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 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.
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
Glomerulonephritis topic kidney related diseaseshiv847105
This document discusses glomerular diseases and classifications of glomerulonephritis. It describes the histopathologic classification of glomerulonephritis based on light microscopy findings, which may include minimal change disease, focal and segmental glomerulosclerosis, membranous glomerulonephritis, and proliferative glomerulonephritis classified by the site of proliferation. Proliferative types include mesangial, membranoproliferative, crescentic, and IgA nephropathy. The document also mentions investigations for kidney diseases include biochemical, microbiologic, immunologic, histopathologic and radiologic tests, with urine examination and blood pressure measurement being initial screening methods.
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.
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.
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.
This document discusses rapidly progressive glomerulonephritis (RPGN) and crescentic glomerulonephritis. It describes the main immunopathologic categories of crescentic glomerulonephritis, which include immune complex crescentic glomerulonephritis, anti-glomerular basement membrane (GBM) disease, and pauci-immune crescentic glomerulonephritis associated with antineutrophil cytoplasmic antibodies (ANCA). Immune complex crescentic glomerulonephritis is most common in children, while pauci-immune crescentic glomerulonephritis is most common in adults. The pathology involves formation of
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.
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
Glomerulonephritis topic kidney related diseaseshiv847105
This document discusses glomerular diseases and classifications of glomerulonephritis. It describes the histopathologic classification of glomerulonephritis based on light microscopy findings, which may include minimal change disease, focal and segmental glomerulosclerosis, membranous glomerulonephritis, and proliferative glomerulonephritis classified by the site of proliferation. Proliferative types include mesangial, membranoproliferative, crescentic, and IgA nephropathy. The document also mentions investigations for kidney diseases include biochemical, microbiologic, immunologic, histopathologic and radiologic tests, with urine examination and blood pressure measurement being initial screening methods.
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.
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.
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.
This document discusses rapidly progressive glomerulonephritis (RPGN) and crescentic glomerulonephritis. It describes the main immunopathologic categories of crescentic glomerulonephritis, which include immune complex crescentic glomerulonephritis, anti-glomerular basement membrane (GBM) disease, and pauci-immune crescentic glomerulonephritis associated with antineutrophil cytoplasmic antibodies (ANCA). Immune complex crescentic glomerulonephritis is most common in children, while pauci-immune crescentic glomerulonephritis is most common in adults. The pathology involves formation of
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 membranoproliferative glomerulonephritis (MPGN), including its classification, pathogenesis, clinical presentation, pathology, and treatment. MPGN is classified based on immunofluorescence and electron microscopy findings. It can be immune-mediated via immune complex deposition or complement-mediated via dysregulation of the alternative complement pathway. On pathology, it is characterized by thickened glomerular basement membranes, mesangial hypercellularity, and endocapillary proliferation. Clinical presentation varies from asymptomatic to nephrotic syndrome or renal failure.
- English version of this lecture is available at:
https://youtu.be/lvcXwE0fb-w
- Arabic version of this lecture is available at:
https://youtu.be/r-fG8bSCqZo
- 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
This document summarizes a nephrology morning session on membranous nephropathy. Membranous nephropathy is one of the most common causes of nephrotic syndrome in adults, accounting for about 1/3 of biopsy diagnoses. It can be idiopathic or secondary. The main clinical features are nephrotic syndrome with preserved kidney function. Treatment involves non-immunosuppressive measures like ACE inhibitors and immunosuppressive regimens like the Ponticelli regimen for patients meeting certain criteria. The prognosis depends on achieving remission, with about 1/3 of patients achieving remission, 1/3 continuing heavy proteinuria, and 1/3 progressing
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.
1 glomerular disease & anatomy pysiology of kidenyEngidaw Ambelu
This document provides an overview of kidney disease and glomerular diseases. It begins with the functions and anatomy of the kidney, focusing on the glomerulus and its role in filtration. It then discusses various glomerular diseases like nephrotic syndrome, nephritic syndrome, acute glomerulonephritis, and common causes like minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Complications of nephrotic syndrome are also covered. The document provides detailed information on the pathology, clinical presentation, and treatment of different glomerular diseases.
Hepatitis C virus infection is associated with many renal diseases.
Renal disease caused by
• Virus itself
• Drugs used for treatment of hepatitis c
• Associated condition with hepatitisadvanced liver cell failure.
A. The renal disease associated with hepatitis c due to advanced liver cell failure:
• Prerenal (Hypovolemia , shock and hepatorenal syndrome )
• ATN ( sepsis or shock)
B. Drugs used for treatment of hepatitis c:
• Interstitial nephritis secondary to Interferon
C. Hepatitis c itself
o Hepatitis c is RNA flavivirus( single strand)
o Has extrahepatic manifestation like arthritis, DM, cryglobulinemia and glomerulonephritis
o Renal diseases associated with hepatitis C
1. The most common types is MPGN with cryoglobulinemia
2. Others are
MPGN without cryoglobulinemia
Membranous nephropathy (MN)
Focal segmental glomerulosclerosis
IgA nephropathy
Fibrillary glomerulopathy
Immunotactoid glomerulopathy
Thrombotic microangiopathy
Amyloid
Vasculitis
Interstitial nephritis secondary to virus
HCV-associated PAN
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.
