This document provides information on various types of primary glomerulonephritis (GN), including acute post-streptococcal GN, rapidly progressive GN, minimal change disease, membranous GN, and membranoproliferative GN. It describes the etiology, pathogenesis, clinical features, laboratory findings, and histopathology of each type of GN. Key details on each type are presented, along with diagrams to illustrate glomerular abnormalities.
This document provides information on various glomerular diseases. It begins by defining glomerulonephritis as inflammation of the glomeruli. The main types of primary glomerular diseases discussed include minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy. For each disease, the document covers pathogenesis, morphology, and clinical manifestations. It provides detailed descriptions of the histologic alterations and immune mechanisms involved in the different glomerular diseases.
Glomerular disease is a group of diseases that affect the glomeruli in an inflammatory manner. They can be primary, arising from issues in the glomeruli themselves, or secondary, arising from other systemic diseases. Primary glomerular diseases include minimal change disease, membranous glomerulonephritis, and IgA nephropathy. Secondary glomerular diseases are often caused by systemic lupus erythematosus, diabetes, or amyloidosis. Glomerular diseases can present as nephrotic syndrome, with heavy proteinuria and edema, or nephritic syndrome, with hematuria and reduced kidney function. Rapidly progressive glomerulonephritis is characterized by a severe loss
This document discusses acute nephritic syndrome, specifically acute post-streptococcal glomerulonephritis (PSGN). It notes that PSGN classically presents after a streptococcal throat or skin infection with hematuria, proteinuria, hypertension, and edema. Investigations may show elevated anti-streptococcal antibodies. On biopsy, there is diffuse mesangial proliferation with immune complex deposition. Management involves controlling symptoms while the infection resolves spontaneously in 6-8 weeks. Complications include hypertension, renal failure, and rarely chronic kidney disease.
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
most of the glomerular diseases , either primary or secondary..touching all the aspects including light microscopy, electron microscopy and immunoflourescence.
1) Nephritic Syndrome (ANS) can be classified clinically, biochemically, or histopathologically. It includes conditions like glomerulonephritis that cause hematuria and proteinuria but not edema.
2) Case studies are presented to demonstrate various etiologies of ANS, including primary membranoproliferative glomerulonephritis (MPGN) type 1 and secondary lupus nephritis.
3) Causes of ANS include primary glomerular diseases like MPGN type 1 as well as secondary glomerular diseases associated with conditions like SLE, hepatitis B/C, and ANCA-associated vasculitis. A thorough evaluation is needed to determine
The KIDNEY - PATHOGENESIS OF GLOMERULAR DISEASESDr. Roopam Jain
The document discusses glomerular diseases, which involve the renal glomeruli. It describes the classification of glomerular diseases into primary and secondary types. The major clinical manifestations are proteinuria, hematuria, hypertension, and impaired renal function. Six major glomerular syndromes are discussed: acute nephritic syndrome, nephrotic syndrome, acute renal failure, chronic renal failure, asymptomatic proteinuria, and asymptomatic hematuria. The pathogenesis of glomerular injury is examined by exploring the roles of endothelial, mesangial, epithelial and parietal cells as well as the glomerular basement membrane. Immunological and non-immunological mechanisms are involved in glomerular disease pathogenesis.
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 provides information on various glomerular diseases. It begins by defining glomerulonephritis as inflammation of the glomeruli. The main types of primary glomerular diseases discussed include minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy. For each disease, the document covers pathogenesis, morphology, and clinical manifestations. It provides detailed descriptions of the histologic alterations and immune mechanisms involved in the different glomerular diseases.
Glomerular disease is a group of diseases that affect the glomeruli in an inflammatory manner. They can be primary, arising from issues in the glomeruli themselves, or secondary, arising from other systemic diseases. Primary glomerular diseases include minimal change disease, membranous glomerulonephritis, and IgA nephropathy. Secondary glomerular diseases are often caused by systemic lupus erythematosus, diabetes, or amyloidosis. Glomerular diseases can present as nephrotic syndrome, with heavy proteinuria and edema, or nephritic syndrome, with hematuria and reduced kidney function. Rapidly progressive glomerulonephritis is characterized by a severe loss
This document discusses acute nephritic syndrome, specifically acute post-streptococcal glomerulonephritis (PSGN). It notes that PSGN classically presents after a streptococcal throat or skin infection with hematuria, proteinuria, hypertension, and edema. Investigations may show elevated anti-streptococcal antibodies. On biopsy, there is diffuse mesangial proliferation with immune complex deposition. Management involves controlling symptoms while the infection resolves spontaneously in 6-8 weeks. Complications include hypertension, renal failure, and rarely chronic kidney disease.
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
most of the glomerular diseases , either primary or secondary..touching all the aspects including light microscopy, electron microscopy and immunoflourescence.
1) Nephritic Syndrome (ANS) can be classified clinically, biochemically, or histopathologically. It includes conditions like glomerulonephritis that cause hematuria and proteinuria but not edema.
2) Case studies are presented to demonstrate various etiologies of ANS, including primary membranoproliferative glomerulonephritis (MPGN) type 1 and secondary lupus nephritis.
3) Causes of ANS include primary glomerular diseases like MPGN type 1 as well as secondary glomerular diseases associated with conditions like SLE, hepatitis B/C, and ANCA-associated vasculitis. A thorough evaluation is needed to determine
The KIDNEY - PATHOGENESIS OF GLOMERULAR DISEASESDr. Roopam Jain
The document discusses glomerular diseases, which involve the renal glomeruli. It describes the classification of glomerular diseases into primary and secondary types. The major clinical manifestations are proteinuria, hematuria, hypertension, and impaired renal function. Six major glomerular syndromes are discussed: acute nephritic syndrome, nephrotic syndrome, acute renal failure, chronic renal failure, asymptomatic proteinuria, and asymptomatic hematuria. The pathogenesis of glomerular injury is examined by exploring the roles of endothelial, mesangial, epithelial and parietal cells as well as the glomerular basement membrane. Immunological and non-immunological mechanisms are involved in glomerular disease pathogenesis.
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 tubulo-interstitial pathology and chronic glomerulonephritis. It defines acute pyelonephritis, its causes and morphology. It describes chronic pyelonephritis and reflux nephropathy, including forms of chronic pyelonephritis and their gross and microscopic morphology. It also discusses drug-induced tubulo-interstitial nephritis, analgesic nephropathy, causes of chronic glomerulonephritis, and interpreting morphology of chronic glomerulonephritis.
Glomerulonephritides are diseases of the glomeruli that constitute major problems in nephrology. The glomerulus consists of a network of capillaries surrounded by epithelial cells. Glomerular diseases can be primary or secondary to other systemic diseases. The pathogenesis involves immune mechanisms such as deposition of immune complexes or antibodies reacting with antigens in the glomerulus. This causes inflammation and injury through activation of complement and recruitment of leukocytes. Conditions like minimal-change disease and focal segmental glomerulosclerosis are common causes of nephrotic syndrome, characterized by massive proteinuria and edema.
