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28 Cards in this Set
- Front
- Back
Renal Diseases which are Secondary to Systemic Diseases
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Systemic Lupus Erythematosus (SLE)
Diabetes Mellitus Amyloidosis Bacterial Endocarditis–Associated Glomerulonephritis Henoch-Schonlein Purpura Fibrillary Glomerulonephritis and Immunotactoid Glomerulopathy Goodpasture syndrome |
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Thickening of GBM and Mesangial expansion (Diffuse glomerulosclerosis)
Kimmelsteil-Wilson nodules (Nodular glomerulosclerosis) Arteriolar hyalinosis (pathognomonic when changes in both afferent and efferent arterioles) |
Diabetic Nephropathy (Nephrotic syndrome)
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Amyloidosis effect on the kidney
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Particularly glomeruli, causes proteinuria, advanced cases uremia and death
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Nephritic syndrome diseases
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IgA nephropathy
Poststreptococcal glomerulonephritis Rapidly progressing glomerulonephritis Membranoproliferative glomerulonephritis |
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What are red cell casts?
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Always pathologic
Yellowish-brown color Generally cylindrical with sometimes ragged edges; their fragility makes inspection of a fresh sample paramount Usually associated with nephritic syndromes Strongly indicative of glomerular damage |
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what are granular casts?
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Result either from the breakdown of cellular casts or the inclusion of aggregates of plasma proteins
Based on size of inclusions, classified as fine or coarse Seen in renal parenchymal disease |
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Appears 1-4 weeks after a group A Beta hemolytic streptococcal infection of pharynx or skin in children 6-10
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Post Streptococcal Glomerulonephritis. Immunologically mediated
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Post Streptococcal Glomerulonephritis lab findings
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elevated antibody titres against streptococcal antigens, lower serum C3 and cryoglobulins in the serum
-Latent period between infection and onset of nephritis is due to the time needed for antibody and immune-complex production |
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Post Streptococcal Glomerulonephritis Immunofluoresence
Electron microscopy |
Immunofluoresnce: Coarse granular immunofluorescence for IgG and C3-lumpy bumpy as in starry sky pattern
EM: Electron dense humps on the epithelial side of the bsmt membrane (subepithelial deposits) |
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Focal proliferative glomerulonephritis
Hematuria Proteinuria Moderate increase in mesangial matrix and mild mesangial hypercellularity |
IgA Nephropathy/Henoch-Schonlein purpura
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IgA Nephropathy
immunofluorescence EM |
Immuno: uniform mesangial positivity for IgA
EM:Mesangial deposits of IgA |
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Clinical-pathologic syndrome characterized by the accumulation of cells in the Bowman space as crescents with rapid decline in renal function
Proliferation of parietal cells in Bowman space Crescents eventually undergo sclerosis |
Crescentic Glomerulonephritis/ Rapidly Progressive Glomerulonephritis
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Rapidly Progressive (Crescentic) Glomerulonephritis Type I:
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Anti-GBM IgG and C3
Idiopathic Goodpasture syndrome |
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Rapidly Progressive (Crescentic) Glomerulonephritis Type II
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: Immune complex
-Idiopathic -Post-infectious -Systemic lupus erythematosus -Henoch-Schonlein purpura (IgA) |
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Rapidly Progressive (Crescentic) Glomerulonephritis Type III
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Pauci-immune (ANCA associated)
Idiopathic Wegener granulomatosis Microscopic polyarteritis nodosa |
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In goodpasture syndrome Rapidly Progressive (Crescentic) Glomerulonephritis presents with
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Nephritic syndrome with hemoptysis and antiglomerular basement membrane antibodies the noncollagenous (NC1) domain of the alpha 3 chain of type IV collagen
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Good pasture syndrome elisa testing
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NEGATIVE
Normal glomerulus incubated with patient’s serum shows no GBM positivity,indicating that no anti-GBM antibody is present in the patient’s serum. + Normal glomerulus stained with serum from a patient who has anti-GBM antibodies |
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Focal Necrotizing glomerulonephritis, Pauci-Immune,
due to Wegener Granulomatosis microscopic findings |
Pulmonary and renal lesions
Serum c-ANCA positive Fibrinoid necrosis Pyknotic nuclei and nuclear fragments Hypercellularity and early crescent formation PAS-fibrin IF-fibrinogen EM-fibrin |
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Thin Basement Membrane DiseaseDifferential Diagnosis with Alport Syndrome
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Bengin familial hematuria
Heredofamilial disorder or sporadic Glomerular basement membrane thinning Hematuria/proteinuria 20-25% of pediatric/adult patients with persistent isolated hematuria ADULTS <250 nm |
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Alport syndrome (Hereditary nephritis) has a triad of symptoms
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Nephritis, nerve deafness, cataracts. It first presents with hematuria and erythrocyte casts
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What causes Alport syndrome?
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X-linked disorder that results in the mutation of the alpha 5 chain of collagen type 4.
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Alport syndrome EM
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Irregular foci of thickening or attenuation in the glomerular basement membrane with longitudinal splitting of the lamina densa
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Diseases Presenting as Both Nephritic and Nephritic Syndrome
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Membranoproliferative Glomerulonephritis
(MPGN) Systemic Lupus Erythematosus |
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Membranoproliferative (Mesangiocapillary) Glomerulonephritis type 1 and 2 general characteristics
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1)mesangiocapillary glomerulonephritis seen in SLE, hep B and c and involves the alternative pathway activation as well as the classical so deposits of C3, C4 and C1q
2) (Dense deposit disease and involves only the alternative pathway so C3 deposits. Recurs in transplant kidney Most pts with Membranoproliferative Glomerulonephritis are under 30! |
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Membranoproliferative Glomerulonephritis type 1 and 2 EM
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TYpe 1: Subendothelial dense deposits
Type 2: Dense sausage-like, deposits within glomerular bsmt membrane |
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Membranoproliferative Glomerulonephritis type 1 and 2 light microscopy reveals a characteristic feat
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Railroad track or tram track appearance of the replicated basement membrane:
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Membranoproliferative Glomerulonephritis type 2 can be screened by circulating antibody
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autoantibody called C3 nephritic factor, which binds to the C3 convertase of the alternative pathway
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The greatest contributions to Chronic glomerulonephritis are
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Rapidly progressive glomerulonephritis
FSGS Membranoproliferative GN |