This document provides information about renal biopsy procedures and pathological interpretation of renal biopsy specimens. It discusses the history and indications for renal biopsy. It describes the procedure, including contraindications, complications, and post-biopsy care. It explains how biopsies are evaluated with light microscopy, immunofluorescence, and electron microscopy. Key terms used to describe histological lesions in the glomeruli, tubules, interstitium, and blood vessels are defined. The document emphasizes the importance of integrating clinical and pathological findings for an accurate diagnosis.
Renal amyloidosis is a condition where an abnormal protein called amyloid builds up in the kidneys. This causes damage to the kidneys and can lead to kidney failure. There are different types of amyloidosis including AL, AA, and hereditary amyloidosis. AL amyloidosis occurs when the bone marrow produces too much of a certain antibody protein. AA amyloidosis develops with chronic infections or inflammatory diseases. Hereditary amyloidosis is genetic and often affects the nerves and kidneys. A biopsy of the affected tissue is usually needed to diagnose amyloidosis. Treatment focuses on decreasing the amyloid-forming protein through drugs, dialysis, or transplant depending on organ involvement.
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.
Approach to the patient with Glomerular Disease.Sufindc
The document discusses the approach to patients with glomerular disease. It describes the structure and function of the glomerulus and capillaries. Common causes of glomerular disease include genetic mutations, infections, autoimmunity, hypertension, and diabetes. Key clinical syndromes are nephritic syndrome, nephrotic syndrome, basement membrane syndrome, glomerular-vascular syndrome, and infectious disease-associated syndrome. The initial workup involves a history, physical exam, urinalysis, and blood tests to help classify the glomerular disease.
This PPT contains only a brief summery about ATN.
for more information about the topic please refer to the book and site found the ppt, or you can get In touch with me .
Nephritis refers to inflammation of the kidneys that can be caused by various factors like infection, autoimmune disease, or kidney disease. It affects the glomeruli, tubules, or surrounding tissue and can lead to impaired kidney function. Symptoms vary depending on the specific type and cause of nephritis but may include blood or protein in the urine, high blood pressure, swelling, and changes in kidney function test results. Treatment involves addressing the underlying cause, managing complications, and potentially using medications, dietary changes, or dialysis.
This document provides tips for using a PowerPoint presentation (PPT) for active learning sessions. Some key points:
- Slides can be freely downloaded, edited, and modified.
- Many slides will be blank except for the title to engage students. The presenter will show a blank slide, ask students what they know about the topic, and then show the content slide.
- This approach will be repeated for three revisions to reinforce learning.
- It can also be used for self-study by viewing blank slides and thinking about the topic before reading the content slide.
The document recommends using this interactive technique to actively involve students and support repeated learning through multiple iterations of showing blank slides and
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
Renal amyloidosis is a condition where an abnormal protein called amyloid builds up in the kidneys. This causes damage to the kidneys and can lead to kidney failure. There are different types of amyloidosis including AL, AA, and hereditary amyloidosis. AL amyloidosis occurs when the bone marrow produces too much of a certain antibody protein. AA amyloidosis develops with chronic infections or inflammatory diseases. Hereditary amyloidosis is genetic and often affects the nerves and kidneys. A biopsy of the affected tissue is usually needed to diagnose amyloidosis. Treatment focuses on decreasing the amyloid-forming protein through drugs, dialysis, or transplant depending on organ involvement.
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.
Approach to the patient with Glomerular Disease.Sufindc
The document discusses the approach to patients with glomerular disease. It describes the structure and function of the glomerulus and capillaries. Common causes of glomerular disease include genetic mutations, infections, autoimmunity, hypertension, and diabetes. Key clinical syndromes are nephritic syndrome, nephrotic syndrome, basement membrane syndrome, glomerular-vascular syndrome, and infectious disease-associated syndrome. The initial workup involves a history, physical exam, urinalysis, and blood tests to help classify the glomerular disease.
This PPT contains only a brief summery about ATN.
for more information about the topic please refer to the book and site found the ppt, or you can get In touch with me .
Nephritis refers to inflammation of the kidneys that can be caused by various factors like infection, autoimmune disease, or kidney disease. It affects the glomeruli, tubules, or surrounding tissue and can lead to impaired kidney function. Symptoms vary depending on the specific type and cause of nephritis but may include blood or protein in the urine, high blood pressure, swelling, and changes in kidney function test results. Treatment involves addressing the underlying cause, managing complications, and potentially using medications, dietary changes, or dialysis.
This document provides tips for using a PowerPoint presentation (PPT) for active learning sessions. Some key points:
- Slides can be freely downloaded, edited, and modified.
- Many slides will be blank except for the title to engage students. The presenter will show a blank slide, ask students what they know about the topic, and then show the content slide.
- This approach will be repeated for three revisions to reinforce learning.
- It can also be used for self-study by viewing blank slides and thinking about the topic before reading the content slide.
The document recommends using this interactive technique to actively involve students and support repeated learning through multiple iterations of showing blank slides and
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
This document discusses various glomerular diseases. It begins with definitions of terms like acute renal failure, chronic renal failure, azotemia and uremia. It then describes different types of glomerular diseases like nephritic syndrome, nephrotic syndrome, acute proliferative glomerulonephritis, rapidly progressive glomerulonephritis and their characteristic features. The document contains detailed information on acute post-streptococcal glomerulonephritis including its etiology, morphology, clinical features and prognosis. Histopathological findings and classifications of various glomerular diseases are also summarized.