The document discusses various hemorrhagic and thrombotic disorders. It describes the normal hemostasis process and key tests used in evaluation. Several specific disorders are then covered in more detail, including immune thrombocytopenic purpura (ITP), hemophilia, von Willebrand disease, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), antiphospholipid syndrome (APS), and various thrombotic disorders. For each condition, it discusses causes, clinical presentation, diagnosis and management.
The document discusses various types of glomerular and tubulointerstitial diseases:
1. Glomerular diseases are caused by damage to the glomerulus and can manifest as nephritic syndrome, nephrotic syndrome, or hematuria. Common glomerular diseases include minimal change disease, membranous nephropathy, and focal segmental glomerulosclerosis.
2. Tubulointerstitial diseases involve damage to the renal tubules and interstitium. Acute interstitial nephritis is often caused by drug reactions while chronic interstitial nephritis can result from various insults like drugs, infections, toxins, and inherited conditions.
3
Platelet and coagulation post graduate lecture Monkez M Yousif
This lecture is prepared for postgraduate students in Internal medicine. It presents a physiologic and basic background of the process of homeostasis followed by a practical approach to diagnosis and brief information of different causes of bleeding disorders
Pancytopenia refers to decreases in all peripheral blood cell lineages. The initial evaluation of pancytopenia includes history, physical exam, screening labs including CBC and peripheral smear. This helps identify potential causes and emergencies requiring prompt treatment or hematology referral. Bone marrow testing may identify primary hematologic disorders but is sometimes unhelpful and specialized testing is preferred in some cases involving peripheral cell destruction.
Pseudomembranous colitis is an inflammatory condition of the colon characterized by elevated yellow-white plaques that coalesce to form pseudomembranes on the mucosa.
The pathogenesis of liver cirrhosis and fibrosisAbbaZarami Bukar
This document summarizes the pathogenesis of liver cirrhosis and fibrosis. It begins with an introduction to liver disease as a major health problem worldwide. It then discusses the epidemiology of cirrhosis, noting its 10th and 12th leading causes of death in the US. The document outlines the classification of cirrhosis based on nodule size, and describes the key events in the pathogenesis of fibrosis, including hepatic stellate cell activation and cytokine signaling pathways. Morphological features of cirrhosis seen on microscopy and complications like portal hypertension are also summarized. The document concludes by stating hepatic fibrogenesis involves both resident and recruited cell types, and advances may help develop effective antifibrotic therapies.
This document discusses tubular and interstitial diseases, focusing on acute kidney injury (AKI) and acute tubular necrosis (ATN). It provides details on:
1) The pathogenesis of AKI involving tubular cell injury from ischemia or toxins, disturbances in blood flow causing vasoconstriction, and the repair process through growth factors and cytokines.
2) The morphology of ischemic AKI, seen as focal tubular necrosis and casts, and the morphology of toxic AKI varying by toxin but often involving necrosis.
3) The clinical course of AKI proceeding through initiation, maintenance, and recovery phases and sometimes being nonoliguric. Prognosis depends on the cause,
This document discusses coagulopathy, which refers to medical disorders involving abnormal blood clotting due to deficiencies or issues with platelets, clotting factors, or the fibrinolytic system. It defines various bleeding disorders and coagulation tests. Specific conditions covered include immune thrombocytopenic purpura (ITP), von Willebrand disease, hemophilia A/B, and disseminated intravascular coagulation (DIC). Treatment involves replacing the deficient clotting factor, managing underlying causes, or administering medications depending on the condition causing the coagulopathy. Complications can include excessive bleeding, joint damage, and transmission of infections.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired hematopoietic stem cell disorder characterized by hemolytic anemia. It arises due to a somatic mutation in the PIGA gene, causing deficiency of glycosylphosphatidylinositol-anchored proteins (GPI-APs) like CD55 and CD59 on the surface of blood cells. This renders the cells highly sensitive to complement-mediated lysis. Diagnosis involves flow cytometry to detect GPI-AP deficiency and tests like Ham and sucrose hemolysis to demonstrate complement sensitivity of the red blood cells. PNH is associated with hemoglobinuria, thrombosis, and bone marrow failure. It requires differentiation
The kidneys filter waste and excess water from the blood to produce urine. Rapidly progressive glomerulonephritis (RPGN) is a severe form of glomerular injury characterized by the rapid loss of kidney function over weeks or months. It is classified based on the type of immune complex deposition, with Type I associated with anti-glomerular basement membrane antibodies, Type II associated with immune complexes, and Type III associated with few or no immune deposits but positive anti-neutrophil cytoplasmic antibodies. Histologically, RPGN is defined by the presence of crescents, which are areas of parietal epithelial cell proliferation that obliterate the Bowman's space.
This document discusses glomerular diseases, including their classification, clinical manifestations, and pathogenesis. It covers the following key points:
- Glomerular diseases are classified as primary (involving the glomeruli predominantly) or secondary (affecting the glomeruli due to systemic/hereditary diseases).
- Major clinical manifestations include proteinuria, hematuria, hypertension, and impaired renal function. The main glomerular syndromes discussed are nephritic, nephrotic, acute/chronic renal failure, and asymptomatic proteinuria/hematuria.
- The pathogenesis involves immunological mechanisms like antibody-mediated immune complex deposition, as well as non-immunological mechanisms. Injury
Approach to the Patient with Renal DiseasePatrick Carter
This document provides an overview of renal disease for medical students. It defines key terms related to renal function and urine findings. It describes tools for detecting renal disease including history, physical exam, urinalysis, and bloodwork. It discusses uremic syndrome and its effects on multiple organ systems. It differentiates between acute and chronic renal failure, nephritic and nephrotic syndrome based on causes, labs, and physical findings. The goal is to review approaches for evaluating and classifying patients with possible renal disease.
Acute Tubular Necrosis | DR RAI M. AMMAR | ALL MEDICAL DATA
by DR RAI M. AMMAR
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www.medicall.com.pk/blog/auther/drraiammar/
For Any Book or Notes Visit Our Website:
www.allmedicaldata.wordpress.com
www.drraiammar.blogspot.com
YOUTUBE CHANNEL :
https://www.youtube.com/channel/UCu-oR9V3OdFNTJW5yqXWXxA
ANY QUESTION ??