This document reviews glomerulonephritis as a cause of acute kidney injury. It discusses several types of glomerulonephritis that can lead to AKI, including anti-GBM disease, small vessel vasculitis, lupus nephritis, IgA nephropathy, and post-streptococcal glomerulonephritis. Kidney biopsy is important for diagnosis but not always possible in critically ill patients. Treatment depends on the specific type of glomerulonephritis and may include corticosteroids, cyclophosphamide, plasma exchange, and immunosuppression. Prognostic markers include the extent of glomerular lesions, need for dialysis, and creatin
This document summarizes IgA nephropathy (IgAN), the most common primary glomerulonephritis globally. Key points include: IgAN is characterized by deposition of IgA in the mesangium. Clinical presentations range from asymptomatic hematuria to rapidly progressive glomerulonephritis. Prognosis depends on factors like proteinuria level and hypertension. Treatment involves renin-angiotensin system blockade, glucocorticoids, and immunosuppression. The Oxford classification uses pathological features to predict prognosis.
This document discusses chronic kidney disease, including its etiology, pathogenesis, and complications. It begins by covering the normal anatomy and embryology of the kidney. It then describes the staging of CKD using the CGA classification system. The main causes of CKD are discussed, including congenital diseases, glomerular diseases, vascular diseases, tubulointerstitial diseases, and obstructive uropathies. The pathogenesis of glomerular injury is examined in depth. Finally, common complications of advanced CKD are outlined, such as anemia, cardiovascular abnormalities, and disorders of calcium and phosphate metabolism.
The document discusses glomerulonephritis, which refers to diseases of the glomeruli in the kidneys mediated by immune mechanisms. It can present as either a nephritic or nephrotic syndrome. Nephritic syndrome is characterized by hematuria, hypertension, and variable proteinuria, while nephrotic syndrome presents with massive proteinuria (>3.5 g/day), edema, hyperlipidemia, and sometimes a hypercoagulable state. The pathogenesis involves immune complex deposition or T-cell mediated responses targeting antigens in the glomerular basement membrane or mesangium. Treatment aims to control symptoms and slow disease progression using immunosuppressants or ACE inhibitors depending on the specific type
IgA nephropathy is characterized by predominant IgA deposition in the glomerular mesangium. It is the most common cause of glomerulonephritis worldwide. Primary IgA nephropathy occurs most commonly in the second and third decades of life and presents with macroscopic hematuria, asymptomatic hematuria with mild proteinuria, or nephrotic syndrome. Treatment involves controlling blood pressure with ACE inhibitors or ARBs, treating any proteinuria or hematuria, and considering corticosteroids for progressive disease. The pathogenesis involves abnormal IgA immune responses leading to pathogenic IgA deposition in the kidney and subsequent glomerular inflammation and injury.
Membranoproliferative glomerulonephritis & c3 glomerulopathyscienthiasanjeevani1
This document provides an overview of membranoproliferative glomerulonephritis (MPGN) and C3 glomerulopathy. It defines MPGN and discusses its pathogenesis, classification based on light microscopy, electron microscopy and immunofluorescence. It describes immune complex-mediated and complement-mediated MPGN, and covers C3 glomerulonephritis in more detail including dense deposit disease. Management strategies are outlined for idiopathic MPGN, Hep C related MPGN, and C3 glomerulopathies depending on disease severity. Treatment may include immunosuppression, plasma exchange, eculizumab, rituximab and addressing identifiable defects. Prognosis is generally poor for dense deposit
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 discusses several types of glomerular diseases: membranous glomerulonephritis, membranoproliferative glomerulonephritis, chronic glomerulonephritis, and Berger disease. Membranous glomerulonephritis involves thickening of the basement membrane from immune complex deposition. Membranoproliferative glomerulonephritis shows proliferation of mesangial and endothelial cells. Chronic glomerulonephritis causes scarring and impaired filtering over time. Berger disease is immunoglobulin A nephropathy where IgA complexes deposit in the mesangium.
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.
