Glomerulonephritis Flashcards
Nephrotic Syn
Urine protein >3500mg/d
Hyercoagulability due to loss of protein C and AT3
Increased risk of infection likely due to immunoglobulin
Minimal change glomerulopathy
Acute onset of edema and weight gain. Urine protein very elevated, complement normal, serology negative
Biopsy: normal glomeruli on light and immunofluorescence. Tubules may have lipid accumulation. Electron shows effacement of epithelial foot processes
Tx with steroids
Secondary causes: NSAIDs, lithium, pamidronate, interferon, hodgkin lymphoma
Membranous glomerulopathy
Edema, nephrotic proteinuria, hypertension, microhematuria, thromboembolic events common (renal vein thrombosis).
Biopsy: glomerular capillary loops that appear thickened w/o proliferative lesions, subepithelial immune dense deposits on electron/immunofluorescence.
1/3 remit spontaneously, generally if no remission after 6-12 months/worsening renal function/thromboembolic events: tx with steroids, cyclophosphamide/calcineurin.
Primary is antibody to phospholipase A2 receptor.
Secondary is malignancy, AI disease, infections.
If cause is secondary, tx precipitating infection or malignancy.
HepB/C, malaria, syphilis, SLE,
Focal Segmental Glomerulosclerosis
Asymptomatic nephrotic proteinuria or edema. Often accompanied by HTN, microscopic hematuria, varying kidney failure.
Serology and complement normal
Biopsy: segmental scars in glomeruli, electron microscopy shows visceral epithelial foot process effacement but no immune deposits
Idiopathic or secondary (HTN, DM, Obesity, sickle cell, HIV, drugs)
HIV is related to collapsing form
Most common form in blacks
Minority of patients have spontaneous remission, otherwise tx with steroids or calcineurin inhibitors
Diabetic Nephropathy
Starts with microalbuminuria, then 10-15 years after DM dx, progresses to overt proteinuria.
Test for proteinuria at dx of DM2 and 5 years after DX of DM1.
Biopsy not indicated unless concerned for alternative pathology.
Tx with ACE or ARB
RPGN
Progression to overt renal failure within weeks.
May be associated with any etiology or idopathic
typically presents with nephritic syn, variable renal failure, systemic signs either vasculitic (arthritis, epistaxis, hemoptysis) or lung hemorrhage (goodpasture).
Serology may reveal cause. CXR may confirm pulmonary hemorrhage.
Tx with steroids then maybe cyclophosphamide or rituximab. Plasmapheresis if pulmonary hemorrhage or severe renal failure.
particularly common with anti-GBM and pauci-immune small vessel vasculitis
Anti-GBM
Antibodies against type IV collagen
Generally presents with neprhitic proteinuria
Complement normal, elevated anti-GBM
Goodpastures is pulmonary + renal involvement
Biopsy: proliferative GN, many crescents, linear IgG deposition
Tx Cylcophosphamide/steroids
Nephritic Syn
hematuria with dysmorphic RBCs with or w/o casts
variable protein
Pauci-immune GN
Microscopic vessel vasculitis.
Generally ANCA: GPA/MPA/EGPA
Can be kidney limited or widespread (palpable purpura, pulm disease).
IgA Nephropathy
Asymptomatic microscopic hematuria with or w/o proteinuria. Episodic gross hematuria following URI (synpharyngitic nephritis - occurs shortly after or concomitant with URI).
Serology and complement normal.
Bx: mesangial proliferation on light micro, IgA deposit on immuno.
20 year survival is 75%, can tx with steroids.
Most frequent cause of GN, particularly Asia/Northern europe. Rare in blacks.
IgA Vascultis
AKA Henoch-Schonlein Purpura
Kidney involvement similar to IgA, also have abdominal findings and palpable purpura.
SLE nephritis
May be presenting finding of SLE.
Likely will have SLE serologies (ANA/DNA, low C3/4).
Biopsy: immune complex deposition in all areas of glomerulus.
Tx: depends on class, if 3-4 use aggressive immunosuppresion.
Post-infectious GN
Immune Complex mediated, typically present with acute nephritic syn.
Low C3, Normal C4, ASO titer positve, Anti-DNAse B
Associated with strep/staph infections. Ecoli is risk factor too. Typically present with 7-10 day latent period after infection.
DM is risk factor.
Tx underlying infection.
Cryoglobulinemia
Very commonly associated with Hep C
Patients with cryoglobulinemia may manifest a spectrum of kidney abnormalities, including mild proteinuria and hematuria, the nephrotic syndrome, and rapidly progressive glomerulonephritis with rapid deterioration of kidney function. C4 (and sometimes C3) complement levels are typically low, and rheumatoid factor is positive.
Membranoproliferative
Histologic findings of mesangial and endocapillary proliferation combined with the thickening of the GBM.
Caused by immune complex deposistion or activation of alternative complement pathway.
Immunoglobulin mediated: SLE, HepC, monoclonal gammopathy
Complement mediated: Dense deposit disease (DDD) or C3 glomerulopathy
