glomerular disease
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this poerpoint includes introduction to kidney disorders - anatomyof kidney, histology of glomeruli , pathogenesis and pathology of glomerular disease
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glomerular disease
- 3. The main purpose of the kidney is to separate urea, mineral salts, toxins, and other waste products from the blood. They also do the job of conserving water, salts, and electrolytes. At least one kidney must function properly for life to be maintained.
- 7. GLOMERULUS: Glomerular capillary wall: 1. Fenestrated endothelium –70 – 100 nm, 2. Glomerular Basement Membrane .. Lamina rara interna, .. Lamina densa, .. Lamina rara externa 3. Visceral epithelial cells (podocytes) 4. Mesangial cells – contract, proliferate, collagen & matrix, secretion;
- 8. Three-dimensional schematic drawing of the glomerulus Afferent arteriole Efferent arteriole Bowman’ s Capsule Basement membrane Visceral Epithelium(Podocyte) Parietal Epithelium Capillary loops Bowman’s Space Endothelial cells Stucture of renal glomerulus Mesangial matrix and cell
- 14. DISEASES OF GLOMERULI DISEASES OF TUBULES DISEASES OF INTERSTITIUM DISEASES OF BLOOD VESSELS
- 15. AZOTEMIA – BUN, Creatinine --- GFR UREMIA – Azotemia + Clinical signs and symptoms + Biochemical abnormalities + Involvement of G I tract, Peripheral nerves .. and heart;
- 19. DEFINITION Abnormalites of glomerular funtion can be caused by damage to the major components of the glomerulus: Epithelium (podocytes), Basement membrane, capillary endothelium, mesangium. Damage manifested by an inflammatory process.
- 21. Histologic alterations a) hypercellularity: i) cell proliferation of mesangial cells or endothelial cells ii) leukocyte infiltration (neutrophils, monocytes and sometimes lymphocytes) iii) formation of crescents - epithelial cell proliferation (from immune/inflammatory injury) - fibrin thought to elicit this injury (TNF, IL-1, IFN- are others) www.freelivedoctor.com
- 22. b) basement membrane thickening - thickening of capillary wall c) hyalinization (hyalinosis) and sclerosis -accumulation of material that is eosinophilic and homogeneous - obliterates capillary lumen of glomerulus (sclerotic feature) www.freelivedoctor.com
- 23. classification is based on histology. Subdivided: a) diffuse (all glomeruli) b) global (entire glomerulus) c) focal (portion of glomeruli) d) segmental (part of each glomerulus) e) mesangial (affecting mesangial region) www.freelivedoctor.com
- 24. What causes glomerular disease ? Most are of immunologic origin, and caused by immune complexes ! • metabolic stress: DN • mechanical stress: • hypertension
- 25. Antibody mediated injury In situ immune complex deposition Fixed intrinsic tissue antigens collagen type4 antigen [anti GBM-nephritis] Heymann antigen [membranous nephropaty Mesangial antigens Circulating immune complex deposition Endogenous antigen[DNA,Nuclear proteins,immunoglobulins,igA] Exogenous antigen [infectiousagents,drugs] Cytotoxic antibodies Cell mediated immune injury Activation of alternative complement pathway
- 27. Pathogenesis of Glomerular Disease Immune mechanisms underlie most cases of primary GN and many of the secondary cases a) 2 forms of Ab-associated injury i) injury resulting from soluble Ag-Ab deposits in glomerulus ii) injury from Ab reacting in-situ with glomerulus www.freelivedoctor.com
- 28. • In Situ Immune Complex Deposition a) Ab act directly with intrinsic tissue Ag “planted” in the glomerulus from the circulation b) 2 forms of Ab-mediated glomerular injury i) anti-GBM Ab-induced nephritis - Ab directed against fixed Ag in ii) Heymann nephritis - a form of membranous GN - Ab bind along GBM in “granular pattern” www.freelivedoctor.com
- 29. Location: Mesangial and sub-endothelial
- 30. Location: GBM sub-epithelial • circulating auto antibodies with intrinsic autoantigens (component of normal parenchyma)
- 31. Location: GBM sub-epithelial Extrinsic antigens planted within the glomerulus
- 33. In situ immune complex Circulating immune complex Activation of T lymphocytes Acitvation of complements cytokines C5b-9 C5a,C3a Epithelial, mesangial, Endothelial cells Macrophagepolynuclear leucocyte, platelets Mesangial cells oxidative stress, protease, matrix accumulations Glomerular Disease