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
Renal impairment is a common complication of multiple myeloma, affecting 20-40% of cases. The most important causes include light chain tubular casts (myeloma kidney), hypercalcemia, light chain deposition disease associated with kappa light chains, and AL amyloidosis associated with lambda light chains. Other potential causes are NSAIDs, hyperuricemia, chemotherapy, IV contrast, and bisphosphonates. While renal impairment was generally associated with a poor prognosis, novel therapies have improved renal prognosis. Treatment involves hydration, correcting contributing factors like hypercalcemia, and using renally safe agents like steroids, melphalan, cyclophosphamide, bortezomib, and thalidomide. Plasmap
Glomerulus and nephrotic & nephritic syndromeessamramdan
This document provides an overview of kidney diseases focusing on glomerular diseases and nephrotic syndrome. It discusses the structure of the kidney and glomerulus. Glomerular diseases are often immunologically mediated involving circulating immune complexes or antibodies reacting within the glomerulus. Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Primary causes include minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Minimal change disease appears normal by light microscopy but shows diffuse foot process effacement by electron microscopy. Membranous glomerulonephritis involves subepithelial immune deposits along the glo
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
हिंदी वर्णमाला पीपीटी, hindi alphabet PPT presentation, hindi varnamala PPT, Hindi Varnamala pdf, हिंदी स्वर, हिंदी व्यंजन, sikhiye hindi varnmala, dr. mulla adam ali, hindi language and literature, hindi alphabet with drawing, hindi alphabet pdf, hindi varnamala for childrens, hindi language, hindi varnamala practice for kids, https://www.drmullaadamali.com
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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 membranoproliferative glomerulonephritis (MPGN), including its classification, pathogenesis, clinical presentation, pathology, and treatment. MPGN is classified based on immunofluorescence and electron microscopy findings. It can be immune-mediated via immune complex deposition or complement-mediated via dysregulation of the alternative complement pathway. On pathology, it is characterized by thickened glomerular basement membranes, mesangial hypercellularity, and endocapillary proliferation. Clinical presentation varies from asymptomatic to nephrotic syndrome or renal failure.
- English version of this lecture is available at:
https://youtu.be/lvcXwE0fb-w
- Arabic version of this lecture is available at:
https://youtu.be/r-fG8bSCqZo
- 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
This document summarizes a nephrology morning session on membranous nephropathy. Membranous nephropathy is one of the most common causes of nephrotic syndrome in adults, accounting for about 1/3 of biopsy diagnoses. It can be idiopathic or secondary. The main clinical features are nephrotic syndrome with preserved kidney function. Treatment involves non-immunosuppressive measures like ACE inhibitors and immunosuppressive regimens like the Ponticelli regimen for patients meeting certain criteria. The prognosis depends on achieving remission, with about 1/3 of patients achieving remission, 1/3 continuing heavy proteinuria, and 1/3 progressing
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.
1 glomerular disease & anatomy pysiology of kidenyEngidaw Ambelu
This document provides an overview of kidney disease and glomerular diseases. It begins with the functions and anatomy of the kidney, focusing on the glomerulus and its role in filtration. It then discusses various glomerular diseases like nephrotic syndrome, nephritic syndrome, acute glomerulonephritis, and common causes like minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Complications of nephrotic syndrome are also covered. The document provides detailed information on the pathology, clinical presentation, and treatment of different glomerular diseases.
Hepatitis C virus infection is associated with many renal diseases.
Renal disease caused by
• Virus itself
• Drugs used for treatment of hepatitis c
• Associated condition with hepatitisadvanced liver cell failure.
A. The renal disease associated with hepatitis c due to advanced liver cell failure:
• Prerenal (Hypovolemia , shock and hepatorenal syndrome )
• ATN ( sepsis or shock)
B. Drugs used for treatment of hepatitis c:
• Interstitial nephritis secondary to Interferon
C. Hepatitis c itself
o Hepatitis c is RNA flavivirus( single strand)
o Has extrahepatic manifestation like arthritis, DM, cryglobulinemia and glomerulonephritis
o Renal diseases associated with hepatitis C
1. The most common types is MPGN with cryoglobulinemia
2. Others are
MPGN without cryoglobulinemia
Membranous nephropathy (MN)
Focal segmental glomerulosclerosis
IgA nephropathy
Fibrillary glomerulopathy
Immunotactoid glomerulopathy
Thrombotic microangiopathy
Amyloid
Vasculitis
Interstitial nephritis secondary to virus
HCV-associated PAN
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.
This document reviews glomerulonephritis as a cause of acute kidney injury. It discusses several types of glomerulonephritis that can lead to AKI, including anti-GBM disease, small vessel vasculitis, lupus nephritis, IgA nephropathy, and post-streptococcal glomerulonephritis. Kidney biopsy is important for diagnosis but not always possible in critically ill patients. Treatment depends on the specific type of glomerulonephritis and may include corticosteroids, cyclophosphamide, plasma exchange, and immunosuppression. Prognostic markers include the extent of glomerular lesions, need for dialysis, and creatin
This document summarizes IgA nephropathy (IgAN), the most common primary glomerulonephritis globally. Key points include: IgAN is characterized by deposition of IgA in the mesangium. Clinical presentations range from asymptomatic hematuria to rapidly progressive glomerulonephritis. Prognosis depends on factors like proteinuria level and hypertension. Treatment involves renin-angiotensin system blockade, glucocorticoids, and immunosuppression. The Oxford classification uses pathological features to predict prognosis.
