Rapidly Progressive Glomerulonephritis , RPGN, Crescentic GN, Extracapillary GN)
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Rapidly progressive glomerulonephritis (RPGN) is characterized by the rapid formation of "crescents" outside the glomerular capillaries that leads to acute kidney failure within weeks or months. It is categorized based on etiology into 3 groups - RPGN associated with systemic diseases, post-infectious RPGN caused by immune complexes, and pauci-immune RPGN. The post-infectious type is identified by crescents forming adhesions between the glomerular tuft and Bowman's capsule, with glomerular hypercellularity and leukocyte infiltration. Prognosis for RPGN is generally poor, though post-infectious cases have a
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This document provides information on rapidly progressive glomerulonephritis (RPGN), including definitions, classifications, pathogenesis, clinical features, pathology, treatment, and epidemiology of the main types. It discusses anti-glomerular basement membrane glomerulonephritis, immune complex-mediated RPGN, and pauci-immune RPGN. The pathology and clinical presentation of each type is described. Treatment typically involves immunosuppression with corticosteroids and cyclophosphamide along with plasmapheresis in severe cases.
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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.
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Rapidly progressive glomerulonephritis
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function,[4][5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months)[5] with glomerular crescent formation seen in at least 50%[5] or 75%[4] of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure[6] and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents (crescent-shaped scars)
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- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
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- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
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Rpgn renal pathology- prof wadie
This document provides an overview of rapidly progressive glomerulonephritis (RPGN) for medical students. It defines RPGN as a clinical syndrome characterized by rapid loss of renal function within 3 months. RPGN can be classified into 3 types based on pathogenesis and immunofluorescence patterns. Type I involves anti-GBM antibodies. Type II features immune complex deposition. Type III, also called pauci-immune RPGN, features neutrophil activation in response to ANCA but no immune complex deposition or anti-GBM antibodies. The diagnosis of RPGN relies on renal biopsy identifying crescents on microscopy along with urine and serum analysis.
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A 12-year-old boy presented with fever, edema, and decreased urine output. He was diagnosed with mesangiocapillary glomerulonephritis (GN) with cellular crescents based on investigations showing hematuria, proteinuria, hypertension, and renal biopsy. He was initially treated with calcium channel blockers, ACE inhibitors, and methylprednisolone + cyclophosphamide IV. His renal function improved and he was discharged on azathioprine and prednisone for maintenance. At last follow up 34 months later, he had normal renal function while continuing immunosuppressants, indicating a good prognosis with aggressive treatment.
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Patient history
Clinical features
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Investigation
Treatment
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- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Approach to Nephritic Syndrome
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
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Hepatorenal
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This document discusses the approach to nephrotic syndrome. It describes the case of a 15-year old male patient presenting with swelling of the face and limbs and decreased urine output. Examinations and investigations revealed nephrotic syndrome. A renal biopsy showed membranoproliferative glomerulonephritis. The document then discusses nephrotic syndrome including definitions, classifications of primary and secondary causes, diagnostic workup including renal biopsy, complications of renal biopsy, and treatment approach.
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Minimal change disease
Minimal Change Disease (MCD), also known as Minimal Change Nephropathy, is a kidney disorder characterized by diffuse effacement and loss of foot processes in the glomeruli seen on electron microscopy. It is the most common cause of nephrotic syndrome in children aged 1-7 years and accounts for about 90% of cases. Boys are more commonly affected than girls. MCD is thought to be caused by an abnormal immune response involving T-cells and cytokines that damages the glomerular filtration barrier. This results in proteinuria but no significant pathology on light microscopy. The clinical features include nephrotic syndrome. The prognosis is generally good as over 90% will respond to corticosteroid therapy
APPROACH TO PANCYTOPENIA
Prepared by Dr Narendra Singh Resident Doctor General Medicine GSVM Medical College and LLRH Hospital Kanpur U.P.
Approach to pancytopenia
This document provides an overview of pancytopenia, including definitions, common causes, clinical evaluation, and diagnostic approach. Pancytopenia is defined as a reduction in all three blood cell lines. The evaluation involves obtaining a complete blood count with peripheral smear, bone marrow aspiration and biopsy, and specific tests depending on findings. The bone marrow examination can help differentiate causes based on cellularity and features seen in erythropoiesis, myelopoiesis, megakaryopoiesis and other cell types. Common causes include bone marrow failure, infiltrative disorders, infections, immune disorders and nutritional deficiencies. A thorough history, examination and systematic evaluation of the bone marrow are required to identify the underlying cause of pancy
Sickle cell disease
The patient is a 20-year-old male with sickle cell disease who presents with several chronic and acute complications. He has a history of delayed puberty, joint pain, weakness and cough. Examination reveals decreased growth, severe anemia, leg ulcers, enlarged spleen and fever. Laboratory tests show hemoglobin of 8g/dL and reticulocyte count of 25%. The most probable cause of the patient's problems is sickle cell disease and its associated complications. The patient is at risk for further complications such as acute chest syndrome, stroke and infection due to his condition.