This document defines and describes different types of vasculitis. It begins by defining vasculitis as inflammation of blood vessel walls. The two main ways of classifying vasculitides are by the size of blood vessels involved and the presence or absence of ANCA. Small vessel vasculitis can be ANCA-positive (e.g. Wegener's granulomatosis, Churg-Strauss syndrome) or ANCA-negative (e.g. Henoch-Schönlein purpura). Medium vessel vasculitides include polyarteritis nodosa and Kawasaki's disease. Large vessel vasculitides include giant cell arteritis, Takayasaki's disease, and poly
Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatologic disease in children. It is classified into several subtypes based on symptoms and physical exam findings. Oligoarticular JIA affects 4 or fewer joints, typically large weight-bearing joints. Polyarticular JIA affects 5 or more joints within the first 6 months. Systemic onset JIA is characterized by spiking fevers and rash. Physical exam may reveal synovitis, limited range of motion, and joint swelling. Screening for uveitis is important for some subtypes.
This document summarizes statin-induced myopathies. It discusses statin mechanisms of action and predisposing factors. It describes different clinical phenotypes including rhabdomyolysis, myalgia with mild CK elevation, self-limited toxic myopathy, and immune-mediated necrotizing myopathy associated with anti-HMGCR antibodies. Immune-mediated necrotizing myopathy is characterized by muscle necrosis, regeneration, and scarce inflammation. Diagnosis involves detecting elevated CK, myopathic EMG findings, and anti-HMGCR antibodies. Treatment depends on severity but may include immunosuppression.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
This document provides an overview of glomerular diseases. It begins by describing the anatomy of the nephron and glomerulus. It then discusses the cells that make up the glomerular filtration membrane and defines glomerular diseases as abnormalities in glomerular function caused by damage to glomerular components like the epithelium, basement membrane, or endothelium. Primary and secondary glomerular diseases are distinguished. Immunological and non-immunological mechanisms of glomerular injury are also summarized. Specific glomerular diseases like membranoproliferative glomerulonephritis, minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, IgA nep
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.
There are several causes for purpuras..... How to clinically approach a patient with purpuric rash???? List of investigations which are helpful in reaching upto the clinical diagnosis....
This document provides an overview of hematuria and glomerular causes of hematuria. It defines macroscopic and microscopic hematuria and discusses various glomerular diseases that can cause hematuria including IgA nephropathy, Alport syndrome, thin basement membrane disease, post-infectious glomerulonephritis, and Henoch–Schönlein purpura. It describes the clinical presentations, pathologies, diagnoses, and treatments of these conditions. Key investigations for glomerular hematuria are outlined.
Anemia is a major public health problem in India, especially among women and children. It can be caused by iron deficiency, vitamin B12 or folate deficiency, chronic illnesses, parasitic infections, and other factors. Common symptoms include fatigue, weakness, dizziness, and pale skin. Diagnosis involves blood tests to measure hemoglobin, red blood cell count, and other indicators. Treatment depends on the underlying cause but often involves dietary changes and iron supplements taken by mouth or via injection. Public health efforts are needed to prevent anemia through nutrition education, parasite control, and antenatal supplementation programs.
This document provides information on hydatid disease, which is caused by the parasitic tapeworm Echinococcus. It begins with a brief history of hydatid disease and descriptions of the Echinococcus species that cause it. It then discusses the life cycle of the parasite, passing between definitive hosts like dogs and intermediate hosts like sheep. Clinical features vary depending on the infected organ but may include abdominal pain or swelling. Diagnosis involves immunological tests and imaging modalities like ultrasound or CT. Untreated cases can lead to organ damage or failure.
Nephrotic syndrome is characterized by proteinuria (>3.5g/24hr), hypoalbuminemia, edema, and other issues. The proteinuria is caused by damage to the glomerular filtration barrier, and the other symptoms are secondary effects of protein loss in the urine. Nephrotic syndrome has potential complications including edema, hyperlipidemia, hypercoagulability, and infection risk. Management involves identifying the underlying cause, treating that cause if possible, controlling proteinuria with ACE inhibitors, and managing complications like edema and hyperlipidemia. Steroids are often used but renal biopsy is usually needed first in adults to guide treatment.
Prostatitis is inflammation of the prostate gland that is caused by infectious agents like bacteria or other conditions. There are four main types: acute bacterial prostatitis, chronic bacterial prostatitis, chronic prostatitis/chronic pelvic pain syndrome where the cause is unclear, and asymptomatic inflammatory prostatitis. Prostatitis causes symptoms like perineal pain and difficulty urinating and is most common in men under 50. Treatment involves antibiotics, alpha-blockers, pain medication, and sitz baths. Chronic forms are difficult to treat due to poor antibiotic diffusion into prostatic fluid.
1. Prostatitis is an inflammation of the prostate gland that can be acute or chronic and is caused by bacterial or non-bacterial factors.
2. It is classified into four categories including acute bacterial, chronic bacterial, chronic pelvic pain syndrome, and asymptomatic inflammatory types.
3. Symptoms vary depending on the type but can include urinary issues, pain, and sexual dysfunction. Diagnosis involves urinalysis, urine culture, and examination of expressed prostatic secretions. Treatment focuses on antibiotics for bacterial infections and supportive care.
Goodpasture syndrome is characterized by the presence of auto-antibodies against the basement membrane of the lungs and kidneys, which causes inflammatory destruction. It was first described in 1919 and can involve either or both the kidneys and lungs. The antibodies specifically target the non-collagenous domains of the alpha-3 chain of collagen type 4, initiating inflammation in the basement membranes of the kidneys and lungs. Treatment involves plasmapheresis, corticosteroids, and immunosuppressive drugs like cyclophosphamide to remove the antibodies from circulation.
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
Appendicitis is a common condition in children that requires surgical removal of the appendix (appendectomy). It occurs when the appendix becomes blocked, usually by lymphoid hyperplasia or fecalith, leading to bacterial infection inside the appendix. This causes abdominal pain localized to the right lower quadrant. Left untreated, the infection and pressure can cause the appendix to perforate, spreading infection into the abdomen. An appendectomy is required once appendicitis is diagnosed to prevent perforation or treat one that has already occurred. Pre-operative resuscitation and antibiotics may be needed for severely infected patients before surgery.