This document discusses chronic kidney disease, including its etiology, pathogenesis, and complications. It begins by covering the normal anatomy and embryology of the kidney. It then describes the staging of CKD using the CGA classification system. The main causes of CKD are discussed, including congenital diseases, glomerular diseases, vascular diseases, tubulointerstitial diseases, and obstructive uropathies. The pathogenesis of glomerular injury is examined in depth. Finally, common complications of advanced CKD are outlined, such as anemia, cardiovascular abnormalities, and disorders of calcium and phosphate metabolism.
The document discusses glomerulonephritis, which refers to diseases of the glomeruli in the kidneys mediated by immune mechanisms. It can present as either a nephritic or nephrotic syndrome. Nephritic syndrome is characterized by hematuria, hypertension, and variable proteinuria, while nephrotic syndrome presents with massive proteinuria (>3.5 g/day), edema, hyperlipidemia, and sometimes a hypercoagulable state. The pathogenesis involves immune complex deposition or T-cell mediated responses targeting antigens in the glomerular basement membrane or mesangium. Treatment aims to control symptoms and slow disease progression using immunosuppressants or ACE inhibitors depending on the specific type
IgA nephropathy is characterized by predominant IgA deposition in the glomerular mesangium. It is the most common cause of glomerulonephritis worldwide. Primary IgA nephropathy occurs most commonly in the second and third decades of life and presents with macroscopic hematuria, asymptomatic hematuria with mild proteinuria, or nephrotic syndrome. Treatment involves controlling blood pressure with ACE inhibitors or ARBs, treating any proteinuria or hematuria, and considering corticosteroids for progressive disease. The pathogenesis involves abnormal IgA immune responses leading to pathogenic IgA deposition in the kidney and subsequent glomerular inflammation and injury.
Membranoproliferative glomerulonephritis & c3 glomerulopathyscienthiasanjeevani1
This document provides an overview of membranoproliferative glomerulonephritis (MPGN) and C3 glomerulopathy. It defines MPGN and discusses its pathogenesis, classification based on light microscopy, electron microscopy and immunofluorescence. It describes immune complex-mediated and complement-mediated MPGN, and covers C3 glomerulonephritis in more detail including dense deposit disease. Management strategies are outlined for idiopathic MPGN, Hep C related MPGN, and C3 glomerulopathies depending on disease severity. Treatment may include immunosuppression, plasma exchange, eculizumab, rituximab and addressing identifiable defects. Prognosis is generally poor for dense deposit
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 discusses several types of glomerular diseases: membranous glomerulonephritis, membranoproliferative glomerulonephritis, chronic glomerulonephritis, and Berger disease. Membranous glomerulonephritis involves thickening of the basement membrane from immune complex deposition. Membranoproliferative glomerulonephritis shows proliferation of mesangial and endothelial cells. Chronic glomerulonephritis causes scarring and impaired filtering over time. Berger disease is immunoglobulin A nephropathy where IgA complexes deposit in the mesangium.
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.
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
Renal impairment is a common complication of multiple myeloma, affecting 20-40% of cases. The most important causes include light chain tubular casts (myeloma kidney), hypercalcemia, light chain deposition disease associated with kappa light chains, and AL amyloidosis associated with lambda light chains. Other potential causes are NSAIDs, hyperuricemia, chemotherapy, IV contrast, and bisphosphonates. While renal impairment was generally associated with a poor prognosis, novel therapies have improved renal prognosis. Treatment involves hydration, correcting contributing factors like hypercalcemia, and using renally safe agents like steroids, melphalan, cyclophosphamide, bortezomib, and thalidomide. Plasmap
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This document provides an overview of kidney diseases focusing on glomerular diseases and nephrotic syndrome. It discusses the structure of the kidney and glomerulus. Glomerular diseases are often immunologically mediated involving circulating immune complexes or antibodies reacting within the glomerulus. Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Primary causes include minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Minimal change disease appears normal by light microscopy but shows diffuse foot process effacement by electron microscopy. Membranous glomerulonephritis involves subepithelial immune deposits along the glo
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Date: May 29, 2024
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MPGN BY DR SAEED KDIGO 2021 UPDATE GUIDELINES.pptx
1. WELCOME TO GUIDELINE PRESENTATION
DR.MD. SAEED HOSSAIN
MD RESIDENT (PHASE B)
DEPARTMENT OF NEPHROLOGY , DMCH.
KDIGO 2021 Clinical Practice Guideline Update
3. Kidney Disease: Improving Global Outcomes
MEMBRANOPROLIFERATIVE
GLOMERULONEPHRITIS
Membranoporoliferative glomerulonephritis (MPGN) is a
pathologic pattern of glomerular injury resulting from
subendothelial & mesangial deposition of immune complexes
and/or complement factors and their products along with
proliferative changes in the glomeruli.