Minimal Change Disease
Minimal Change Disease (MCD) is a type of nephrotic syndrome characterized by proteinuria and swelling without significant findings on light microscopy. It is caused by a circulating permeability factor that leads to foot process effacement on electron microscopy. MCD is most common in children and responds well to steroid treatment, though relapses are common. Second line treatments include cyclophosphamide or rituximab if relapses are frequent or the patient is steroid dependent.
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This document discusses thrombocytopenia (low platelet count) and its causes and evaluation. It describes the normal physiology of platelets and hemostasis. Common causes of thrombocytopenia include decreased platelet production (bone marrow problems), increased platelet destruction (immune mechanisms like ITP), and increased consumption (DIC). Evaluation involves history, exam, blood smear review, and identifying potential causes like drugs, infections, malignancies or autoimmune disorders. Specific conditions discussed in detail include ITP, HIT, DIC, and thrombocytopenia in cardiac patients.
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This document provides an overview of rapidly progressive glomerulonephritis (RPGN) for medical students. It defines RPGN as a clinical syndrome characterized by rapid loss of renal function within 3 months. RPGN can be caused by immune complex deposition or associated with anti-neutrophil cytoplasmic antibodies. The document classifies RPGN into 3 types - type I involves anti-GBM antibodies, type II immune complex deposition, and type III is pauci-immune and associated with ANCA-associated vasculitis. The diagnosis of RPGN involves renal biopsy showing crescents, elevated creatinine and urea, hematuria and proteinuria on urine examination.
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Rapidly progressive glomerulonephritis (RPGN) is characterized by the rapid formation of "crescents" outside the glomerular capillaries that leads to acute kidney failure within weeks or months. It is categorized based on etiology into 3 groups - RPGN associated with systemic diseases like anti-GBM disease, post-infectious RPGN caused by immune complexes, and pauci-immune RPGN. The prognosis for RPGN is generally poor but post-infectious cases have a somewhat better outcome and potential for recovery.
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This document provides an overview of rapidly progressive glomerulonephritis (RPGN) for medical students. It defines RPGN as a clinical syndrome characterized by rapid loss of renal function within 3 months. RPGN can be classified into 3 types based on pathogenesis and immunofluorescence patterns. Type I involves anti-GBM antibodies. Type II features immune complex deposition. Type III, also called pauci-immune RPGN, features neutrophil activation in response to ANCA but no immune complex deposition or anti-GBM antibodies. The diagnosis of RPGN relies on renal biopsy identifying crescents on microscopy along with urine and serum analysis.
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- The pathogenesis involves immunological mechanisms like antibody-mediated immune complex deposition, as well as non-immunological mechanisms. Injury
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1) Acute nephritic syndrome is characterized by sudden onset of hypertension, hematuria, mild to moderate proteinuria, and red blood cell casts. It is caused by acute glomerular inflammation and results in a fall in GFR and renal failure.
2) Rapidly progressive glomerulonephritis (RPGN) similarly presents with renal failure over weeks to months along with nephritic urinary sediment and proteinuria.
3) The main categories of acute nephritic syndrome and RPGN are immune complex mediated, anti-GBM antibody mediated, and pauci-immune mediated glomerulonephritis. A renal biopsy is needed for diagnosis.
RPGN in Children.pptx
A 5-year-old female presented with respiratory distress, hemoptysis, dark urine, and decreased urine output. Laboratory findings showed kidney dysfunction and a positive myeloperoxidase antibody. This suggests a diagnosis of pauci-immune rapidly progressive glomerulonephritis likely caused by anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
Rapidly progressive glomerulonephritis.pptx
Rapidly progressive glomerulonephritis (RPGN) is a type of nephritic syndrome characterized by extensive glomerular crescent formation in over 50% of glomeruli that can progress to end-stage renal disease within weeks to months if untreated. It has several etiologies including post-infectious, autoimmune, drug-induced, and underlying connective tissue diseases. Clinically it presents with hematuria, proteinuria, renal dysfunction and can involve pulmonary hemorrhage. Diagnosis involves lab tests, serology and renal biopsy showing immune complex or antibody deposition. Treatment aims to suppress inflammation and immune response with corticosteroids, immunosuppressants, and plasma exchange depending on
clinical approach to Rapidly Progressive Glomerulonephritis
This document discusses rapidly progressive glomerulonephritis (RPGN). It begins by describing the original use of the term RPGN and the discovery of anti-glomerular basement membrane (GBM) antibody's role in Goodpasture syndrome. It then discusses three main types of RPGN - anti-GBM antibody disease, immune complex disease, and pauci-immune disease. The document provides details on the clinical presentation, pathogenesis, treatment and prognosis of each type. It highlights that plasmapheresis and immunosuppression can benefit 40-45% of patients with anti-GBM antibody RPGN by preventing progression to end-stage renal disease or death.
Glomerulonephritis at a glance
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.