- 34. Glomerular Diseases PRIMARY GLOMERULOPATHIES Acute proliferative glomerulonephritis Post- infectious Rapidly progressive (crescentic) glomerulonephritis Membranous glomerulopathy Minimal-change disease Focal segmental glomerulosclerosis Membranoproliferative glomerulonephritis IgA nephropathy Chronic glomerulonephritis SYSTEMIC DISEASES WITH GLOMERULAR INVOLVEMENT Systemic lupus erythematosus Diabetes mellitus Amyloidosis Goodpasture syndrome Microscopic polyarteritis/polyangiitis Wegener granulomatosis Henoch-Schönlein purpura Bacterial endocarditis HEREDITARY DISORDERS Alport syndrome Thin basement membrane disease
- 35. Various types of glomerulopathies are characterized by one or more of four basic tissue reactions: 1. Hypercellularity 2. Basement membrane thickening 3. Hyalinosis 4. Sclerosis
- 37. Common form of GN in developing countries. 6 to 10yrs of age 1 - 4 weeks after a streptococcal infection of pharynx or skin (Impetigo) Group A β-haemolytic streptococci - types 12, 4, 1 Immunologically mediated disease Immune Complex mediated Anti - endostreptosin & other cationic antigens . Serum – C
- 38. Glomeruli- Enlarged , hypercellular glomeruli - infiltration by leukocytes - proliferation of endothelial & mesangial cells, - crescent formation (severe cases) - obliteration of capillary lumen Fibrin deposition in capillary lumen & mesangium. Interstitial edema and leucocytic infiltration Tubules contain red cell cast. Diffuse
- 43. Immunofluorescence: - granular deposits of IgG , IgM , C3 in mesangium , along BM
- 44. Electron microscopy: Discrete , amorphous , electron dense deposits on epithelial side of BM often having the appearance of “humps
- 46. Sudden onset in a young child - malaise, fever , nausea , oliguria , hematuria, Edema , mild - moderate hypertension , elevation of BUN Urine - RBC casts, proteinuria Lab - antistreptococcal antibody titre , C3
- 47. 95% -- children recover, < 1% - rapidly progressive GN 1-2% - slow progression to chronic GN, Persistent proteinuria, Abnormal GFR Adults Poor prognosis
- 49. Severe glomerular injury Does not denote a specific etiologic form of GN Clinically - rapid & progressive loss of renal function & death within weeks to months Crescents in most glomeruli – parietal epithelial cells proliferation;
- 50. Type - I RPGN ( Anti-GBM antibody induced disease) .. Idiopathic, .. Goodpasture syndrome; Type - II RPGN (immune Complex) .. Idiopathic, postinfecious, SLE, Henoch-Schonlein purpura (IgA), others; Type - III RPGN ( Pauci-immune ) .. ANCA associated, Idiopathic, Wagener granulomatosis, PAN;
- 51. Linear deposits of IgG , C3 in GBM Cross reaction with pulmonary alveolar BM Good - Pasture’s antigen located in noncollagenous portion of α3 domain of collagen type - IV
- 52. Immune complex mediated disease Complication of immune complex nephritides - Post infectious GN , SLE , IgA nephropathy Granular deposit of immune complexess of IgG and C3 along glomerular capillary walls. IF - lumpy bumpy granular pattern
- 53. Lack of anti GBM antibody , immune complexes by IF , EM ANCA present- defect in humoral immunity. Usually a component of systemic vasculitis - Wegeners Granulomatosis , Polyarteritis Idiopathic
- 54. Gross : Kidneys enlarged , pale ,smooth outer surface. C/S petechial hemorrhages on cortical surface
- 55. Crescents proliferation of parietal cells migration of monocytes ,macrophages into Bowmans space Crescents obliterate Bowman’s space , compress glomerular tuft Fibrin strands are prominent between cellular layers in the cresents.
- 58. Crescents Sclerosis EM : subepithelial deposits ruptures in GBM IF : Postinfectious cases - granular Good Pastures syndrome - linear Idiopathic - granular / linear
- 59. Electron micrograph showing characteristic wrinkling of GBM with focal disruptions (arrows).
- 61. Hematuria , RBC casts , proteinuria Hypertension , Edema Good - Pastures syndrome - Hemoptysis Anti - GBM , antinuclear , ANCA Renal involvement - progressive
- 62. a) massive proteinuria (> 3.5 g/day) b) hypoalbuminemia c) generalized edema d) hyperlipidemia and lipiduria
- 64. Latent GN (asymptomatic urinary abnormalities) Nephrotic syndrome Acute GN RPGN Chronic GN microscopic or Macroscopic hematuria Proteinuria Dysmorphic Glomerular erythrocytes Proteinuria>3.5g/d Hypoalbuminemia Hyperlipidemia Edema Hematuria Proteinuria (1-3g/d) ARF Edema Hypertension Red cell casts •Rapidly deterioration of renal function •Hematuria, Proteinuria • oliguria or anuria Red cell casts •With or without systemic symptom •Hematuria Proteinuria •Hypertens on •Reduced GFR
Editor's Notes
- Deposite
- attack