4. Kidney Disease: Improving Global Outcomes
MPGN is a light- microscopic pattern of injury. This pattern does
not represent a disease entity rather it can occur as a result of
different pathologic processes. Other name is Lobular
glomerulonephritis and Mesangiocapillary glomerulonephritis
(MCGN).
5. Kidney Disease: Improving Global Outcomes
FORMER CLASSIFICATION
Traditionally, MPGN was classified based on the ultrastructural
characteristics on Electron-microcopy as :
• MPGN type I: mesangial & subendothelial deposit.
• MPGN type II: Mesangial & intramembranous highly electron
dense deposit.Also called Dense Deposit Disease (DDD).
• MPGN type III: subendothelial, intramembranous &
subepithelial electron dense deposit.
6. Kidney Disease: Improving Global Outcomes
HISTOLOGY-LIGHT MICROSCOPY
• Mesangial hypercellularity & matrix expansion.
• Leucocyte infiltration leading to lobular pattern of glomerular
tufts.
• Interposition of mesangial cell cytoplasm between
endothelium & GBM along the capillary wall giving rise to
double contour or basement membrane splitting appearance.
• Crescent may be seen.
7. Kidney Disease: Improving Global Outcomes
Light Microscopy
Figure showing
glomerulus increased
of size, with mesangial
hypercellularity and
lobulated aspect; this
appearance is very
characteristic of
membranoproliferative
GN , more accentuated
in some areas
(arrows).
8. Kidney Disease: Improving Global Outcomes
IMMUNOFLUORESCENCE MICROSCOPY
• Deposition of C3 and immunoglobulin (IgM/ IgG) in a
granular fashion along capillary wall.
• C1q or C4 may also be present.
9. Kidney Disease: Improving Global Outcomes
Immunofluorescence
Microscopy :
Immunofluorescence
microscopy showing
bright granular staining
for (B) IgM, and (C) C3
10. Kidney Disease: Improving Global Outcomes
Direct
immunofluorescence
for C3 in a case of
dense deposits
disease. Observe
strong staining, like
"ribbons", on
capillary walls. This
immunostaining is
only for C3.
11. Kidney Disease: Improving Global Outcomes
ELECTRON MICROSCOPY
• Subendothelial & mesangial electron dense deposit (Type 1).
• Continuous dense ribbon like intramembranous deposits along
the GBM, tubule & Bowman’s capsule(Type 2).
• Subendothelial, intamembranous & sub epithelial electron
dense deposit(Type 3).
• Effacement of foot process (podocycytes).
12. Kidney Disease: Improving Global Outcomes
Electron
Microscopy
(D) Figure showing
subendothelial
electrondense deposits
and double contour
formation.
(F)Figure showing
subendothelial
electron-dense
deposits and double
contour formation.
13. Kidney Disease: Improving Global Outcomes
NEWER CLASSIFICATION
(MAYO CLINIC CLASSIFICATION)
The Mayo Clinic classification of MPGN divides MPGN based
on two broad pathogenetic pathways:
(i)immune complex or monoclonal immunoglobulin
deposition in the glomeruli with or without complement
deposition.
(ii)complement deposition subsequent to dysregulation of
the complement system.
14. Kidney Disease: Improving Global Outcomes
A third pathogenic pathway with an MPGN pattern can be seen in the
absence of immune complex or complement deposition in the setting
of chronic endothelial injury or chronic thrombotic micro-angiopathy.
16. Kidney Disease: Improving Global Outcomes
IMMUNOGLOBIN/IMMUNE COMPLEX
MEDIATED MPGN
A. Immune complex-mediated GN (ICGN) with an MPGN
pattern: ICGN is characterized by the deposition of immune
complexes containing both polyclonal immunoglobulins and
complement (excludes IgAN). This lesion classically results from
chronic antigenemia with or without circulating immune
complexes. ICGN may manifest with the MPGN pattern of injury
or other proliferative glomerular lesions.
17. Kidney Disease: Improving Global Outcomes
ICGN is usually due to:
• Infections: Hepatitis C and B viral infections are among the
most common underlying causes of ICGN, but bacterial and
protozoal infections can also cause ICGN.
• Autoimmunity: ICGN can be associated with certain
autoimmune disorders, such as SLE, Sjögren's syndrome, and
Rheumatoid arthritis.
18. Kidney Disease: Improving Global Outcomes
B. Glomerulonephritis with monoclonal immunoglobulin
deposits: Proliferative patterns of kidney injury secondary to
deposition of monoclonal immunoglobulins are observed in
patients with monoclonal gammopathies. These disorders are
infrequently found in patients without overt hematological
disease, such as multiple myeloma, Waldenström
macroglobulinemia, or B-cell lymphoma.
