Glomerular Diseases Flashcards
What are the mechanisms of all glomerular diseases?
- Endothelial injury: TMAs
- Structural abnormality of GBM: thin BM and Alports
- Immune complex mediated: in situ formation( intrinsic or planted antigen) or circulating complexes
- Direct antibody attack: AntiGBM and ANCA
- Complement dysregulation: atypical HUS and C3 GN
- Podocyte dysregulation or injury: FSGS
Hydralazine associated ANCA vasculitis few words:
-Necrotizing crescentic GN, MPO ANCA predominates and titer is elevated, frequent presence of ANA, anti-histone and antidsDNA, hypocomplementemia is common
Mention the old and new classification of MPGN
- Old: I, II and III
- New: complement and Ig +, complement positive Ig -
Causes of nephrotic syndrome in IgA nephropathy
- advanced glomerular sclerosis
- diffuse proliferative glomerulonephritis involving all glomeruli
- overlap of IgA with MCD and other glomerular disease
What are the predictors of poor renal outcome in IgA?
- Serum Cr
- HTN
- Proteinuria >1 gm: single biggest
AntiGBM+ ANCA overlap disease characteristics
-presents as antiGBM disease, relapse as ANCA disease
When do you think is the best to obtain spot urine protein/cr ration?
-probably second void, First void proteinuria is at lowest
Cautions in using/ interpreting urine albumin/Cr
-causes of decrease in urine Cr excretion like decreased muscle mass, age, vegetarian diet etc
-causes of increase in urine Cr excretion high red meat diet, muscle breakdown
etc will alter ratio
Categories of proteinuria
Glomerular, Tubular, Overflow, Tissue, Physicochemical
Overflow: paraprotein, hemoglobin, myoglobin, Lysozyme, mucoprotein from malignant tumors
Physicochemical: best eg is glycated albumin in DM
MCD that hasnt responded well to steroids?
Think of Glomerular tip lesion or FSGS
One situation to suspect C3 GN
-Post infectious GN that hasnt gone away
What happens to complements in Hydralazine induced ANCA vasculitis?
may be low, and + ANA, Antihistone, antidsDNA