IgA nephropathy (IgAN) is characterized by diffuse mesangial deposition of IgA. It is the most common primary glomerulonephritis worldwide. Clinical presentations vary from asymptomatic microscopic hematuria to gross hematuria, nephrotic syndrome, and acute kidney injury. Histologically, it ranges from isolated mesangial hypercellularity to endocapillary hypercellularity and crescents. Treatment involves supportive care like blood pressure control and ACE inhibitors. Immunosuppression may be considered for patients at high risk of progression despite supportive care. Two recent trials found no benefit of corticosteroids when supportive care was optimized.
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.
This document provides an overview of pleural effusions including definition, composition of pleural fluid, etiology, classification, symptoms, clinical findings, investigations and diagnosis, and management. Key points include that pleural effusions occur when fluid formation exceeds absorption or absorption is reduced. Etiologies include conditions that increase fluid formation or decrease absorption. Investigations include chest x-ray, thoracentesis, and analysis of pleural fluid. Management depends on the underlying cause and may include antibiotics, diuretics, chest tube placement, chemical pleurodesis, or VATS.
A renal biopsy is a procedure used to obtain renal tissue samples through a needle. The tissue is analyzed to diagnose underlying renal conditions ranging from infections to tumors. Indications for biopsy include unexplained kidney failure or dysfunction, nephrotic syndrome, and kidney masses. Complications can include bleeding or the formation of abnormal vessel connections. The biopsy samples are prepared and examined under the microscope using stains to identify structures and diagnose kidney diseases.
This document provides an overview of kidney biopsy procedures and pathological examination of biopsy samples. It discusses indications for kidney biopsy, techniques for performing native and transplant biopsies, post-biopsy care, adequacy of samples, transport and processing of samples. Microscopic examination of glomerular, vascular and tubulointerstitial features is described. Common abnormalities and lesions seen are outlined. Staining techniques, immunohistochemistry, immunofluorescence and interpretation of biopsy results are also summarized.
This document discusses various glomerular diseases. It begins with definitions of terms like acute renal failure, chronic renal failure, azotemia and uremia. It then describes different types of glomerular diseases like nephritic syndrome, nephrotic syndrome, acute proliferative glomerulonephritis, rapidly progressive glomerulonephritis and their characteristic features. The document contains detailed information on acute post-streptococcal glomerulonephritis including its etiology, morphology, clinical features and prognosis. Histopathological findings and classifications of various glomerular diseases are also summarized.
This document defines and describes different types of vasculitis. It begins by defining vasculitis as inflammation of blood vessel walls. The two main ways of classifying vasculitides are by the size of blood vessels involved and the presence or absence of ANCA. Small vessel vasculitis can be ANCA-positive (e.g. Wegener's granulomatosis, Churg-Strauss syndrome) or ANCA-negative (e.g. Henoch-Schönlein purpura). Medium vessel vasculitides include polyarteritis nodosa and Kawasaki's disease. Large vessel vasculitides include giant cell arteritis, Takayasaki's disease, and poly
Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatologic disease in children. It is classified into several subtypes based on symptoms and physical exam findings. Oligoarticular JIA affects 4 or fewer joints, typically large weight-bearing joints. Polyarticular JIA affects 5 or more joints within the first 6 months. Systemic onset JIA is characterized by spiking fevers and rash. Physical exam may reveal synovitis, limited range of motion, and joint swelling. Screening for uveitis is important for some subtypes.
This document summarizes statin-induced myopathies. It discusses statin mechanisms of action and predisposing factors. It describes different clinical phenotypes including rhabdomyolysis, myalgia with mild CK elevation, self-limited toxic myopathy, and immune-mediated necrotizing myopathy associated with anti-HMGCR antibodies. Immune-mediated necrotizing myopathy is characterized by muscle necrosis, regeneration, and scarce inflammation. Diagnosis involves detecting elevated CK, myopathic EMG findings, and anti-HMGCR antibodies. Treatment depends on severity but may include immunosuppression.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
This document provides an overview of glomerular diseases. It begins by describing the anatomy of the nephron and glomerulus. It then discusses the cells that make up the glomerular filtration membrane and defines glomerular diseases as abnormalities in glomerular function caused by damage to glomerular components like the epithelium, basement membrane, or endothelium. Primary and secondary glomerular diseases are distinguished. Immunological and non-immunological mechanisms of glomerular injury are also summarized. Specific glomerular diseases like membranoproliferative glomerulonephritis, minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, IgA nep
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.
There are several causes for purpuras..... How to clinically approach a patient with purpuric rash???? List of investigations which are helpful in reaching upto the clinical diagnosis....
This document provides an overview of hematuria and glomerular causes of hematuria. It defines macroscopic and microscopic hematuria and discusses various glomerular diseases that can cause hematuria including IgA nephropathy, Alport syndrome, thin basement membrane disease, post-infectious glomerulonephritis, and Henoch–Schönlein purpura. It describes the clinical presentations, pathologies, diagnoses, and treatments of these conditions. Key investigations for glomerular hematuria are outlined.
Anemia is a major public health problem in India, especially among women and children. It can be caused by iron deficiency, vitamin B12 or folate deficiency, chronic illnesses, parasitic infections, and other factors. Common symptoms include fatigue, weakness, dizziness, and pale skin. Diagnosis involves blood tests to measure hemoglobin, red blood cell count, and other indicators. Treatment depends on the underlying cause but often involves dietary changes and iron supplements taken by mouth or via injection. Public health efforts are needed to prevent anemia through nutrition education, parasite control, and antenatal supplementation programs.
This document provides information on hydatid disease, which is caused by the parasitic tapeworm Echinococcus. It begins with a brief history of hydatid disease and descriptions of the Echinococcus species that cause it. It then discusses the life cycle of the parasite, passing between definitive hosts like dogs and intermediate hosts like sheep. Clinical features vary depending on the infected organ but may include abdominal pain or swelling. Diagnosis involves immunological tests and imaging modalities like ultrasound or CT. Untreated cases can lead to organ damage or failure.