Most commonly occur in the setting of an indolent clonal, plasma
cell, or lymphocytic disorder, and may be classified as a
monoclonal gammopathy of renal significance (MGRS).
19. Kidney Disease: Improving Global Outcomes
COMPLEMENT MEDIATED MPGN
• C3 Glomerulopathy (C3G) is a rare entity that is defined by
C3 dominant glomerulonephritis (a proliferative histologic
lesion with C3 deposition at least two orders of magnitude
greater than any other immune reactant) on kidney biopsy IF.
Characteristically, glomeruli show strong immunohistologic
staining for C3 without significant staining for
immunoglobulins or for components of the classic pathway of
complement activation, C1q and C4. This includes:
1.DDD &
2.C3 glomerulonephritis(C3GN).
20. Kidney Disease: Improving Global Outcomes
Whereas DDD is defined by highly electron-dense osmophilic,
predominantly intramembranous deposits, C3GN is characterized
by mesangial and capillary wall deposits of lesser intensity. Other
C3 dominant glomerular lesions (i.e., infection-related GN) must
be excluded by history where possible.
21. Kidney Disease: Improving Global Outcomes
Masked monoclonal immunoglobulin deposits should be
considered in patients with a pattern of C3GN when IF shows a
small amount of IgG deposition admixed with C3 deposits. IF
studies on paraffin-embedded tissue after protease digestion may
be useful to detect masked glomerular deposits of monoclonal Ig.
22. Kidney Disease: Improving Global Outcomes
• C4 glomerulopathy, C4G:
A new entity of complement-mediated GN that is characterized
by bright C4d staining but with no or minimal C3 or
immunoglobulin deposits on IF studies. Further studies are
required to determine its underlying cause.
23. Kidney Disease: Improving Global Outcomes
KDIGO 2021 UPDATE AT A GLANCE..
• Evaluation of MPGN
-Diagnosis of Idiopathic ICGN.
-Diagnosis of C3 glomerulopathy.
• Treatment of Idiopathic ICGN.
-Indolent ICGN.
-Subnephrotic range proteinuria.
-Nephrotic range proteinuria without renal impairment.
-Renal impairment without crescentic involvement.
- Rapidly progressive crescentic idiopathic ICGN.
- eGFR <30 ml/min/1.73m2
• Treatment of C3 glomerulopathy.
24. Kidney Disease: Improving Global Outcomes
DIAGNOSIS & TREATMENT (KDIGO 2021)
• 8.1. Diagnosis
• 8.1.1. Evaluate patients with ICGN for underlying disease.
Consider:
1) Infection such as HBV and HCV infection, chronic bacterial
infection (e.g., endocarditis, shunt nephritis, abscesses),
fungal, and, particularly in the developing world, parasitic
infections (e.g., schistosomiasis, echinococcosis, malaria).
Streptococcal serology should be performed in patients with
recent history of infection;
25. Kidney Disease: Improving Global Outcomes
2) Autoimmune disorders such as SLE (particularly in the chronic
phase of LN) and less often, Sjögren’s syndrome or rheumatoid
arthritis. Besides autoimmunity, an underlying immune
abnormality may be a trigger for ICGN. ICGN may be associated
with malignancy; therefore, age appropriate cancer screening may
be warranted.
26. Kidney Disease: Improving Global Outcomes
• Practice Point 8.1.2. Evaluate patients with GN and
monoclonal immunoglobulin deposits for a hematological
malignancy.
Patients with PGNMID(Proliferative GN with monoclonal
deposit) by IF must undergo a complete evaluation for a
hematological malignancy or an indolent plasma cell or
lymphocytic disorder, regardless of age, and must include:
27. Kidney Disease: Improving Global Outcomes
1) Serum and urine protein electrophoresis;
2) Serum and urine immunofixation;
3) Measurement of serum-free light chain levels;
4) Hematology consultation to further evaluate for the presence of an
underlying B-cell/plasma cell clone producing the monoclonal Ig.
28. Kidney Disease: Improving Global Outcomes
• Practice Point 8.1.3. If no underlying etiology is found for
immunoglobulin/ICGN after extensive workup, evaluate for
complement dysregulation.
A complete complement workup includes an assessment of
overall complement activity, measurement of serum levels of
complement proteins and in select cases, screening for
autoantibodies against complement regulatory proteins and
genetic studies .
30. Kidney Disease: Improving Global Outcomes
• Practice Point 8.1.4. Rule out infection-related GN or
post-infectious GN prior to assigning the diagnosis of C3G.
Both infection-related GN (i.e., in the presence of active
infection) and post-infectious GN (i.e., in patients with a
preceding infection that resolved) are presumed to be non-
recurrent, acute disease processes requiring only a limited
workup.
31. Kidney Disease: Improving Global Outcomes
Treatment is best focused on resolving the infection while
supporting kidney function. Immunosuppression is unlikely to be
required except in extreme cases (i.e., rapidly progressive loss of
kidney function and/or crescentic glomerular disease) and only
after concurrent infection is controlled.
