematuria and glomerular causes of hematuria. It defines macroscopic and microscopic hematuria and discusses various glomerular diseases that can cause hematuria including IgA nephropathy, Alport syndrome, thin basement membrane disease, post-infectious glomerulonephritis, and Henoch–Schönlein purpura. It describes the clinical presentations, pathologies, diagnoses, and treatments of these conditions. Key investigations for glomerular hematuria are outlined.
Glomerular diseases account for a significant proportion of acute and chronic kidney disease and can have various causes including immune system problems, inherited conditions, and protein deposition in the glomeruli. The response of the glomerulus depends on the type of injury and may cause blood or protein in the urine, as well as high blood pressure or impaired kidney function. Diagnosis involves urine and blood tests to examine for blood, protein, and kidney function. Common glomerular diseases include minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy.
Based on the information provided, the most likely diagnosis is idiopathic nephrotic syndrome. Some key points:
- The child is 5 years old, which is a common age for nephrotic syndrome to present.
- There is generalized body swelling (edema), hypoalbuminemia (serum albumin 17), heavy proteinuria (4+ on urine dipstick), and hyperlipidemia (cholesterol 12), meeting the criteria for nephrotic syndrome.
- No obvious underlying cause is identified, so it is likely primary/idiopathic in nature.
The main possible etiologies/causes of nephrotic syndrome include minimal change disease, focal segment
Glomerulonephritis is inflammation of the glomeruli in the kidneys. It can be acute or chronic. Acute glomerulonephritis usually develops after a streptococcal infection and causes rapid damage to the glomeruli, reducing kidney function. Chronic glomerulonephritis develops gradually over years and can lead to irreversible kidney damage and failure if left untreated. The document discusses the causes, pathophysiology, clinical manifestations, diagnosis, and management of both acute and chronic glomerulonephritis.
2. Glomerulonephritis & hypertension in children 01.04.15 lecture.pptxIvwananjisikombe1
Acute glomerulonephritis (AGN) is characterized by edema, hematuria, proteinuria, and hypertension resulting from inflammation of the glomeruli. It is commonly caused by a prior streptococcal infection. The inflammation damages renal tissue through immune complex deposition and cellular proliferation. Treatment focuses on controlling blood pressure and fluid balance. Medical management includes diuretics, ACE inhibitors, calcium channel blockers, and other antihypertensives. Outcomes are generally good if the inflammatory process is self-limited, but progressive kidney damage can occur if inflammation persists long-term.
This document discusses generalized edema, proteinuria, nephrotic syndrome, and nephritic syndrome. It defines the conditions and describes their signs, symptoms, causes, investigations, treatment, prognosis, and complications. Nephrotic syndrome is characterized by heavy proteinuria, low serum albumin, edema, and high cholesterol. The most common cause is minimal change disease. Nephritic syndrome indicates glomerular inflammation with hematuria, hypertension, edema and mild proteinuria. Common causes include post-streptococcal glomerulonephritis and IgA nephropathy. Corticosteroids are first-line treatment for nephrotic syndrome while nephritic syndrome is usually managed supportively.
1. Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Common causes include minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy.
2. Patients with nephrotic syndrome are at increased risk of thromboembolic complications such as deep vein thrombosis and pulmonary embolism due to hypercoagulability. They also face higher risks of acute kidney injury, infections, anemia, and protein malnutrition.
3. Prophylactic anticoagulation is often used to prevent thromboembolic events, with treatment choices dependent on albumin levels and bleeding risk. Managing underlying infections
This document provides information about nephrotic syndrome including its definition, causes, signs and symptoms, investigations, management, and complications. Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be caused by primary/idiopathic conditions like minimal change disease or secondary causes such as SLE, diabetes, or drugs. Management involves dietary modifications, diuretics, steroid therapy, and immunosuppressive drugs depending on disease severity and response to treatment. Complications include thrombosis, peritonitis, and hypovolemia which require prompt intervention.
This document provides information on rapidly progressive renal failure (RPRF), including its definition, causes, investigations, diagnosis, and treatment. Key points:
- RPRF is characterized by progressive renal failure over weeks that is not due to acute kidney injury or chronic kidney disease. The kidney biopsy often shows lesions in the glomerular, tubulointerstitial, or vascular compartments.
- Common causes of RPRF include crescentic glomerulonephritis (seen in 54% of cases), acute interstitial nephritis (18%), and IgA nephropathy (15%).