Nephrotic syndrome is characterized by proteinuria (>3.5g/24hr), hypoalbuminemia, edema, and other issues. The proteinuria is caused by damage to the glomerular filtration barrier, and the other symptoms are secondary effects of protein loss in the urine. Nephrotic syndrome has potential complications including edema, hyperlipidemia, hypercoagulability, and infection risk. Management involves identifying the underlying cause, treating that cause if possible, controlling proteinuria with ACE inhibitors, and managing complications like edema and hyperlipidemia. Steroids are often used but renal biopsy is usually needed first in adults to guide treatment.
Prostatitis is inflammation of the prostate gland that is caused by infectious agents like bacteria or other conditions. There are four main types: acute bacterial prostatitis, chronic bacterial prostatitis, chronic prostatitis/chronic pelvic pain syndrome where the cause is unclear, and asymptomatic inflammatory prostatitis. Prostatitis causes symptoms like perineal pain and difficulty urinating and is most common in men under 50. Treatment involves antibiotics, alpha-blockers, pain medication, and sitz baths. Chronic forms are difficult to treat due to poor antibiotic diffusion into prostatic fluid.
1. Prostatitis is an inflammation of the prostate gland that can be acute or chronic and is caused by bacterial or non-bacterial factors.
2. It is classified into four categories including acute bacterial, chronic bacterial, chronic pelvic pain syndrome, and asymptomatic inflammatory types.
3. Symptoms vary depending on the type but can include urinary issues, pain, and sexual dysfunction. Diagnosis involves urinalysis, urine culture, and examination of expressed prostatic secretions. Treatment focuses on antibiotics for bacterial infections and supportive care.
Goodpasture syndrome is characterized by the presence of auto-antibodies against the basement membrane of the lungs and kidneys, which causes inflammatory destruction. It was first described in 1919 and can involve either or both the kidneys and lungs. The antibodies specifically target the non-collagenous domains of the alpha-3 chain of collagen type 4, initiating inflammation in the basement membranes of the kidneys and lungs. Treatment involves plasmapheresis, corticosteroids, and immunosuppressive drugs like cyclophosphamide to remove the antibodies from circulation.
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
Appendicitis is a common condition in children that requires surgical removal of the appendix (appendectomy). It occurs when the appendix becomes blocked, usually by lymphoid hyperplasia or fecalith, leading to bacterial infection inside the appendix. This causes abdominal pain localized to the right lower quadrant. Left untreated, the infection and pressure can cause the appendix to perforate, spreading infection into the abdomen. An appendectomy is required once appendicitis is diagnosed to prevent perforation or treat one that has already occurred. Pre-operative resuscitation and antibiotics may be needed for severely infected patients before surgery.
IgA nephropathy (IgAN) is characterized by diffuse mesangial deposition of IgA. It is the most common primary glomerulonephritis worldwide. Clinical presentations vary from asymptomatic microscopic hematuria to gross hematuria, nephrotic syndrome, and acute kidney injury. Histologically, it ranges from isolated mesangial hypercellularity to endocapillary hypercellularity and crescents. Treatment involves supportive care like blood pressure control and ACE inhibitors. Immunosuppression may be considered for patients at high risk of progression despite supportive care. Two recent trials found no benefit of corticosteroids when supportive care was optimized.
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.
This document provides an overview of pleural effusions including definition, composition of pleural fluid, etiology, classification, symptoms, clinical findings, investigations and diagnosis, and management. Key points include that pleural effusions occur when fluid formation exceeds absorption or absorption is reduced. Etiologies include conditions that increase fluid formation or decrease absorption. Investigations include chest x-ray, thoracentesis, and analysis of pleural fluid. Management depends on the underlying cause and may include antibiotics, diuretics, chest tube placement, chemical pleurodesis, or VATS.
A renal biopsy is a procedure used to obtain renal tissue samples through a needle. The tissue is analyzed to diagnose underlying renal conditions ranging from infections to tumors. Indications for biopsy include unexplained kidney failure or dysfunction, nephrotic syndrome, and kidney masses. Complications can include bleeding or the formation of abnormal vessel connections. The biopsy samples are prepared and examined under the microscope using stains to identify structures and diagnose kidney diseases.
This document provides an overview of kidney biopsy procedures and pathological examination of biopsy samples. It discusses indications for kidney biopsy, techniques for performing native and transplant biopsies, post-biopsy care, adequacy of samples, transport and processing of samples. Microscopic examination of glomerular, vascular and tubulointerstitial features is described. Common abnormalities and lesions seen are outlined. Staining techniques, immunohistochemistry, immunofluorescence and interpretation of biopsy results are also summarized.
This document provides an overview of kidney biopsy procedures and pathological examination of biopsy samples. It discusses indications for kidney biopsy, techniques for performing native and transplant biopsies, post-biopsy care, adequacy of samples, and transportation of samples. It also describes examination of samples including staining, microscopy, immunohistochemistry, and interpretation. Key abnormalities that can be seen including glomerular, vascular, tubular, and interstitial lesions are summarized.
This document discusses renal biopsy procedures and indications. It provides details on the history and technique of renal biopsy. Key points include that renal biopsy can provide a diagnosis in over 95% of patients with a complication rate of less than 0.1%. An adequate biopsy sample contains 10-15 glomeruli. Tissue is divided for light microscopy, immunofluorescence, and electron microscopy. Complications include hematuria and pain in 3-4% of patients. Indications for biopsy include nephrotic syndrome, acute kidney injury, systemic diseases affecting the kidneys, and unexplained chronic kidney disease.