32. Kidney Disease: Improving Global Outcomes
• Practice Point 8.1.5. Evaluate for the presence of a
monoclonal protein in patients who present for the first
time with a C3G diagnosis at >50 years of age.
C3G in its classic form is a disease of children and young adults
related to autoantibody (nephritic factor)-mediated dysregulation
of the enzyme complexes of the alternative pathway of
complement, or to other key complement pathway proteins, and
to a lesser extent is associated with mutations in genes encoding
Factor H, Factor I, the complement factor H-related (CFHR)
proteins, or C3.
33. Kidney Disease: Improving Global Outcomes
Recently, the association between the production of a monoclonal
protein in older adults and the development of C3G has been
described. In patients over the age of 50 with C3G, the
prevalence of monoclonal gammopathy ranges from 31% to 83%
versus approximately 3% in age-matched controls.
34. Kidney Disease: Improving Global Outcomes
• 8.2. Treatment
• 8.2.1. ICGN
Prior guidelines supported the use of oral cyclophosphamide or
MMF plus low-dose, alternate-day, or daily corticosteroids as a
therapeutic approach to ICGN, particularly in those with
idiopathic disease and NS and/or rapidly progressive diseases.
35. Kidney Disease: Improving Global Outcomes
Data no longer support the global application of broad-spectrum
immunosuppression as in prior recommendations, but a more
individualized approach. Treatment is often influenced and
determined by the severity of proteinuria and kidney dysfunction.
36. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.1.1. When the cause of ICGN is
determined, the initial approach to treatment should focus
on the underlying pathologic process.
After identification of the underlying trigger for ICGN, the most
effective therapy is to treat the primary disease process. In
addition, all patients with ICGN are likely to benefit from the
usual, routine care considered for other active glomerular disease
patients.
37. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.1.2 Indolent ICGN, whether idiopathic
or linked to a primary disease process, is best managed
with supportive care and only carefully considered use of
immunosuppression.
Patients with indolent disease may present late when active
inflammation has subsided. Such patients may have a bland urine
sediment with a variable degree of proteinuria and elevation in
SCr. Such patients should be treated with RASi alone unless the
kidney biopsy shows signs of active inflammation.
38. Kidney Disease: Improving Global Outcomes
Patients who present with advanced kidney disease and severe
tubulointerstitial fibrosis on kidney biopsy are less likely to
benefit from immunosuppressive therapy even if there is still
some active inflammation in the kidneys, so assessment of the
extent of chronicity on the kidney biopsy may help in deciding
whether or not to treat with immunosuppression.
39. Kidney Disease: Improving Global Outcomes
Practice Point 8.2.1.3. For patients with idiopathic ICGN and
proteinuria <3.5 g/day, the absence of the nephrotic
syndrome, and a normal eGFR, we suggest supportive
therapy with RAS inhibition alone.
No evidence exists to support a benefit from immunosuppressive
therapy in adults. Since disease progression can occur, regular
monitoring of SCr, proteinuria and the urinalysis is
recommended.
40. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.1.4. For patients with idiopathic ICGN
nephrotic syndrome and normal or near-normal serum
creatinine, try a limited treatment course of
corticosteroids.
Prednisone (or its equivalent) can be initiated at 1 mg/kg per day
(maximum dose of 60 to 80 mg/day) for 12 to 16 weeks. If the
patient responds, prednisone may be gradually tapered to
alternate-day therapy over six to eight months. If there is <30%
reduction in proteinuria after 12 to 16 weeks, we recommend
tapering and discontinuation of prednisone.
41. Kidney Disease: Improving Global Outcomes
Patients with a contraindication to corticosteroids or unwilling to
take steroids can be treated with a CNI. We do not encourage the
extended use of steroids, where a steroid-sparing option may be
available, particularly in children.
42. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.1.5. For patients with idiopathic ICGN,
abnormal kidney function (but without crescentic involvements),
active urine sediment, with or without nephrotic-range
proteinuria, add corticosteroids and immunosuppressive therapy
to supportive care.
Prednisone (or its equivalent) can be initiated at 1 mg/kg per day
(maximum dose 60 to 80 mg/day) for 12 to 16 weeks. Patients who
respond with stabilization or improvement in kidney function or ≥30%
reduction in proteinuria are considered to have a satisfactory response
to initial therapy. In such patients, gradually taper and discontinue
prednisone.
43. Kidney Disease: Improving Global Outcomes
Patients that experience worsening kidney function and/or <30%
reduction in proteinuria after 12 to 16 weeks are considered to
have had an unsatisfactory response. In such patients, reduce the
dose of prednisone to 20 mg a day and add MMF. If, after 6 to 12
months of combined therapy, there is no improvement in kidney
function, hematuria, or proteinuria, discontinue therapy, and
consider a repeat kidney biopsy. If the kidney biopsy continues to
show active GN, consider using cyclophosphamide or rituximab.