Get in touch with us at Any of the Above Social Media or Email at
drraiammar@gmail.com
allmedicaldata@gmail.com
Edema is the accumulation of excessive body fluid in interstitial spaces or serous cavities due to diseases rather than being a disease itself. It can be classified based on its range (generalized vs local) or cause (renal, hepatic, cardiac, etc.). Edema develops due to an imbalance in fluid exchange between plasma and tissues or due to renal sodium and water retention. Causes include increased capillary pressure, decreased plasma proteins, obstructed lymphatics, increased capillary permeability, and renal issues. Edema fluid characteristics depend on capillary permeability and it can be pitting or recessive with distribution influenced by factors like gravity. Edema generally harms tissues but may help dilute toxins in
Leukocytosis is an increased white blood cell count in the blood. There are five main types: neutrophilia, lymphocytosis, monocytosis, eosinophilia, and basophilia. Neutrophilia is most common and usually due to bacterial infection. Eosinophilia can be caused by allergic disorders, parasites, and some cancers. Lymphocytosis is seen with viral infections and lymphomas. Leukopenia and neutropenia involve decreased white blood cell and neutrophil counts respectively, increasing infection risk. Lymphoma involves abnormal lymphocyte proliferation. Leukemia includes acute and chronic forms, with acute being more aggressive and involving immature cells.
Glomerulonephritis is a type of kidney disease that causes inflammation of the glomeruli, the small blood vessels in the kidneys that filter waste from the blood. Common symptoms include blood and protein in the urine, swelling, high blood pressure, and general fatigue. The cause is often unknown but can be related to immune system problems, infections, cancer, or exposure to toxins. Diagnosis involves urinalysis and imaging tests to check for blood and protein in the urine. Treatment focuses on controlling blood pressure with medications and suppressing the immune system if it is causing the issue. The prognosis ranges from temporary to leading to chronic kidney disease, so patients need ongoing monitoring.
This document discusses two types of nephrosclerosis: benign and malignant. Benign nephrosclerosis is caused by thickening of renal arterioles over time from aging, hypertension, or diabetes. It can cause scarring and loss of renal function. Malignant nephrosclerosis involves a worsening of hypertension that damages renal vessels, causing ischemia and sudden loss of function. The pathology involves fibrinoid necrosis and intimal thickening of arteries. Aggressive treatment of high blood pressure is needed to prevent permanent kidney damage in malignant nephrosclerosis.
This document provides information on different types of primary glomerulonephritis (GN), including acute post-streptococcal GN, rapidly progressive GN, minimal change disease, and membranous GN. It describes the key characteristics of each such as typical age of onset, clinical presentation, pathogenesis, histopathological features on light microscopy, immunofluorescence and electron microscopy. Acute post-streptococcal GN commonly follows a streptococcal infection and presents as acute nephritic syndrome in children. Rapidly progressive GN can lead to acute renal failure in weeks and is characterized by crescent formation. Minimal change disease is the most common cause of nephrotic syndrome in children and shows no
The KIDNEY: SPECIFIC TYPES OF GLOMERULAR DISEASESDr. Roopam Jain
This document discusses different types of glomerular diseases. It provides details on acute post-streptococcal glomerulonephritis, including its etiology, pathogenesis, clinical features, and microscopic appearance. It also describes rapidly progressive glomerulonephritis, minimal change disease, and membranous glomerulonephritis, noting key distinguishing characteristics such as presentation, prognosis, and histopathological findings of each type. Comparative features of major forms of primary glomerulonephritis are analyzed.
This document discusses tubulo-interstitial pathology and chronic glomerulonephritis. It defines acute pyelonephritis, its causes and morphology. It describes chronic pyelonephritis and reflux nephropathy, including forms of chronic pyelonephritis and their gross and microscopic morphology. It also discusses drug-induced tubulo-interstitial nephritis, analgesic nephropathy, causes of chronic glomerulonephritis, and interpreting morphology of chronic glomerulonephritis.
Glomerulonephritides are diseases of the glomeruli that constitute major problems in nephrology. The glomerulus consists of a network of capillaries surrounded by epithelial cells. Glomerular diseases can be primary or secondary to other systemic diseases. The pathogenesis involves immune mechanisms such as deposition of immune complexes or antibodies reacting with antigens in the glomerulus. This causes inflammation and injury through activation of complement and recruitment of leukocytes. Conditions like minimal-change disease and focal segmental glomerulosclerosis are common causes of nephrotic syndrome, characterized by massive proteinuria and edema.
The document discusses various hemorrhagic and thrombotic disorders. It describes the normal hemostasis process and key tests used in evaluation. Several specific disorders are then covered in more detail, including immune thrombocytopenic purpura (ITP), hemophilia, von Willebrand disease, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), antiphospholipid syndrome (APS), and various thrombotic disorders. For each condition, it discusses causes, clinical presentation, diagnosis and management.
The document discusses various types of glomerular and tubulointerstitial diseases:
1. Glomerular diseases are caused by damage to the glomerulus and can manifest as nephritic syndrome, nephrotic syndrome, or hematuria. Common glomerular diseases include minimal change disease, membranous nephropathy, and focal segmental glomerulosclerosis.
2. Tubulointerstitial diseases involve damage to the renal tubules and interstitium. Acute interstitial nephritis is often caused by drug reactions while chronic interstitial nephritis can result from various insults like drugs, infections, toxins, and inherited conditions.
3
Platelet and coagulation post graduate lecture Monkez M Yousif
This lecture is prepared for postgraduate students in Internal medicine. It presents a physiologic and basic background of the process of homeostasis followed by a practical approach to diagnosis and brief information of different causes of bleeding disorders
Pancytopenia refers to decreases in all peripheral blood cell lineages. The initial evaluation of pancytopenia includes history, physical exam, screening labs including CBC and peripheral smear. This helps identify potential causes and emergencies requiring prompt treatment or hematology referral. Bone marrow testing may identify primary hematologic disorders but is sometimes unhelpful and specialized testing is preferred in some cases involving peripheral cell destruction.
Pseudomembranous colitis is an inflammatory condition of the colon characterized by elevated yellow-white plaques that coalesce to form pseudomembranes on the mucosa.
The pathogenesis of liver cirrhosis and fibrosisAbbaZarami Bukar
This document summarizes the pathogenesis of liver cirrhosis and fibrosis. It begins with an introduction to liver disease as a major health problem worldwide. It then discusses the epidemiology of cirrhosis, noting its 10th and 12th leading causes of death in the US. The document outlines the classification of cirrhosis based on nodule size, and describes the key events in the pathogenesis of fibrosis, including hepatic stellate cell activation and cytokine signaling pathways. Morphological features of cirrhosis seen on microscopy and complications like portal hypertension are also summarized. The document concludes by stating hepatic fibrogenesis involves both resident and recruited cell types, and advances may help develop effective antifibrotic therapies.
This document discusses tubular and interstitial diseases, focusing on acute kidney injury (AKI) and acute tubular necrosis (ATN). It provides details on:
1) The pathogenesis of AKI involving tubular cell injury from ischemia or toxins, disturbances in blood flow causing vasoconstriction, and the repair process through growth factors and cytokines.