This document discusses renal biopsy procedures and indications. It provides details on the history and technique of renal biopsy. Key points include that renal biopsy can provide a diagnosis in over 95% of patients with a complication rate of less than 0.1%. An adequate biopsy sample contains 10-15 glomeruli. Tissue is divided for light microscopy, immunofluorescence, and electron microscopy. Complications include hematuria and pain in 3-4% of patients. Indications for biopsy include nephrotic syndrome, acute kidney injury, systemic diseases affecting the kidneys, and unexplained chronic kidney disease.
This document discusses renal biopsy procedures. It provides details on the history, technique, adequacy, contraindications, complications and indications for renal biopsy. Some key points include:
- Renal biopsy has evolved since the 1950s and can now provide a tissue diagnosis in over 95% of patients with a life-threatening complication rate of less than 0.1%.
- An adequate biopsy sample contains 10-15 glomeruli and provides samples for histology, immunofluorescence and electron microscopy.
- Contraindications include bleeding diathesis and inability to comply with instructions. Relative contraindications include hypertension and infection.
- Complications are rare but can include hematuria, pain, and rarely death from
This document provides information on interpreting renal biopsies. It begins with the anatomy and location of the kidneys. It then discusses the history and development of renal biopsy techniques. The main indications for kidney biopsy are listed as nephrotic syndrome, acute renal failure, chronic renal failure, hematuria, asymptomatic proteinuria, and transplant. The document outlines the procedure for native and transplant kidney biopsies. Key pathology findings are described for various glomerular diseases including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, C1q nephropathy, and more. Interpretation of biopsy samples and electron microscopy are also discussed.
This document discusses renal biopsy procedures. It begins with definitions and history of renal biopsies. The aim is to determine the cause, severity, and treatment of kidney disorders and the procedure provides a diagnosis in over 95% of cases. Indications include nephrotic syndrome, atypical nephrotic features in children, acute or progressive renal failure, and transplant dysfunction. Contraindications include refusal, bleeding disorders, infections, and anatomical abnormalities. The procedure involves ultrasound-guided collection of tissue samples for analysis. Patients are monitored afterwards for pain and bleeding complications, which are usually minor.
The document provides information on hydatid cyst of the liver caused by the larva of the dog tapeworm Echinococcus granulosus. It discusses the life cycle of the parasite, symptoms, investigations including imaging techniques, classification of cysts, treatment options including surgery, percutaneous drainage (PAIR procedure), and chemotherapy. PAIR involves puncturing the cyst, injecting a scolicidal agent, and reaspirating the contents to treat the cyst minimally invasively.
The document discusses hydatid cyst of the liver caused by the larva of the dog tapeworm Echinococcus granulosus. It summarizes the life cycle, pathology, clinical features, investigations including imaging techniques, and treatment options for hydatid cyst. Treatment options include medical treatment with albendazole, percutaneous drainage using the PAIR technique, endoscopic management for biliary involvement, and surgical options. PAIR involves puncturing the cyst under imaging guidance, injecting a scolicidal agent, and reaspirating the contents.
Renal biopsy is a procedure used to obtain a small piece of kidney tissue to examine under a microscope in order to diagnose the specific cause of kidney disease or damage. Some key points:
- Renal biopsy has been performed since the 1930s and modern techniques now use real-time ultrasound guidance.
- Indications for renal biopsy include nephrotic syndrome, acute kidney injury, unexplained chronic kidney disease, and renal transplant dysfunction.
- Complications can include bleeding, but are usually minor. The patient must follow post-biopsy monitoring and restrictions like bed rest to reduce risks.
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.
This document provides an overview of lymphoma, including:
- Lymphoma is a heterogeneous group of neoplasms originating from lymphoid tissue that are divided into Hodgkin's and non-Hodgkin's lymphoma.
- The lymphoid system includes central (bone marrow, thymus) and peripheral (lymph nodes, spleen, mucosa-associated lymphoid tissue) tissues.
- Hodgkin's lymphoma is characterized by the presence of Reed-Sternberg cells and is typically diagnosed based on lymph node biopsy and staging. Treatment involves radiation, chemotherapy, or a combination.
- Non-Hodgkin's lymphomas are more diverse and have
This document provides information about renal biopsy procedures. It defines a renal biopsy as a procedure where renal tissue is obtained from the kidney using a biopsy gun under ultrasound guidance. It lists the indications for biopsy as hematuria, proteinuria, unexplained kidney failure, and diagnosing glomerular diseases. The pre-operative preparation, procedure, and post-operative care are described. Potential complications include pain, hemorrhage, infection, and incorrect tissue acquisition, though death is rare at 0.02%.
This document provides information about bone marrow examination. It discusses:
1. Bone marrow is located within bone cavities and contains hematopoietic cells, sinusoids, fibroblasts, fat cells, and macrophages. There are two types - red (active) marrow and yellow marrow.
2. Hematopoietic cells are arranged between sinusoids and supported by fibroblasts. Erythroid precursors cluster near sinusoids while granulocytes are near bone. Megakaryocytes are near sinusoid walls.
3. Bone marrow aspiration and biopsy are the main examination methods and each provides different information. Aspiration assesses cell morphology while biopsy studies architecture and fibrosis. Indications
Histology of Renal Tubule and its Variation in relation to FunctionSaran A K
The structural and functional unit of kidney, the nephron is highly specialized in view of its function. Here we look at the various histological variations/modification in relation to its function of the Renal Tubule
Intravenous urography and its modifications.pptx 01SUJAN KARKI
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
3. Background
• The first published report of the use of kidney biopsy in the
diagnosis of medical kidney disease was in 1951.
• Before this, although clinicians recognized clinical syndromes
such as acute nephritis, nephrosis, asymptomatic hematuria,
and chronic kidney failure, how these related to distinct
pathologic processes remained obscure.
• Over the past 50years, renal pathology has evolved gradually
and, by the turn of the century, our ability to diagnose kidney
disease outstripped our knowledge of pathogenesis.