- Diagnosis involves ruling out other causes through history, physical exam, labs, and
A 7-year-old boy was admitted with facial puffiness, passing smoky urine, and decreased urine output for 1 week. Examination showed pallor, high blood pressure, and a skin lesion on his elbow. Tests found protein and red blood cells in his urine, and raised blood urea. An ultrasound showed enlarged pale kidneys. The document discusses nephrotic syndrome, including its definition, causes, presentation, diagnosis, management, and nursing care. Nephrotic syndrome results from kidney damage that allows protein to leak into the urine, lowering blood protein levels and causing edema. Management focuses on fluid control, diuretics, ACE inhibitors, and sometimes steroids to preserve kidney function.
Primary glomerular diseases include various forms of glomerulonephritis and nephrotic syndrome. Acute glomerulonephritis is defined by the sudden onset of hematuria, proteinuria, and red blood cell casts. It is caused by an immunological reaction, often due to a streptococcal infection, that results in inflammation and proliferation in the glomerulus. Symptoms include edema, hypertension, and decreased kidney function. Treatment involves a low sodium diet, fluid restriction, antibiotics, corticosteroids, diuretics, and dialysis if needed. With treatment, most cases of acute glomerulonephritis resolve though some may progress to chronic kidney disease.
Nephrotic syndrome affects 1-3 per 100,000 children below age 16. It is most commonly caused by minimal change disease in children, responding to corticosteroid therapy in 80% of cases. A kidney biopsy is generally not required initially as most children will respond to corticosteroids. For steroid-sensitive nephrotic syndrome, treatment involves prednisone for 12 weeks including 4-6 weeks daily followed by alternate-day dosing for 2-5 months. Frequently relapsing or steroid-dependent cases may be treated with corticosteroid-sparing agents such as cyclophosphamide, levamisole, or calcineurin inhibitors.
The document discusses nephritic syndrome and its causes. It provides details on:
1. Acute post-streptococcal glomerulonephritis (APSGN), a classical illness resulting from prior streptococcal infection that presents with hematuria, edema, and hypertension.
2. Hemolytic uremic syndrome (HUS), mostly affecting children under 4, that follows gastroenteritis and presents with anemia, hematuria, edema, oliguria, and hypertension.
3. Differentiating features between nephrotic and nephritic syndrome based on onset, edema, blood pressure, proteinuria, and hematuria.
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.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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 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.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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4. Responses of glomerulus to injury
.
◦ It can leak protein
◦ It can leak blood
◦ It can lose filtration function
◦ It can cause hypertension
Diseases that cause haematuria cause proteinuria if
they leave scarring or progress.
5. Proteinuric diseases
Historically termed ‘nephrosis’
◦ Subtle abnormalities in podocytes
◦ Abnormal glomerular matrix, including the scarring laid down by
inflammatory diseases
6. Diseases that cause proteinuria
Podocyte is central to proteinuria.
◦ Minimal change disease —podocyte dysfunction
◦ Membranous nephropathy—podocyte attack by autoantibodies
◦ Focal segmental glomerulosclerosis —podocyte injury or death
Most of the genetic causes of nephrotic syndrome, almost all involve
podocyte genes
The major metabolic and systemic diseases causing nephrotic syndrome
disturb the function of these highly specialized, highly differentiated cell
7. Haematuric diseases
Breaks in the GBM
◦ Characterized by inflammatory disruption of the glomerular basement
membrane (GBM) (‘nephritis’)
◦ Fragile GBM without inflammation
8. Chapter: Mechanisms of glomerular injuryoverview Author(s): Neil Turner From: Oxford Textbook of Clinical Nephrology
9.