2) The morphology of ischemic AKI, seen as focal tubular necrosis and casts, and the morphology of toxic AKI varying by toxin but often involving necrosis.
3) The clinical course of AKI proceeding through initiation, maintenance, and recovery phases and sometimes being nonoliguric. Prognosis depends on the cause,
This document discusses coagulopathy, which refers to medical disorders involving abnormal blood clotting due to deficiencies or issues with platelets, clotting factors, or the fibrinolytic system. It defines various bleeding disorders and coagulation tests. Specific conditions covered include immune thrombocytopenic purpura (ITP), von Willebrand disease, hemophilia A/B, and disseminated intravascular coagulation (DIC). Treatment involves replacing the deficient clotting factor, managing underlying causes, or administering medications depending on the condition causing the coagulopathy. Complications can include excessive bleeding, joint damage, and transmission of infections.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired hematopoietic stem cell disorder characterized by hemolytic anemia. It arises due to a somatic mutation in the PIGA gene, causing deficiency of glycosylphosphatidylinositol-anchored proteins (GPI-APs) like CD55 and CD59 on the surface of blood cells. This renders the cells highly sensitive to complement-mediated lysis. Diagnosis involves flow cytometry to detect GPI-AP deficiency and tests like Ham and sucrose hemolysis to demonstrate complement sensitivity of the red blood cells. PNH is associated with hemoglobinuria, thrombosis, and bone marrow failure. It requires differentiation
The kidneys filter waste and excess water from the blood to produce urine. Rapidly progressive glomerulonephritis (RPGN) is a severe form of glomerular injury characterized by the rapid loss of kidney function over weeks or months. It is classified based on the type of immune complex deposition, with Type I associated with anti-glomerular basement membrane antibodies, Type II associated with immune complexes, and Type III associated with few or no immune deposits but positive anti-neutrophil cytoplasmic antibodies. Histologically, RPGN is defined by the presence of crescents, which are areas of parietal epithelial cell proliferation that obliterate the Bowman's space.
This document discusses glomerular diseases, including their classification, clinical manifestations, and pathogenesis. It covers the following key points:
- Glomerular diseases are classified as primary (involving the glomeruli predominantly) or secondary (affecting the glomeruli due to systemic/hereditary diseases).
- Major clinical manifestations include proteinuria, hematuria, hypertension, and impaired renal function. The main glomerular syndromes discussed are nephritic, nephrotic, acute/chronic renal failure, and asymptomatic proteinuria/hematuria.
- The pathogenesis involves immunological mechanisms like antibody-mediated immune complex deposition, as well as non-immunological mechanisms. Injury
Approach to the Patient with Renal DiseasePatrick Carter
This document provides an overview of renal disease for medical students. It defines key terms related to renal function and urine findings. It describes tools for detecting renal disease including history, physical exam, urinalysis, and bloodwork. It discusses uremic syndrome and its effects on multiple organ systems. It differentiates between acute and chronic renal failure, nephritic and nephrotic syndrome based on causes, labs, and physical findings. The goal is to review approaches for evaluating and classifying patients with possible renal disease.
Acute Tubular Necrosis | DR RAI M. AMMAR | ALL MEDICAL DATA
by DR RAI M. AMMAR
www.facebook.com/drraiammar
www.twitter.com/drraiammar
www.instagram.com/drraiammar
www.linkedin.com/in/drraiammar
www.medicall.com.pk/blog/auther/drraiammar/
For Any Book or Notes Visit Our Website:
www.allmedicaldata.wordpress.com
www.drraiammar.blogspot.com
YOUTUBE CHANNEL :
https://www.youtube.com/channel/UCu-oR9V3OdFNTJW5yqXWXxA
ANY QUESTION ??
Get in touch with us at Any of the Above Social Media or Email at
drraiammar@gmail.com
allmedicaldata@gmail.com
Edema is the accumulation of excessive body fluid in interstitial spaces or serous cavities due to diseases rather than being a disease itself. It can be classified based on its range (generalized vs local) or cause (renal, hepatic, cardiac, etc.). Edema develops due to an imbalance in fluid exchange between plasma and tissues or due to renal sodium and water retention. Causes include increased capillary pressure, decreased plasma proteins, obstructed lymphatics, increased capillary permeability, and renal issues. Edema fluid characteristics depend on capillary permeability and it can be pitting or recessive with distribution influenced by factors like gravity. Edema generally harms tissues but may help dilute toxins in
Leukocytosis is an increased white blood cell count in the blood. There are five main types: neutrophilia, lymphocytosis, monocytosis, eosinophilia, and basophilia. Neutrophilia is most common and usually due to bacterial infection. Eosinophilia can be caused by allergic disorders, parasites, and some cancers. Lymphocytosis is seen with viral infections and lymphomas. Leukopenia and neutropenia involve decreased white blood cell and neutrophil counts respectively, increasing infection risk. Lymphoma involves abnormal lymphocyte proliferation. Leukemia includes acute and chronic forms, with acute being more aggressive and involving immature cells.
Glomerulonephritis is a type of kidney disease that causes inflammation of the glomeruli, the small blood vessels in the kidneys that filter waste from the blood. Common symptoms include blood and protein in the urine, swelling, high blood pressure, and general fatigue. The cause is often unknown but can be related to immune system problems, infections, cancer, or exposure to toxins. Diagnosis involves urinalysis and imaging tests to check for blood and protein in the urine. Treatment focuses on controlling blood pressure with medications and suppressing the immune system if it is causing the issue. The prognosis ranges from temporary to leading to chronic kidney disease, so patients need ongoing monitoring.
This document discusses two types of nephrosclerosis: benign and malignant. Benign nephrosclerosis is caused by thickening of renal arterioles over time from aging, hypertension, or diabetes. It can cause scarring and loss of renal function. Malignant nephrosclerosis involves a worsening of hypertension that damages renal vessels, causing ischemia and sudden loss of function. The pathology involves fibrinoid necrosis and intimal thickening of arteries. Aggressive treatment of high blood pressure is needed to prevent permanent kidney damage in malignant nephrosclerosis.
