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Glomerular diseases
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- 2. ANATOMY AND FUNCTION •A renal corpuscle consists of: • Glomerulus – tuft of fenestrated capillaries • Glomerular (Bowman’s) capsule • Parietal layer – simple squamous epithelium • Visceral layer – consists of podocytes • Blood travels from efferent arteriole to peritubular capillaries • Blood leaves the nephron via the efferent arteriole
- 3. Three-dimensional schematic drawingof the glomerulus Afferent arteriole Efferent arteriole Endothelial cells Capillary loops Mesangial matrix and cell Bowman’s Space
- 4. Light micrograph ofglomerulus showing Normal cellularity with patent capillary lumen
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- 7. WHAT CAUSES GLOMERULAR DISEASES Glomerulardiseases results from: • Immunological Injury(Glomerulonephritis) • Inherited(Alport’s Syndrome) • Metabolic stress(Diabetes mellitus) • Deposition of extraneous materials(Amyloidosis)
- 8. MECHANISM OF IMMUNOLOGICAL INJURY •Most types of glomerulonephritis are immune mediated and respond to immunosuppressive drugs • Mechanisms of immune mediated injury involve • circulating immune complexes • In-situ immune complexes • Circulating immune complexes and in situ immune deposits lead to the activation of complement complexes which result in glomerular injury,as shown
- 9. Activation of complements cytokines C5b-9C5a,C3a oxidative stress, protease, matrix accumulations Glomerular Disease
- 10. GLOMERULAR DISEASES CLASSIFICATION &CLINICAL FEATURES
- 11. CLASSIFICATION & CLINICAL FEATURES Clinically,a glomerular disease can be classified as being in one of two spectra— either in the nephritic spectrum or the nephrotic spectrum
- 12. NEPHROTIC SPECTRUM • Thenephrotic spectrum comprises diseases that present with • Proteinuria • Hypoalbuminuria • Edema • Hyperlipidemia • Diseases falling in nephritic spectrum include: • Minimal change disease • FSGS • Membranous nephropathy • Focal segmental glomerulosclerosis • Diabetic Nephropathy
- 13. NEPHRITIC SPECTRUM • Nephriticspectrum glomerular diseases presents with • Hematuria • Proteinuria (0.3–3 g/d) • Hypertension • Edema, if present, in dependent (e.g., periorbital or scrotal) areas • Diseases falling in nephritic spectrum include: • Post streptococcal glomerulonephritis • IgA nephropathy • Sle
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- 15. MINIMAL CHANGE DISEASE •Occurs as sudden onset nephrotic syndrome in children • Electron microscopy shows fusion of podocyte foot processes • Good response to steroids(Prednisolone 1mg/Kg for 6 weeks) • Does not progress to CKD
- 16. Electron Microscopy: effacementand fusion of foot processes
- 17. FOCAL SEGMENTAL GLOMERULOSECLEROSIS • Focalprocess • Primary FSGS • Presents with idiopathic nephrotic syndrome • Poor response to steroids • Progresses to CKD • Recurs after transplant • Secondary FSGS • Variable presentation and outcome • Histology: Segmental scars in glomeruli • Associations: Local glomerular Injury • ,HIV infection, Heroin misuse, Morbid obesity
- 18. MEMBRANOUS NEPHROPATHY • Commonin Adults • Nephrotic presentation • Histology:Thickening of GBM,progressing to matrix deposition and glomerulosclerosis with granular sub epithelial IgG deposits • Pathogenesis:Antibodies to podocyte surface antigens with complement dependent podocyte injury • Course: • 1/3 remits spontaneously • 1/3 remains in nephrotic state • 1/3 progressive loss of renal function
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- 20. ELECTRON MICROSCOPY SUB EPITHELIAL ELECTRON DENSE MATERIAL
- 21. IGA NEPHROPATHY • Presentswith Hematuria, Proteinuria HTN • Leads to ESRD • Histology: Increased mesengial matrix and cells Mesengial IgA deposits • Poor response to immunosuppressive therapy
- 22. LIGHT MICROSCOPY DIFFUSE MENINGEALHYPER CELLULARITY
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- 24. POST STREPTOCOCCAL GLOMERULONEPHRITIS • Morecommon in children • Follows streptococcal throat or skin infection • Presentation: • Acute nephritic syndrome of varying severity • Hematuria • Characteristic “smoky/red urine” • Hypertension • Edema • Decreased GFR
- 25. POST STREPTOCOCCAL GLOMERULONEPHRITIS • Histology •Diffuse endothelial and mesengial cell proliferation • Neutrophils and macrophage infiltration • Sub endothelial electron dense deposits
- 26. POST STREPTOCOCCAL GLOMERULONEPHRITIS Lumpy-bumpy depositsof immunoglobulin G and complement C3 along the capillary loops and within the mesangium Immunofluorescence •Sub epithelial electron-dense deposits or “humps” Electron microscope
- 27. POST STREPTOCOCCAL GLOMERULONEPHRITIS • Laboratoryfindings: • Low serum complements levels of C3 and C4 • Aso titre raised • Positive culture of throat swab Treatment: • Fluid and sodium restriction • Diuretics • Control of HTN • Resolves Completely
- 28. RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS • Presentswith Rapid deterioration of renal function • Oliguria and obvious macroscopic hematuria • Crescent formation>50% often associated with necrotizing lesions within glomerulus
- 29. RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS • Seenin Good pasture’s disease, SLE and Small vessel vasculitides • Need aggressive therapy with large dose steroids • Prognosis: poor, most require dialysis.
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- 31. ALPORT ‘S SYNDROME •X-linked recessive disorder characterized by • hematuria progressing to ESRD • Sensorineural hearing loss • Caused by mutation of COL4A5 gene on X chromosome which encodes type IV collagen • Abnormal collagen results in degradation on GBM and ocular abnormalities. • Female carriers presents with hematuria and does not progress to ESRD • No definitive treatment available.
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