10. Progressive renal disease after glomerular injury
◦ Haemodynamic—increased glomerular perfusion pressure or stretches
Podocyte—podocyte stress and death
◦ Toxicity of proteinuria—proteinuria creates progression by its effects on
the tubulointerstitium
◦ Disordered repair and replacement of cells
11. Nephrotic syndrome
Characterized by
◦ A urine protein excretion of greater than 3500 mg per 24 hours or, iurine
protein-to-creatinine ratio is greater than 3000 mg/g in an adult
◦ Hypoalbuminemia, usually less than 3.5 g/dL
◦ Edema (peripheral or periorbital, occasionally ascites or pleural
effusions)
◦ Hyperlipidemia
◦ Lipiduria
12. Presentation
◦ Edema is the most common presenting feature
◦ Features of complication:
• infections like spontaneous peritonitis in children with ascites
• venous thrombosis or thromboembolism
• manifestations of hyperlipidemia
13. Nephrotic edema
In adults, retention of up to 4 L of salt and water remains undetectable
◦ around the eyes in the morning
◦ around the ankles in the evening
The five characteristics of nephrotic edema
◦ gradually increasing
◦ gravitational
◦ generalized
◦ pitting
◦ softness
18. Evaluation of nephrotic syndrome
Kidney biopsy
Kidney biopsy may be deferred in certain patients:
◦ If there is an obvious etiology
◦ If amyloidosis is suspected in a patient with a monoclonal gammopathy
◦ If the patient with nephrotic syndrome has a positive anti-phospholipase A2
receptor (anti-PLA2R) autoantibody
◦ If a biopsy cannot be performed or is refused (later stages of pregnancy )
◦ If ages of 1 and 10 years, with normal renal function, normal complement levels
without hypertension or haematuria
◦ Frail elderly or others with severe comorbid conditions where a pathological
diagnosis is very unlikely to alter best management.
19. Evaluation of nephrotic syndrome
Laboratory tests
◦ Glycated hemoglobin (HbA1C, to diagnose diabetes)
◦ Antinuclear antibody and anti-double stranded DNA (dsDNA) antibody
◦ Anti-PLA2R autoantibody
◦ In patients older than 50 years – serum free light chains and serum protein
immunofixation
◦ Tests for hepatitis B and C viruses and the human immunodeficiency virus
◦ Serum C3 and C4 complement levels
Other serologic, microbiological, and genetic tests are sometimes performed in
patients once a specific histologic diagnosis is established.
20. Causes of nephrotic
Syndrome
In US adult
Primary nephrotic syndrome
◦ FSGS (35%)
◦ Membranous GN(33%)
◦ Minimal change disease (15%)
◦ Membranoproliferative GN (14%).
Secondary nephrotic syndrome
◦ Diabetes
◦ Lupus
◦ Amyloid
21. Management
Conservative
◦ Monitor U&E, BP, fluid balance, weight
◦ Salt and fluid restriction
◦ Avoid high protein diet
Medical
◦ Diuretics
◦ ACE-inhibitors/ARBs
◦ Lipid lowering agents
◦ Corticosteroids/immunosuppression
◦ Dialysis
◦ Anticoagulation
Nephrectomy
o Chemical
o Embolization
o Surgical
22. Management
Salt restriction
oBelow 50-70 mmol/day (about 4 g)
oPatients are advised to avoid salty food, use no added salt
Protein restriction
o0.8 g of protein of high biological value/kg/24 hours, plus 1 g protein per
gram of proteinuria
Diuretics
o 2-3 L of fluid loss per day for short periods
Anticoagulation
o Membranous nephropathy, albumin < 20gm/L
23. Complications
Increased susceptibility to infection
o Due to reduced serum IgG, reduced complement activity,
reduced T cell function
o Immunization against pneumococci
o Varicella/chicken pox prophylaxis for non immune contact
o Prompt discontinuation of cytotoxic therapy
Thromboembolism
Hyperlipidaemia
AKI
25. Nephritic syndrome
Caused by glomerular inflammation
oOliguria
oHematuria
oHypertension
oVariable degrees of proteinuria
oLeukocyturia
oRenal insufficiency
oInvolvement of other organ
systems
• Pulmonary hemorrhage
• Palpable purpura
• Arthritis
28. Evaluation
Renal Biopsy
Laboratory tests
◦ Serum C3 and C4 complement levels
◦ Antineutrophil cytoplasmic autoantibodies
◦ Anti-glomerular basement membrane (GBM) autoantibodies
◦ Antinuclear antibodies
◦ Anti-dsDNA antibodies
◦ Serology for hepatitis C virus, hepatitis B virus, and HIV
◦ Serum free light chains and serum immunofixation
29. Evaluation
Other laboratory tests based on clinical context or biopsy findings
A cryocrit
oIf there are features of cryoglobulinemia or a known history of hepatitis C
virus infection.
Blood cultures
oIF persistent fever or other signs of chronic infection
30. Differential diagnosis
Based on serum complement levels
Complement levels are normal
◦ Anti-GBM disease
◦ Pauci-immune glomerulonephritis
Complement levels are typically low
◦ Immune complex-mediated glomerulonephritis (except IgA nephropathy)
◦ PSGN low C3
◦ Dense deposit disease low C3
◦ SLE both C3, C4 low
31. Differential diagnosis
Based on clinical findings
Gross hematuria with upper respiratory infection
oLatent period 7 to 10 days
o Poststreptococcal glomerulonephritis (especially in children)
oConcurrently ("synpharyngitic glomerulonephritis")
o IgA nephropathy.