4. Contd.
The kidney biopsy is an effective, valuable and safe procedure
that provides insight into the:
1. Diagnosis of kidney disease,
2. Assess prognosis,
3. Monitor disease progression,
4. Aid in the selection of therapy and
5. Follow the response to treatment.
6. Contraindication
Absolute
1. Sepsis,
2.Severe uncontrolled hypertension,
3. A hemorrhagic diathesis,
4. Known or suspected renal
parenchymal infection or malignancy,
5. Solitary ectopic or horseshoe
kidney (except the transplanted
kidney),
6. Patient who is uncooperative.
7. Acute pyelonephritis/perinephritic
abscess
8. Uremia
Relative
Platelet dysfunction often can be
corrected by administration of
desmopressin (DDAVP) which is a
vasopressin analogue that stimulates
platelet aggregation.
Hypertension may represent a
relative contraindication, assuming it
is brought under adequate control
before the biopsy procedure.
7. Pre–kidney biopsy evaluation.
Counseling and consent from parents
History
Bleeding diathesis, allergy to agent
Use of aspirin, NSAIDs, H/O HTN
Physical examination
• Blood pressure
• Biopsy site assessment
Laboratory evaluation
• CBC,BT, CT, PT, blood grouping, HBsAg, Anti-HCV
• Urine R/E, C/S
Ultrasonography of KUB
8. Contd.
Special attention
1. If child on oral anticoagulants, anti-platelet agents or NSAIDs
should be stopped 7 days before biopsy and will restart after
1-2 weeks after biopsy.
2. If child on HD, renal biopsy should performed at least 6
hours after haemodialysis and halt heparin for next 24
hours.
3. A18 gauze needle is used in newborn or infant and in
allograft kidney biopsy. Allograft biopsy approach is from
anterior abdominal wall.
9. Contd.
Biopsy
equipments
• Biopsy gun
• Two test
tubes
• Others
Medicine
• Midazolam
• 2% Lignocaine
• Emergency
medicines
Procedure
• Prone
position,
pillow/sand
bag under
abdomen
• Left kidney
Post biopsy
care &
monitoring
10. Contd.
• The current standard procedure for kidney biopsy involves the
use of real-time ultrasound to guide an automated spring-
loaded biopsy device percutaneously.
• Computed tomography–guided renal biopsy is an alter native
imaging tool, but it exposes the patient to the risks of
radiation.
• Other procedure for renal biopsy are written in book are open
kidney biopsy, laparoscopic kidney biopsy and transjugular
kidney biopsy in special situation.
12. Post Biopsy Care
• Following kidney biopsy, vitals are checked at frequent
intervals for initial few hours.
• Bed rest is advised for initial 8-10 h.
• In some centers, kidney biopsy is performed as an outpatient
procedure, but in majority of centers, it is an inpatient
procedure.
• Routine post-biopsy ultrasound is not recommended but we
do because sometimes silent perinephric hematoma
occurred.
13. Contd.
Time F/Up
Just arrival at bed Vitals
After 2 hours Vitals +urine output & colour+ local area
After 4 hours Vitals + urine output & colour
After 6 hours Vitals + urine output & colour
After 24 hours Renal biopsy+ dressing off
15. Contd.
The diagnosis of glomerular disease in renal biopsy specimens
often has at least 5 steps that may occur in different
sequences:
• Preliminary review of available clinical data prior to
specimen examination,
• Light microscopic examination,
• Immunohistologic examination,
• Electron microscopic examination, and
• Integration of all pathologic and clinical data into a final
interpretation and diagnosis.
16. Adequacy of sample
Two biopsy cylinders with a minimal length of 1 cm and a
diameter of at least 1.2 mm.
• Usually 10–15 glomeruli are optimal; very often 6–10
glomeruli are sufficient
• Some cases even one glomerulus is enough(Membranous
nephropathy)
Cortex and medulla Examination
1-2 glomeruli Electron microscope
3-5 glomeruli Immunofluroscence
6 glomeruli Light microscopy(native kidney)
10 glomeruli Light microscopy(renal allograft)
17. Sectioning and staining
• After histologic processing and paraffin embedding, the
tissues are sectioned by microtome.
• Sections are prepared as thin as 3 μm or less for light
microscopy, at least two sections should be placed on each
slide.
• Thicker sections is needed in congo red and
Immunohistochemistry staining.
• There are many acceptable staining protocols; most include
staining alternating slides with hematoxylin and eosin stain
(H&E), periodic acid–Schiff reaction (PAS), silver methenamine
and Massons trichrome, JMS and congo red.
18. Contd.
• Hematoxylin and eosin
(H and E)
• Periodic Schiff (PAS)
• Silver methanamine
stain
• Trichrome
• Others-Congo red for
amyloidosis
21. Staining
• The antigens that should be routinely examined include:
1. Immunoglobulins (primarily IgG, IgM and IgA),
2. Complement components (primarily C3, C1q, and C4), fibrin, and
kappa and lambda light chains.
• Additional antibodies may be required in specific circumstances, for
example:
1. Amyloid speciation,
2. Collagen IV alpha chains in hereditary nephritis,
3. IgG subclasses, virus identification,
4. Lymphocyte phenotyping in allografts in suspected cases of PTLD,
5. C4d in allograft biopsies.
22. Contd.
• The tissue for EM may be fixed in 2–3% glutaraldehyde or 1–4%
paraformaldehyde.
• Toluidine blue-stained, 1 μm thick, so-called ‘thick’ sections, are
examined to identify appropriate structures for thin sectioning
and examination with the electron microscope.
• Thick sections are also useful to supplement the paraffin
material (eg a lesion of focal segmental sclerosis may only be
present on the thick section).
• In general, one or two glomeruli are examined
ultrastructurally. Low-, medium- and high-magnification
photographs are taken to include both capillary loops and
mesangial areas.
