Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
20 Cards in this Set
- Front
- Back
|
When would you consider doing a kidney biopsy in a diabetic patient? (4)
|
Features suggesting systemic disease other than diabetes
Hematuria Lack of retinopathy Fulminant course |
|
|
What are features seen on light microscopy of a kidney biopsy from a patient with diabetic nephropathy? (3)
|
Mesangial expansion
Diffuse glomerular BM thickening Nodular clomerulsclerosis (Kimmelstiel-Wilson nodules) |
|
|
What is the pathogenesis of diabetic nephropathy?
|
AGE, sorbitol pathway and protein kinase C all cause increase in reactive oxygen species which results in microvascular damage in kidney
|
|
|
How would you manage diabetic nephropathy?
|
Control glucose
Treat associated dyslipidemia Control BP to <130/80 using ACEi/ARB or ACEi+ARB Control proteinuria |
|
|
What is the pathogenesis of HIV associated nephropathy (HIVAN)?
|
Viral infection of epithelial cells in glomerulus and tubules causes cell hyperplasia
|
|
|
What is the treatment for HIVAN?
|
Treat HIV infection (HAART)
Treat glomerular disease with ACEi/ARB Immunosuppression in some cases |
|
|
What is the differential for nephritic syndrome (blood and RBC casts in urine) with normal GFR ?
|
Primary - IgA nephropathy, idiopathic mesangial proliferative GN
Secondary - Alport's syndrome, Henoch-Schonlein pupura, SLE |
|
|
What is the pathogenesis of IgA nephropathy?
|
IgA is abnormally glycosylated so that it cannot be taken up the liver for break down.
High levels of IgA bind to mesangial cells forming complexes Triggers inflammation and mesangial cell proliferation/glomerular injury |
|
|
What are subtypes of IgA nephropathy? (5)
|
Benign recurrent hematuria
IgA with associated minimal change disease IgA with progressive chronic kidney disease Crescentic IgA nephropathy IgA with systemic disease (Henoch-Schoenlein purpura) |
|
|
What is the pathogenesis of mesangial proliferative GN?
|
IgG or IgM antibody deposition in mesangial cells causing proliferation and glomerular injury
|
|
|
How do you treat IgA nephropathy? (according to subtpye)
|
Benign recurrent hematuria - nothing
With minimal change disease - steroids +/- immunosuppression with progressive CKD - ACEi/ARB, consider immunosuppression |
|
|
What is the differential diagnosis for nephritic syndrome that is rapidly progressing (RPGN)? (3)
|
Immune complexes: primary (IgA neprhopathy, idiopathic memranoproliferative GN), secondary (SLE, post strep GN, Henoch-Schenlein purpura, Endocarditis, cryoglobulinemia due to HCV or lymphoproliferative disorder)
Antibody to basement membrane: primary (anti-GBM Ab disease), secondary (Goodpasture's syndrome) ANCA: primary (idiopathic ANCA associated RPGN), secondary (Wegener's granulomatosis, microscopic poyangitis, Churg-Strauss syndrome) |
|
|
What is cryoglobulin?
|
Ab to immunoglobulin that precipitates in the cold and are associated with formation/deposition of immune complexes
|
|
|
What triggers cryoglobulinemia? (2)
|
Hepatitis C virus
lymphoproliferative disorder |
|
|
What is RPGN also known as?
|
Crescentic GN
|
|
|
How do you treat RPGN due to anti-GBM or ANCA-associated antibodies?
|
High dose prednisone: pulse to start, begin tapering at 2 months over next 4 months
Cyclophosphamide: 6 months Plasmaphoresis: if have pulmonary hemorrhage |
|
|
How do you treat RPGN due to an underlying infection?
|
Treat infection
Prednisone or immunosuppression occasionally |
|
|
How do you classify lupus nephritis? (6)
|
Class I - minimal lupus glomerulonephritis
Class II - mesangial proliferative LGN Class III - Focal LGN (<50% glomeruli) Class IV - Diffuse LGN (>50% glomeruli) Class V - Membranous LGN Class VI - Advanced sclerotic LGN (>90% sclerosis) |
|
|
What is the pathogenesis of Lupus nephritis? (3)
|
Autoantibodies (against glomeruli) and immune complexes
Complement activation T and B cell abnormalities |
|
|
How do you treat lupus neprihitis? (based on class)?
|
Diffuse proliferative: Induction with corticosteroids and cyclophosphamide for 3-6 months then maintenance with low dose corticosteroids
Focal proliferative: corticosteroids only with high dose then taper Membranous: corticosteroids plus cyclosporin or cyclophosphamide |