This document provides information on different types of primary glomerulonephritis (GN), including acute post-streptococcal GN, rapidly progressive GN, minimal change disease, and membranous GN. It describes the key characteristics of each such as typical age of onset, clinical presentation, pathogenesis, histopathological features on light microscopy, immunofluorescence and electron microscopy. Acute post-streptococcal GN commonly follows a streptococcal infection and presents as acute nephritic syndrome in children. Rapidly progressive GN can lead to acute renal failure in weeks and is characterized by crescent formation. Minimal change disease is the most common cause of nephrotic syndrome in children and shows no
The KIDNEY: SPECIFIC TYPES OF GLOMERULAR DISEASESDr. Roopam Jain
This document discusses different types of glomerular diseases. It provides details on acute post-streptococcal glomerulonephritis, including its etiology, pathogenesis, clinical features, and microscopic appearance. It also describes rapidly progressive glomerulonephritis, minimal change disease, and membranous glomerulonephritis, noting key distinguishing characteristics such as presentation, prognosis, and histopathological findings of each type. Comparative features of major forms of primary glomerulonephritis are analyzed.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is caused by increased permeability of the glomerular capillary wall due to damage or abnormalities of the glomerular basement membrane or podocytes. There are several histological types including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and membranoproliferative glomerulonephritis. Treatment involves controlling symptoms through dietary changes and medications, with corticosteroids often used to treat the underlying condition.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is caused by increased permeability of the glomerular capillary wall due to damage or abnormalities of the glomerular basement membrane or podocytes. There are several histological types including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and membranoproliferative glomerulonephritis. Treatment involves controlling symptoms with diuretics and albumin supplementation, and treating the underlying kidney damage with corticosteroids, immunosuppressants, or other medications. Complications can include edema, infections, hypercoagulability, and kidney failure
This document outlines the objectives and content for two pathology lectures on renal glomerular syndromes including nephrotic syndrome and nephritic syndrome. The lectures will cover the clinical presentation and pathological findings of key renal diseases like minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, acute post-streptococcal glomerulonephritis, lupus nephritis, IgA nephropathy, and rapidly progressive glomerulonephritis. The lectures will discuss kidney biopsy techniques and the role of light microscopy, immunofluorescence and electron microscopy in the diagnosis of renal diseases. Key pathological mechanisms like the location of immune deposits and pathogenesis of glomerular
Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis characterized by thickening of the glomerular basement membrane, proliferation of mesangial cells and capillary loops, and activation of the complement system. There are two main types - type I is caused by immune complex deposition and type II (dense deposit disease) results from abnormal alternative complement pathway regulation leading to dense material deposition in the glomerular basement membrane. MPGN follows a progressive clinical course and can lead to end stage renal disease within 10 years if left untreated. Treatment aims to slow disease progression and control symptoms.
ANTI GBM DISEASE final hellllo hiiiii.pptxManoj Aryal
This document provides an overview of anti-GBM disease and Goodpasture's syndrome. It discusses the epidemiology, etiology, pathogenesis, clinical presentation, diagnosis, pathology, treatment and prognosis. The key points are:
- It is a rare disease caused by autoantibodies against type IV collagen in the glomerular basement membrane, leading to lung hemorrhage and rapidly progressive glomerulonephritis.
- Treatment involves plasma exchange to remove antibodies, immunosuppression with cyclophosphamide and steroids, and supportive care. Prognosis is good with over 90% survival if treated early, though kidney recovery depends on disease severity at presentation.
- Smoking cessation is important
This document discusses several types of glomerular diseases that present with a membranoproliferative pattern of injury on histology, including membranoproliferative glomerulonephritis (MPGN) types I, II, and III, cryoglobulin-associated glomerulonephritis, lupus nephritis class IV, and thrombotic microangiopathies (both acute and chronic). It provides details on the etiology, clinical features, histopathology, immunofluorescence, and electron microscopy findings of each condition.
This document provides information on membranoproliferative glomerulonephritis (MPGN). It discusses the histological characteristics of MPGN including thickening of the glomerular basement membrane and increased mesangial and endocapillary cellularity. It presents a new classification system for MPGN that is based on pathogenesis, categorizing it as immune complex-mediated, complement-mediated, or other rare causes. Immune complex-mediated MPGN can result from infections, autoimmune diseases, or monoclonal gammopathies. Complement-mediated MPGN includes dense deposit disease and C3 glomerulonephritis, which are caused by dysregulation of the alternative complement pathway.
MPGN BY DR SAEED KDIGO 2021 UPDATE GUIDELINES.pptxDr-Saeed Hossain
This document provides an overview of the 2021 KDIGO Clinical Practice Guideline update for membranoproliferative glomerulonephritis (MPGN). It discusses the classification, pathophysiology, diagnosis, and treatment recommendations for immune complex-mediated MPGN, complement-mediated MPGN including C3 glomerulopathy, and monoclonal immunoglobulin deposition disease. Key updates from KDIGO include more individualized treatment approaches for idiopathic immune complex glomerulonephritis based on disease severity and proteinuria levels.
This document discusses glomerulonephritis, which is inflammation of the glomeruli in the kidney. It can be classified as primary, affecting only the kidney, or secondary, affecting the kidney and other organs. The main types are acute post-streptococcal glomerulonephritis, rapidly progressive glomerulonephritis, and membranoproliferative glomerulonephritis. Clinical manifestations include nephritic syndrome, nephrotic syndrome, and hematuria. The document provides details on pathogenesis, morphological features, and treatment of different glomerular diseases.
Glomerulonephritis refers to inflammation of the glomeruli in the kidney. It can be primary, affecting only the kidney, or secondary, affecting the kidney and other organs. It causes nephritic or nephrotic syndrome. Common types include post-streptococcal glomerulonephritis, minimal change disease, membranous glomerulonephritis, and rapidly progressive glomerulonephritis. Symptoms range from hematuria and proteinuria to edema, hypertension and renal failure depending on type and severity.
This document discusses the histopathological features of several types of crescentic glomerulonephritis (GN), including anti-glomerular basement membrane (GBM) disease, pauci-immune GN, immune complex-mediated GN, lupus nephritis class IV, IgA nephropathy, and post infectious GN. Key findings include fibrinoid necrosis, crescent formation, immune complex deposition patterns on immunofluorescence, and electron-dense deposits, effacement of foot processes, and basement membrane abnormalities on electron microscopy. The diseases are distinguished by their pathogenic mechanisms and specific immune staining and ultrastructural characteristics.
Nephrotic syndrome is a kidney disorder characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is mostly seen in children and is usually caused by minimal change disease or focal segmental glomerulosclerosis. Treatment involves corticosteroids, which are effective in resolving symptoms in 80% of children. Relapses are common and managed with additional courses of steroids. The document provides details on the definition, causes, pathology, clinical manifestations, investigations, and management of nephrotic syndrome.
The document discusses different types of kidney diseases and disorders:
- It describes the normal anatomy and histology of the kidney, including structures like the glomerulus.
- Nephrotic syndrome is discussed, which is characterized by proteinuria and low albumin levels, causing fluid retention and edema. Investigations include urine tests and kidney biopsies.
- Different glomerular diseases are described based on their pathology, including membranous glomerulonephritis, minimal change disease, focal segmental glomerulosclerosis (FSGS), and membranoproliferative glomerulonephritis. Their features on light microscopy, immunofluorescence and electron microscopy are provided.