23. Interpretation
• The evaluation of a kidney biopsy includes examination of
multiple serial sections each with several tissue slices, stained
with a variety of stains to be examined by LM and IHC.
• Careful evaluation of glomeruli, tubules, the interstitium and
the vessels is required.
• The final report should provide a glomerular count with the
number showing global and/or segmental sclerosis.
• In certain situations, other glomerular lesions should be
counted (eg number of crescents, subtyped into cellular,
fibrocellular and fibrous, etc).
24. Contd.
• A description of alterations in tubules, interstitium and vessels
should also be included.
• Two days for LM and IF, and 3–5 days for EM should be
considered routine.
• A nephropathologist must have a thorough understanding of
renal disease as well as good communication with the
nephrologists caring for the patients for correct final
diagnosis.
25. Contd.
Under the microscope, first a low-power screening
examination helps in localizing the defect is in glomerulus,
tubule, and interstitium, and/or blood vessels.
In addition to the site of lesions, the distribution of lesion is
also important from the pathology point of view.
• Diffuse change: Changes occurring in all the glomeruli.
• Focal changes: Changes occurring in few glomeruli only.
• Global changes: Whole glomerulus is involved.
• Segmental changes: Only some part of glomerulus is involved.
The next issue is to categorize whether the lesion is active or
chronic type.
26. A. Light microscopy(LM)
PAS & TRICHROME SILVER
• Basement membrane --red deep blue black
• Mesangial matrix --red deep blue black
• Interstitial collagen --pale blue
• Cell cytoplasm --rust/orange
• Granular Immune complex deposit -/+ bright red orange,
homogenous
• Fibrin- weakly, Bright red orange,
• fibrillar ---- amyloid -------- Light blue orange
28. Contd.
• Glomeruli Tubules Interstitium Vessels
A. Injury Localization: Glomerular/Vascular/Tubulointerstitial
B. Category of Injury: Active Versus Fibrosing
1. Active lesions a. Proliferation b. Necrosis c. Crescents d. Edema e. Active
inflammation (eg, glomerulitis, tubulitis, vasculitis)
2. Fibrosing a. Glomerulosclerosis b. Fibrous crescents c. Tubular atrophy
d. Interstitial fibrosis e. Vascular sclerosis
C. Types of Lesions
Determination of the nature and pathogenesis of lesions: examination by IF,
EM and LM
30. Glomeruli
• Glossary of terms used to describe histologic lesions in glomeruli
• Focal-Involving <50% of glomeruli
• Diffuse-Involving 50% or more of glomeruli
• Segmental-Involving part of a glomerular tuft
• Global-Involving all of a glomerular tuft
• Minimal change: Normal appearance by LM, fusion of podocyte foot processes by
EM
• Mesangial hypercellularity-4 or more nuclei in a peripheral mesangial segment
• Endocapillary hypercellularity-Increased cellularity internal to the GBM composed
of leukocytes, endothelial cells and/or mesangial cells
• Extracapillary hypercellularity-Increased cellularity in Bowman’s space, i.e. > one
layer of parietal or visceral epithelial cells, or monocytes/macrophages.
31. Contd.
• Crescent- Extracapillary hypercellularity collection of cells in Bowman’s
space in response to glomerular damage.
• Fibrinoid necrosis- Lytic destruction of cells and matrix with deposition of
acidophilic fibrin- rich material.
• Mesangiolysis- lysis of mesangial matrix
• Hyaline-Glassy acidophilic extracellular material
• Sclerosis-Increased collagenous extracellular matrix that is expanding the
mesangium, obliterating capillary lumens or forming adhesions to
Bowman’s capsule
32. Contd.
• Membranoproliferative-Combined capillary wall thickening and
endocapillary hypercellularity
• Lobular -Consolidated expansion of segments that are demarcated by
intervening urinary space.
• Humps : Deposits of Ig and complement in a sub- epithelial site
• Spikes : Projections of basement membrane between regular subepithelial
deposit
• Basket weave GBM : The disordered replication of lamina densa of GBM
33. Contd.
No abnormality by light microscopy
1. Glomerular disease with no light
microscopic changes (e.g. minimal
change glomerulopathy, thin
basement membrane nephropathy).
3. Mild or early glomerular disease (e.g.
Class I lupus nephritis, IgA
nephropathy, C1q nephropathy,
Alport syndrome, etc.)
Thick capillary walls without
hypercellularity or mesangial
expansion
1. Membranous glomerulopathy
(primaryor secondary)(>Stage I)
2. Thrombotic microangiopathy with
expanded subendothelial zone
3. Preeclampsia/eclampsia with
endothelial swelling
4. Fibrillary glomerulonephritis with
predominance of capillary wall
deposits
34. Contd.
Mesangial or endocapillary hypercellularity:
• Focal or diffuse mesangioproliferative glomerulonephritis
• Focal or diffuse (endocapillary) proliferative glomerulonephritis
• Acute (“exudative”) diffuse proliferative postinfectious glomerulonephritis
• Membranoproliferative glomerulonephritis (type I, II or III)
Extracapillary hypercellularity:
• ANCA crescentic glomerulonephritis (paucity of immunoglobulin by IFM)
• Immune complex crescentic glomerulonephritis ((granular
immunoglobulin by IFM)
• Anti-GBM crescentic glomerulonephritis (linear immunoglobulin by IFM)
• Collapsing variant of focal segmental glomerulosclerosis (including HIV
nephropathy)
39. Tubule
Characterized morphologically by destruction/severe injury of the renal
tubular epithelium
• Two major causes are-toxins & ischaemia
Evidence of ATN/injury are-
• Degeneration & necrosis of individual tubular epithelial cells
• Swelling of tubular epithelium(ballooning)
• Detachment of tubular epithelium from underlying BM
• Loss of PAS positive brush border of PCT
• Thinning of tubular epithelium
• Dilatation of tubular Lumina
• Interstitial edema
• Casts ( hyaline, pigmented, eosinophilic, cellular, granular debris)
• Tubular lumen contains sloughed epithelial cells, leukocytes, cellular
debris
• Rupture of tubular BM
40. Contd.
• Lymphocytes or other inflammatory cells on epithelial side of tubular BM
infiltrating the tubular epithelium
Marker of active tubulointerstitial inflammation.