Ac nephritic synd
Acute nephritic syndrome is characterized by inflammation of the glomeruli that can damage the basement membrane. It is typically caused by a preceding streptococcal infection. The classic presentation includes hematuria, edema, and hypertension. Workup involves renal function tests, urinalysis showing hematuria and proteinuria, and evidence of prior streptococcal infection via antibody titers. Treatment is symptomatic with diuretics for edema and blood pressure control. Renal biopsy may be needed if atypical or persistent features are present.
Primary glomerulonephritis
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.
ANTI GBM DISEASE final hellllo hiiiii.pptx
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
5 1093438501069783057
Rapidly progressive glomerulonephritis (RPGN) is characterized by a rapid loss of renal function over a short period of time. It is classified as primary or secondary RPGN based on its underlying causes. The pathogenesis involves crescent formation in glomeruli due to proliferation of cells and inflammation. Clinically, it presents with hematuria, proteinuria, hypertension, and declining kidney function. Diagnosis involves lab tests showing abnormalities in urine, blood counts, complement levels, and antibodies. Renal biopsy revealing crescentic lesions in glomeruli is diagnostic. Treatment depends on the specific type but often includes steroids, plasmapheresis and cyclophosphamide to slow kidney damage. Prognosis depends
Glomerulonephritis.pptx..................
Glomerulonephritis refers to inflammation of the glomeruli in the kidney. It can be caused by various factors like infections, autoimmune diseases, or genetic conditions. Patients may experience symptoms like blood or protein in the urine. Diagnosis involves urinalysis, kidney biopsy, and tests for antibodies. Treatment depends on the underlying cause and severity of symptoms, but often includes medications to reduce inflammation and protect kidney function. The prognosis can range from spontaneous remission to progressive kidney damage and failure.
Lupus Nephritis-Diagnosis and management
Based on the information provided, the most likely diagnosis is:
Behçet's disease.
Key characteristics that support this diagnosis include:
- Recurring rash on the face, arms and hands. Rash is a common manifestation of Behçet's disease.
- Painless mouth ulcers. Oral ulcers are a hallmark feature seen in over 90% of patients with Behçet's disease.
- No other medical conditions reported. Behçet's disease typically presents in otherwise healthy young adults.
- Sexual activity mentioned. Behçet's disease has been associated with sexual transmission in some cases.
Other conditions that can cause mouth ul
glomerulonephritis (5).pptx
1) Glomerulonephritis refers to inflammation of the glomeruli in the kidney that can be caused by various immune-mediated mechanisms.
2) It is characterized by hematuria, proteinuria, and reduced kidney function. On biopsy, it shows immune complex deposition, thickening of the glomerular basement membrane, and cellular proliferation within the glomerular tuft.
3) There are different clinical presentations including asymptomatic urinary abnormalities, acute glomerulonephritis, rapidly progressive glomerulonephritis, nephrotic syndrome, and chronic glomerulonephritis. The pathology and treatment varies depending on the specific type and cause of glomerulonephritis.
Lupus nephritis nids
Lupus nephritis is a serious manifestation of systemic lupus erythematosus where the kidneys are damaged. It is characterized by autoantibodies that form immune complexes and deposit in the glomeruli, causing inflammation. A renal biopsy is required for diagnosis and classification. Treatment depends on the class, with classes III and IV requiring aggressive immunosuppression including corticosteroids and other agents to reduce inflammation and prevent loss of renal function. Factors like genetics, estrogen, and ultraviolet light exposure are believed to contribute to lupus development.
NEPHRITIC SYNDROME. Clinical Manifestations
Etiology- genetic mutations, infection, toxin exposure, autoimmunity, atherosclerosis, hypertension, emboli, thrombosis, or diabetes mellitus.
Even after careful study, however, the cause often remains unknown, and the lesion is called idiopathic.
Inflammation of the glomerular capillaries is called glomerulonephritis.
Persistent glomerulonephritis that worsens renal function is always accompanied by interstitial nephritis, renal fibrosis, and tubular atrophy.
Similar to Rapidly Progressive Glomerulonephritis , RPGN, Crescentic GN, Extracapillary GN) (20)
The KIDNEY: Rapidly Progressive Glomerulonephritis
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Renal pathology lecture 6 Rapid Progressive Glomerulonephritis & Chronic Kidn...
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clinical approach to Rapidly Progressive Glomerulonephritis
clinical approach to Rapidly Progressive Glomerulonephritis
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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.
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Pathogenesis of Cell Injury
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.
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FIRST GENERATION ANTIHISTAMINICS-
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Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
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These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
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Rapidly Progressive Glomerulonephritis , RPGN, Crescentic GN, Extracapillary GN)
- 1. The KIDNEY - RPGN DR. ROOPAM JAIN PROFESSOR & HEAD, PATHOLOGY
- 2. Rapidly Progressive Glomerulonephritis (Synonyms: RPGN, Crescentic GN, Extracapillary GN)
- 3. 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.
- 4. 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)
- 5. Distinguishing features of 3 main categories of RPGN
- 7. 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.
- 8. RPGN diagrammatic representation of ultrastructure of a portion of glomerular lobule showing epithelial crescent formation & subepithelial granular deposits.
- 9. 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.