- IgA nep
This document discusses acute glomerulonephritis, specifically acute post-streptococcal glomerulonephritis (APSGN). It begins by introducing acute glomerulonephritis and dividing it into post-streptococcal and non-streptococcal types. It then focuses on APSGN, describing how it typically affects children after a streptococcal throat or skin infection. The pathogenesis involves an immune response against streptococcal antigens. Clinically, APSGN presents as acute nephritic syndrome with hematuria, proteinuria, hypertension, and edema. Microscopically, there is proliferation of glomerular cells and neutrophil infiltration.
1. The document discusses glomerular diseases in children, describing the anatomy of the kidneys and glomerulus.
2. It then focuses on acute glomerulonephritis (AGN), the most common form in children which typically follows a streptococcal infection.
3. AGN is characterized by hematuria, proteinuria, edema, hypertension, and other symptoms. It results from immune complexes depositing in the glomerular basement membrane.
Membranous GN
MOST COMMON cause is idiopathic (85%); peak age 30-50; male:female, 2:1
May be secondary to:
Drugs-captopril, penicillamine, gold, mercury, trimethadione, NSAIDS
Infections-malaria (P. malariae), leprosy, schistosomiasis, syphilis, hepatitis B and C, filariasis, hydatid disease and enterococcal endocarditis
Diseases-malignancy (Carcinoma of breast, lung, colon, stomach, and esophagus) melanoma, renal cell CA, SLE, sarcoidosis, diabetes, thyroiditis, sickle cell anemia, Crohn’s disease
This document discusses acute glomerulonephritis, specifically acute post-streptococcal glomerulonephritis. It begins by defining acute glomerulonephritis and noting that it typically presents as acute nephritic syndrome following an acute infection. It then describes acute post-streptococcal glomerulonephritis in more detail, indicating it is most common in children following a streptococcal throat or skin infection, with onset of symptoms 1-2 weeks later. Symptoms include hematuria, proteinuria, hypertension, edema and occasionally oliguria. The document discusses the etiology and pathophysiology of acute post-streptococcal glomerulonephritis in more detail.
Necrosis and apoptosis are two types of cell death. Necrosis is caused by external factors like hypoxia or toxins and results in the uncontrolled death and degradation of cells. Apoptosis is a programmed and controlled form of cell death that plays an important role in normal development and tissue homeostasis. It is characterized by cell fragmentation into membrane-bound vesicles that are phagocytosed by other cells. Apoptosis is involved in physiological processes like tissue sculpting and involution as well as pathological processes including cancer, viral infections, and neurodegenerative diseases.
This document summarizes different types of reversible cell injury seen microscopically, including hydropic change, hyaline change, mucoid change, and fatty change. Hydropic change is characterized by cytoplasmic vacuolation and swelling of cells. Hyaline change results in a glassy, eosinophilic appearance of intracellular or extracellular proteins. Mucoid change describes excess intracellular or extracellular mucin accumulation. Fatty change or steatosis involves intracellular accumulation of neutral fats within cells. Each type of change is described in detail with examples and microscopic images.
Cell injury can be reversible or irreversible. Reversible injury is caused by decreased ATP and acidosis within cells. Irreversible injury occurs when mitochondrial and cell membrane dysfunction cannot be reversed, leading to calcium influx, membrane damage, and cell death. Free radicals generated during ischemia-reperfusion can also cause irreversible injury through lipid peroxidation, protein and DNA oxidation, and cytoskeletal damage. Stress proteins help cells cope with injury by moving molecules within the cell.
This document discusses cell injury, cellular adaptations, and cellular aging. It covers various causes of cell injury including hypoxia, physical agents, chemicals, microbes, immunologic factors, nutritional imbalances, and aging. It describes the pathogenesis of injury from these various sources and the cellular responses, which can be reversible or irreversible. Reversible changes include hydropic swelling, hyaline changes, mucoid changes, and fatty changes. The document outlines various morphologic features of reversible cell injury and discusses cellular adaptations like stress protein production in response to injury.
USMLE Style case based study & MCQs Neoplasia Dr. Roopam Jain
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CELL INJURY, CELLULAR ADAPTATION by DR. ROOPAM JAINDr. Roopam Jain
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The document provides an introduction to the pathology department and describes the various subspecialties and benches within histopathology. It discusses that pathology is the study of disease processes and changes in cells, tissues, and organs. The key benches in histopathology are processing, grossing, tissue processing, embedding, cutting, histochemistry, immunohistochemistry, special stains, cytology, and cytogenetics. Each bench performs specific functions in examining tissues at the macroscopic and microscopic level to arrive at diagnoses.
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INFECTIOUS DISEASES by DR. ROOPAM JAIN for NEET PGDr. Roopam Jain
This document discusses infectious diseases and provides an overview of routes of microbial infection, techniques for diagnosing infectious agents, the spectrum of inflammatory responses to infection, and a classification of important sexually transmitted diseases.
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This document provides an overview of various infectious diseases caused by bacteria, viruses, and fungi. It discusses staphylococcal infections caused by Staphylococcus aureus, including skin infections, respiratory infections, bone infections, and more. It also covers streptococcal infections caused by different streptococcal species, clostridial diseases including gas gangrene and tetanus, mycotic diseases such as mycetoma and candidiasis, and selected viral diseases including viral hemorrhagic fevers, influenza, dengue fever, chikungunya, and bird flu.
INFECTIOUS DISEASE - Human Viruses & Viral Diseases by Dr. Roopam JainDr. Roopam Jain
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The document discusses several fungal diseases including mycetoma, candidiasis, cutaneous superficial mycosis, and viral haemorrhagic fevers. Mycetoma is a chronic infection of the limbs characterized by draining sinuses discharging grains. Candidiasis is an opportunistic infection most commonly caused by Candida albicans. Cutaneous superficial mycosis includes infections caused by dermatophytes like Microsporum and Trichophyton. Viral haemorrhagic fevers covered are yellow fever, dengue fever, chikungunya virus infection, and influenza virus infections.
Hemodynamic disorders - Edema, Hyperemia, Hemorrahge by DR. ROOPAM JAINDr. Roopam Jain
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Embolism occurs when a solid, liquid, or gaseous mass travels through the bloodstream and lodges in a blood vessel distant from the site of origin. Embolisms are classified based on direction of travel and composition. Pulmonary embolisms involve the lungs while systemic embolisms affect other organs. Common causes of embolism include blood clots, fat droplets, air bubbles, and infectious materials. Symptoms vary depending on the size and location of the embolism but may include dyspnea, chest pain, and coughing. Diagnosis involves blood tests, imaging, and scans. Consequences depend on factors like vessel size and collateral blood flow.