• Hyaline casts
• WBC casts
• Epithelial / granular casts
• RBC casts
• Large hyaline fractured casts
• Myoglobin/hemoglobin casts
Tubules are non functioning & it is no longer capable of regenerating and
resuming function. Tubular BM are thickened & wrinkled.
44. Contd.
Interstitial expansion by neoplastic cells-
• Lymphoma
• Leukemia
• Primary renal ca
• Metastasis
• Crystals & mineral deposits
• Nephrocalcinosis(ca carbonate)
• ARF(ca oxalate)
• Uric acid(gout)
• Cholesterol(glomerular disease with nephrotic syndrome)
45. B. Immunofluresence study(DIF)
Directed at identification of pathogenic Immunoglobulin (Ig) and
complement.
Antibody used routinely-IgG, IgA, IgM, Kappa & lambda light
chains, C3, C4, C1q, fibrinogen
• Glomerular/extraglomerular location, intensity & pattern of
staining
• Glomerular staining catagorized as-mesangial, capilary wall
or both
• Capillary staining –granular, linear, band like
46. Contd.
Linear/ Granular mesangial and capillary wall deposition:
• WHO Class II lupus( full house)
• Finely granular (membranous GN with/without SLE)
• Coarsely granular (MPGN, WHO Class III, or IV lupus)
• Scattered ,coarse granules (poststreptococcal GN)
• Dense deposit disease( ribbonlike,thick C3)
• IgA nephropathy
• C1q nephropathy
• IgM is idiopathic nephrotic syndrome
• Fibrillary GN(IgG)
• Anti GBM disease(IgG, C3)
• Monoclonal Ig deposition disease(mostly kappa chain)
• Primary amyloidosis(usually λ)
47. Contd.
• Dark-field immunofluorescent microscopy is usually graded using a
semiquantitative scale, such as 0, trace, 1+, 2+, and 3+. Some
laboratories divide a positive reaction into 0 to 4+.
• The glomerulus is the usual site of interest, the tubulointerstitium and
the vessels may also react with various antibodies, and a description of
these changes is also required.
• An experienced observer will be familiar with background fluorescence
and the positive control area for each immunoreactant.
• Immunohistochemical staining, most often using diaminobenzidine to
reveal the reactive products, should also be graded and described
fully.
49. C. Electron Microscopy
• Electron microscopy, the tool of promise in the 1960s and 1970s, has little
diagnostic utility in the daily practice of anatomic pathology, having been
almost completely replaced by diagnostic immunohistochemical
examination of pathologic tissues.
• The tissue for EM may be fixed in 2-3% glutaraldehyde or 1-4%
paraformaldehyde.
• Tissue can be reprocessed from the paraffin or the frozen block if no
glomeruli are available in the EM sample. However, such reprocessed
tissue will have poor morphologic preservation.
• Toluidine blue-stained 1-μm thick sections are examined to identify
appropriate structures for thin sectioning and examination with the
electron microscope.
50. Contd.
In general, one or two
glomeruli are examined
ultrastructurally.
1. When there is a family
history of renal disease.
2. Hematuria, especially
microscopic, with or
without proteinuria.
3. When there is a
symptomatic proteinuria,
with normal renal
excretory function.
Indication
51. Contd.
• The EM report should include a description of the glomerular
basement membranes, presence or absence of deposits or
infiltrative processes, the status of the foot processes, and changes
in the endothelium.
• Abnormalities of the glomerular basement membranes, such as
wrinkling, folding, collapse, sclerosis, or duplication, thickness
should be described.
• A description of deposits should contain information on location,
density, granularity or fibrillarity, size, and frequency.
• Hypercellularity should be documented, including degree, location,
and cell type, if possible.
• Changes noted in the tubules, the interstitium, or the blood vessels
should also be described.
54. Contd.
• Immunohistochemistry
• IHC detects specific proteins by mono-or polyclonal antibodies raised
against that protein in biopsy. Some of the examples for such proteins are:
Hepatitis B virus and SV40 antigen for BK Polyoma virus infection.
• In-situ Hybridization
• ISH uses labeled cDNA or RNA probes. It localizes specific DNA/RNA
sequence in tissue section which is then quantitated using
autoradiography or fluorescence microscopy. The commonly used ones
are as follows:
• BK virus.
• EB virus probes in the diagnosis of PTLD.
• Pathogenic cytokines such as platelet-derived growth factor, epithelial
growth factor, etc.
55. Final report
• A glomerular count with a statement regarding the number of
obsolescent glomeruli.
• In the case of crescentic glomerulonephritis, the number of
glomeruli with crescents, and of those, the number that are,
for example, cellular, fibrocellular, and fibrous should be
documented.
• A description of the changes seen in the glomerular capillaries
and the mesangium should be given, including information on
alternations in the glomerular basement membranes,
hypercellularity, leukocyte infiltration, matrix expansion, and
the presence of deposits or thrombotic changes, among
others.
56. Contd.
• The other renal compartments should be described as well,
including descriptions of the tubules, the interstitium, and the
blood vessels.
• Occasionally, the only slide containing the pathologic feature
of interest is the toluidine blue–stained, thick section,
produced for EM, which emphasizes the importance of a
careful examination of all available material.
• Finally, detailed communication with the nephrologist or
other clinician caring for the patient leads to an accurate
clinicopathologic correlation and the correct diagnosis.