32. Differential diagnosis
Based on clinical findings
oThe presence of palpable purpura or a petechial rash
oVasculitis
oThe presence of renal failure and pulmonary hemorrhage
oVasculitis
oIn patients with an acute presentation of microangiopathic hemolytic
anemia, thrombocytopenia, and kidney failure
oThrombotic microangiopathy (TMA)
33. Post-streptococcal glomerulonephritis
A complication of Streptococcal infections that is responsible for classic
acute nephritic syndrome, mostly seen in children
oAcute nephritis associated with
oEdema
oHypertension and
oHematuria
oSerum C3 levels are characteristically very low
oRBC cast in urine RME
34. In temperate climates
◦ Pharyngitis and tonsillitis are the usual sites of antecedent infection In the
winter and the spring
In the tropics
◦ Impetigo is more frequent in the summer months
The latent period
◦ Throat infections (about 2weeks)
◦ After pyodermitis (several weeks)
35. Clinical manifestations of
acute PSGN
The clinical features of
PSGN are different in
adults and in children
Male: Female ratio 2:1
Typical age 4–14 years
36. Clinical manifestations of acute PSGN
Typical presentation
◦ Hematuria
◦ Edema
◦ Hypertension
◦ Oliguria
At least two of these manifestations are present in almost all patients
The full clinical picture in about 40% of the patients
37. oImprovement is observed within 2 to 7 days with increasing urine volume
resolution of edema and return of the blood pressure to normal levels
oSerum complement returns to normal usually within 1 month in patients
with uncomplicated PSGN.
oGross hematuria is present in one-third of the patients. Microscopic
hematuria usually persists for many months. Disappears usually within 1
year and always within 4 years in children
39. Evaluation
Lab test
o Urine RME: RBC cast
o High ASO titer in 70% to 80% of throat infection
o High anti-DNAse B titers in about 70% of the cases with pyodermitis
o The streptozyme test, (DNAse B, Streptolysin O, hyaluronidase and
streptokinase) elevated in nearly 80% of the cases
o Serum C3 low, C4 minimally low or normal
40. Evaluation
Lab test
o Serum IgG and IgM are elevated in 80% of the cases
o Serum IgA level is normal
o Cryoglobulins, elevated rheumatoid factor, and anti-C1q antibodies are
present in up to one-third of patients
o Rarely low titters of anti-DNA and ANCA
41.
42. Renal Biopsy
Indication of renal biopsy In children
oNephrotic range proteinuria
oProgressive azotaemia suggesting crescentic GN
oIf serum complement levels not depressed in the acute phase
oIf serum complement levels remain reduced for > 1 month
In adult patients, kidney biopsy is the norm
43.
44.
45. Management
◦ Hospitalization if symptomatic
◦ Salt water restriction
◦ Loop diuretics
◦ Treatment of the infection if still present
◦ Prophylactic antibiotic treatment for household members of index cases
◦ Antihypertensive agents
◦ Management of hyperkalemia
◦ Severe cases may require dialysis
High-dose corticosteroids have often been given in severe crescentic
disease, but there is no evidence that they are effective
46. Prognosis
In children
oRecovery of renal function is often excellent
oThough long-term studies now suggest that it may represent a risk factor
for the development of chronic kidney disease.
In older patients with comorbid conditions and atypical presentations
oResolution may be less complete than in children
47. Prognosis
◦ The early mortality is very low in children but significant in adults
◦ Cardiovascular complications are the main cause of death in acute PSGN
◦ Irreversible renal failure may follow acute GN if widespread extra capillary
(crescentic) proliferation develops
◦ Associations of PSGN with positive ANCA or haemolytic uremic syndrome
carry a worse prognosis
◦ The incidence of abnormal laboratory findings during the follow-up varies
from 3.5% to 60%
◦ Subgroup of adult patients with massive proteinuria as the initial
manifestation had an incidence of chronic renal failure as high as 77%
50. syndrome in elderly patients.
Chapter: Nephrotic syndrome Author(s): Premil Rajakrishna, Stewart Cameron, and Neil Turner From: Oxford Textbook of Clinical Nephrology