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This document discusses chronic venous congestion (CVC) and its effects on various organs. It describes how CVC results in localized blood volume increase within dilated vessels. It then summarizes the gross and microscopic findings of CVC in the lungs, liver, spleen, and kidneys. The lungs show brown induration and thickened alveolar septa. The liver has a nutmeg appearance and centrilobular necrosis. The spleen exhibits congestion and fibrosis. The kidneys demonstrate mild degenerative changes. Hemorrhage and its causes, effects based on amount/speed of blood loss are also outlined.
The document discusses homeostasis and fluid balance in the human body. It begins by defining the internal environment and homeostasis. It then describes the distribution of body water and electrolytes, including that total body water is 60% of body weight, with two-thirds being intracellular fluid and one-third extracellular fluid. Extracellular fluid is further divided into interstitial fluid, blood plasma, and other minor components. Common disturbances to body water balance discussed are edema, dehydration, and overhydration. The key causes and features of different types of edema like renal, cardiac, pulmonary, and cerebral edema are summarized.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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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.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
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Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
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).
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
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2. I. PRIMARY GLOMERULONEPHRITIS
• Acute Glomerulonephritis
• Synonyms:
• Acute Diffuse Proliferative GN,
• Diffuse Endocapillary GN
3. Acute Glomerulonephritis
• Acute GN is known to follow acute infection and characteristically
presents as acute nephritic syndrome.
• Based on etiologic agent, acute GN is subdivided into 2 main groups:
• acute post-streptococcal GN & (more common)
• acute non-streptococcal GN
4. ACUTE POST-STREPTOCOCCAL GN (APSGN)
• common form of GN in developing countries,
• mostly affecting children between 2 to 14 years of age but 10% cases
are seen in adults above 40 years of age.
• The onset of disease is generally sudden after 1-2 weeks of
streptococcal infection, most frequently of the throat (e.g. streptococcal
pharyngitis) and sometimes of the skin (e.g. streptococcal impetigo).
5. ACUTE POST-STREPTOCOCCAL GN (APSGN)
ETIOPATHOGENESIS
• The relationship between streptococcal infection and this form of GN is now well establish
• The evidences cited in support are as under:
• i) There is epidemiological evidence of preceding streptococcal sore throat or skin infection
about 1-2 weeks prior to the attack.
• ii) The latent period between streptococcal infection and onset of clinical manifestations of
the disease is compatible with the period required for building up of anti bodies.
• iii) Streptococcal infection may be identified by culture or may be inferred from elevated
titres of antibodies against streptococcal antigens.
• a) anti-streptolysin O (ASO);
• b) anti-deoxyribonuclease B (anti-DNAse B);
• c) anti-streptokinase (ASKase);
• d) anti-nicotinyl adenine dinucleotidase (anti-NADase); and
• e) anti-hyaluronidase (AHase).
• iv) hypocomplementaemia indicating involvement of complement in the glomerular deposits.
• v) identify antigenic component of streptococci which is cytoplasmic antigen, endostreptosin.
6. Acute post-streptococcal GN
Light microscopic appearance. There is increased cellularity due to proliferation of
mesangial cells, endothelial cells and some epithelial cells and infi ltration of the tuft by
neutrophils and monocytes.
7. APSGN - MORPHOLOGIC FEATURES - GROSS
• Grossly, the kidneys are
symmetrically enlarged,
weighing one and a half to
twice the normal weight. Th
e cortical as well as sectio
ned surface show petechial
haemorrhages giving the
characteristic appearance of
fl ea-bitten kidney (Fig
Flea-bitten kidney
The kidney is enlarged in size and
weight.
The cortex shows tiny petechial
haemorrhages visible through
9. ACUTE POST-STREPTOCOCCAL GN
CLINICAL FEATURES
• young child, presenting with acute nephritic syndrome,
• having sudden and abrupt onset following an episode of sore throat or
skin infection
• microscopic or intermittent haematuria,
• red cell casts,
• mild non-selective proteinuria (less than 3 gm per 24 hrs),
• hypertension,
• periorbital oedema
• variably oliguria.
• In adults, the features are atypical and include sudden hypertension,
oedema and azotaemia.
11. RPGN
• RPGN presents with an acute reduction in renal function resulting in
acute renal failure in a few weeks or months.
• It is characterised by formation of ‘crescents’ (crescentic GN) outside the
glomerular capillaries (extracapillary GN)
• RPGN occurs most frequently in adults
• slight male preponderance.
• Prognosis of RPGN in general is dismal.
12. RPGN - ETIOPATHOGENESIS
• A number of primary glomerular and systemic diseases are characterised
by formation of crescents.
• Based on the etiologic agents and pathogenetic mechanism, patients
with RPGN are divided into 3 groups (Table):
• 1. RPGN in systemic diseases (anti-GBM type)
• 2. Post-infectious RPGN (immune-complex type)
• 3. Pauci-immune RPGN.
• Following three serologic markers are used for categorising RPGN:
• i) serum C3 level,
• ii) anti-GBM antibody; and
• iii) anti-neutrophil cytoplasmic antibody (ANCA)
15. RPGN (post-infectious type),
Light microscopic appearance.
There are crescents in Bowman’s space forming adhesions between
the glomerular tuft and Bowman’s capsule.
The tuft shows hypercellularity & leucocytic infiltration.
16. RPGN
diagrammatic representation of ultrastructure of a portion of glomerular
lobule showing epithelial crescent formation & subepithelial granular
deposits.
17. RPGN CLINICAL FEATURES
• Generally, the features of postinfectious RPGN are similar to those of
acute GN, presenting as acute renal failure.
• The patients of Goodpasture’s syndrome may present as acute renal
failure and/or associated intrapulmonary haemorrhage
producing recurrent haemoptysis.
• Prognosis of all forms of RPGN is poor.
• However, post-infectious cases have somewhat better outcome and
may show recovery.
19. Minimal Change Disease
• condition in which the nephrotic syndrome is accompanied by no
apparent change in glomeruli by light microscopy.
• Its other synonyms, lipoid nephrosis and foot process disease,
are descriptive terms for fatty changes in the tubules and electron
microscopic appearance of flattened podocytes respectively.
• Minimal change disease accounts for 80% cases of nephrotic
syndrome in children under 16 years of age with preponderance in
boys (ratio of boys to girls 2:1).
• In fact, historically, lipoid nephrosis was the first condition associated
with nephrotic syndrome.
20. Minimal Change Disease
ETIOPATHOGENESIS
i) Idiopathic (majority of cases).
ii) Cases associated with systemic diseases (Hodgkin’s disease, HIV
infection) & drug therapy (e.g. NSAIDs, rifampicin, interferon- ).
Possible immunologic pathogenesis for MCD:
• i) Absence of deposits by immunofluorescence microscopy.