44. Kidney Disease: Improving Global Outcomes
Initiate daily oral cyclophosphamide (2 mg/kg per day; maximum
200 mg/day in adults) with prednisone (10 mg/day) for 3 to 6
months. The cyclophosphamide dose should be reduced by 25%
in older adults (age >60 years) and adjusted appropriately for
abnormal kidney function.
45. Kidney Disease: Improving Global Outcomes
Alternatively, in adults, initiate rituximab at 1 gram followed 14
days later a second dose of 1 gram, and repeat this 2 gram regime
at 6 months.
46. Kidney Disease: Improving Global Outcomes
• In patients with persistent disease activity despite at least 6
months of MMF plus low dose prednisone or after 3 to 6
months of daily oral CYC plus prednisone or rituximab,
discontinue corticosteroids and immunosuppression and
continue supportive therapy.
47. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.1.6. For patients presenting with a
rapidly progressive crescentic idiopathic ICGN, treat with
high-dose corticosteroids and cyclophosphamide.
Initiate treatment with intravenous methylprednisolone (1-3 g)
followed by oral glucocorticoids and oral cyclophosphamide or
oral glucocorticoids and rituximab using a regimen similar to that
used for patients with ANCA- associated vasculitis.
48. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.1.7. For most patients with idiopathic
ICGN presenting with an eGFR <30 ml/min/1.73m2 treat
with supportive care alone.
Unless kidney biopsy shows an active necrotizing crescentic
glomerulonephritis or other reason that could support use of
immunosuppression (i.e., minimal interstitial fibrosis or
concomitant acute tubule-interstitial nephritis), these patients
should be treated conservatively with referral for kidney
transplant evaluation in due course.
49. Kidney Disease: Improving Global Outcomes
• 8.2.2. C3 glomerulopathy:
An optimal treatment strategy for C3 glomerulopathy using
currently available therapeutics has not been established.
Expert opinion has encouraged the usual supportive measures, as
well as the use of immunosuppression in the setting of moderate
to severe disease, defined as moderate-to-marked proliferation on
biopsy and proteinuria (>2g/d).
50. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.2.1. In the absence of a monoclonal
gammopathy, C3G in patients with moderate-to-severe
disease should be treated initially with MMF, and if this
fails, Eculizumab.
Consider treating patients with C3G who have proteinuria >1 g/d
and hematuria or have declining kidney function for at least 6
months. The reported effectiveness of immunosuppressive
treatment in C3G has been variable.
51. Kidney Disease: Improving Global Outcomes
• Practice Point 8.2.2.2. Patients who fail to
respond to the treatment approaches should
be considered for a clinical trial where
available(Discussed in 8.2.2.1)
52. Kidney Disease: Improving Global Outcomes
TAKE-HOME MESSAGE
1. Idiopathic ICGN e Proteinuria <3.5 g/day e absence of NS e normal eGFR ===
Supportive therapy with RASi alone
2. Idiopathic ICGN e Proteinuria >3.5 g/day e presence of NS e Normal or near
normal SCr ===Limited treatment course of Glucocorticoids
(Prednisone 1mg/kg/day for 12-16 weeks)
53. Kidney Disease: Improving Global Outcomes
3. Idiopathic ICGN e abnormal kidney function (but without crescentic involvements) e active urine sediment,with or
without nephrotic-range proteinuria ===
Prednisone 60 to 80 mg/day for 12 to 16 weeks
If < 30% reduction of proteinuria ,then it is unsatisfactory
Reduce the dose of Prednisone 20 mg/day + add MMF for 6 to 12 months
After 6-12 months of treatment, if there is no improvement of --- kidney function,hematuria or proteinuria discontinue
therapy and consider repeat “ Kidney Biopsy”
If kidney biopsy continues to show active GN,consider using Cyclophosphamide or Rituximab
Oral Cyclophosphamide 2 mg/kg/day e Prednisone 10 mg/day for 3 to 6 months,Alternatively
Rituximab 1g repeated in 14 days apart and this 2 gm repeated at 6 months after
If all fails continue supportive therapy e RASi
54. Kidney Disease: Improving Global Outcomes
4. Patients presenting with a Rapidly Progressive Crescentic Idiopathic ICGN = = =
High-dose Glucorticosteroids and Cyclophosphamide.
5. Patients with Idiopathic ICGN presenting with an eGFR <30 ml/min/1.73m2 = =
= Supportive care alone(RASi)
6. In the absence of a Monoclonal gammopathy, C3G in patients with moderate-to-
severe disease = = = = Treated initially with MMF plus Glucocorticoids , and if
this fails, Eculizumab.
7. Patients who fail to respond to the treatment approaches, should be considered
for a Clinical Trial where available.