• ii) Normal circulating levels of complement
• iii) Universal satisfactory response to steroid therapy.
• iv) Evidence of increased suppressor T cell activity with elaboration of
cytokines
• v) Detection of a mutation in nephrin gene
21. Minimal Change Disease
A, Light microscopy shows a normal glomerulus while
B, Diagrammatic representation tubules show cytoplasmic vacuolation and
proteinaceous material. of ultrastructure of a portion of glomerular lobule showing
diffuse fusion or flattening of foot processes of visceral epithelial cells (podocytes).
The GBM is normal and there are no deposits.
22. Minimal-change disease.
A, Glomerulus stained with PAS. Note normal basement membranes and
absence of proliferation.
B, Ultrastructural characteristics of minimal-change disease include
effacement of foot processes (arrows) and absence of deposits. CL, Capillary
lumen; M, mesangium; P, podocyte cell body.
23. Minimal Change Disease
CLINICAL FEATURES
• The classical presentation of MCD is of fully-developed nephrotic
syndrome with massive and highly selective proteinuria;
hypertension is unusual.
• Most frequently, the patients are children under 16 years (peak
incidence at 6-8 years of age).
• The onset may be preceded by an upper respiratory infection, atopic
allergy or immunisation.
• The disease characteristically responds to steroid therapy.
• In spite of remissions and relapses, long-term prognosis is very
good and most children become free of albuminuria after several years.
25. • Membranous nephropathy is characterized by
diffuse thickening of the glomerular capillary wall
due to the accumulation of deposits containing Ig
along the subepithelial side of the basement
membrane.
• uniform, diffuse thickening of the glomerular capillary
wall
27. Membranous
GN
Diagrammatic representation of ultrastructure of a portion of glomerular lobule
showing subepithelial deposits of electron-dense material so that the basement
membrane material protrudes between these deposits.
28. Membranous nephropathy. A, Silver methenamine stain. Note the marked diffuse
thickening of the capillary walls without an increase in the number of cells. There are
prominent “spikes” of silver-staining matrix (arrow) projecting from the basement
membrane lamina densa toward the urinary space, which separate and surround deposited
immune complexes that lack affinity for the silver stain.
B, Electron micrograph showing electron-dense deposits (arrow) along the epithelial side of
the basement membrane (B). Note the effacement of foot processes overlying deposits. CL,
Capillary lumen; End, endothelium; Ep, epithelium; US, urinary space. C
31. Membranous GN
CLINICAL FEATURES
• insidious onset of nephrotic syndrome in an adult.
• The proteinuria is usually of non-selective type.
• microscopic haematuria and hypertension
• Progression to impaired renal function and endstage renal disease with
progressive azotaemia occurs in approximately 50% cases within a span
of 2 to 20 years.
• Renal vein thrombosis (due to hypercoagulability)
• The role and beneficial effects of steroid therapy with or without the
addition of immunosuppressive drugs is debatable
33. MPGN
ETIOPATHOGENESIS
• evidence of preceding streptococcal infection.
• 3 types of MPGN
• Type I or classic form is an example of immune complex disease and
comprises more than 70% cases
• Type II or dense deposit disease is the example of alternate pathway
disease (page 651) and constitutes about 30% cases.
• Type III is rare and shows features of type I MPGN and membranous
nephropathy in association with systemic diseases or drugs.
34. MPGN
The glomerular tufts show lobulation and mesangial hypercellularity.
There is increase in the mesangial matrix between the capillaries.
There is widespread thickening of the GBM.
35. MPGN
diagrammatic representation of ultrastructure of a portion of glomerular lobule showing
features of type I (left half) and type II (right half) MPGN.
Type I (classic form) shows the characteristic subendothelial electron-dense deposits
Type II (dense deposit disease) is characterised by intramembranous dense deposits
36. MPGN - CLINICAL FEATURES
• The most common age at diagnosis is between 15 and 20 years.
• Approximately 50% of the patients present with nephrotic syndrome;
• about 30% have asymptomatic proteinuria;
• and 20% have nephritic syndrome at presentation.
• proteinuria is non-selective.
• Haema turia and hypertension are frequently present.
• Hypo complementaemia is a common feature.
• With time, majority of patients progress to renal failure
38. A, Focal GN : The characteristic feature is the cellular proliferation in
some glomeruli and in one or two lobules of the affected glomeruli i.e.
focal and segmental proliferative change.
B, C, Focal segmental glomerulosclerosis. The features are focal and
segmental involvement of the glomeruli by sclerosis and hyalinosis and
mesangial hypercellularity
39. MPGN
MPGN, showing mesangial cell proliferation, increased mesangial matrix
(staining black with silver stain), basement membrane thickening with
segmental splitting, accentuation of lobular architecture, swelling of
cells lining peripheral capillaries, and influx of leukocytes
(endocapillary proliferation).
40. CLINICAL FEATURES
• The clinical features vary according to the condition causing it.
• Haematuria is one of the most common clinical manifestation.
• Proteinuria is frequently mild to moderate but
• hypertension is uncommon.
43. IgA Nephropathy - ETIOPATHOGENESIS
• remains unclear: i) It is idiopathic in most cases.
• ii) Seen as part of Henoch-Schonlein purpura.
• iii) Association with chronic inflammation in various body systems (e.g.
• chronic liver disease,
• inflammatory bowel disease,
• interstitial pneumonitis,
• leprosy,
• dermatitis herpetiformis,
• uveitis,
• ankylosing spondylitis,
• Sjögren’s syndrome,
• monoclonal IgA gammopathy
45. Chronic Glomerulonephritis
• Chronic GN is the final stage of a variety of glomerular diseases which
result in irreversible impairment of renal function. Th e conditions which
may progress to chronic GN, in descending order of frequency, are as
under:
• i) Rapidly progressive GN (90%)
• ii) Membranous GN (50%)
• iii) Membranoproliferative GN (50%)
• iv) Focal segmental glomerulosclerosis (50%)
• v) IgA nephropathy (40%)
• vi) Acute post-streptococcal GN (1%). However, about 20% cases of
chronic GN are idiopathic without evidence of preceding GN of any type.
46. End-stage kidney, gross appearance of short contract kidney in CGN.
The kidney is small & contracted.
The capsule is adherent to the cortex and has diffusely granular
cortical surface.
47. End-stage kidney in chronic GN, light microscopy.
Glomerular tufts are acellular and completely hyalinised.
Blood vessels in the interstitium are hyalinised and thickened while the
interstitium shows fine fibrosis & a few chronic inflammatory cells
48. Chronic Glomerulonephritis
CLINICAL FEATURES
• The patients are usually adults
• characterised by hypertension, uraemia & progressive deterioration
of renal function
• variety of systemic manifestations of uraemia
• These patients eventually die if they do not receive a renal transplant