Nephrology- Glomerular Disease Flashcards
S&S minimal change disease
Edema (periorbital, scrotal, tibial)
Fatigue
Abdominal pain
proteinuria
Mechanism of minimal change disease
Dysregulation of T-cells. Release cytokines that damage the capillary wall of the glomerulus. Epithelial podocyte injury and loss of charge selectivity
Diagnosis of MCD
Clinical. Biopsy only in atypical cases. Diffuse podocyte effacement on EM
Mechanism of PSGN
immune complex deposition
Nephrotic diseases
Minimal change disease Focal segmental glomerulosclerosis Membranous nephropathy Membranoproliferative Glomerulonephritis (if severe) DM nephropathy Systemic Amyloidosis
Nephritic diseases
PSGN
Diffuse proliferative glomerulonephritis (DPGN)
Membranoproliferative Glomerulonephritis (commonly)
Rapidly progressive glomerulonephritis
IgA Nephropathy
Alport Syndrome
Causes of rapidly progressive glomerulonephritis
Linear: Goodpasture Syndrome
Granular: PSGN, DPGN
Negative: Granulomatosis with polyangiitis, Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis
Nephrotic characteristics
Proteinuria >3.5g/day Fatty casts Edema Hypercoag state (loss antithrombin III) Hyperlipidemia/cholesterolemia Hypogammaglobulinemia
Nephritic characteristics
Inflammation <3.5 g/day protein RBC casts Hematuria HTN Oliguria
Granular subepithelial IgG, C3 immune deposits
Differential
PSGN: hematuria, HTN
Membranous nephropathy: Capillary loops involved, proteinuria
Assosiations with membranous nephropathy
Malignancy
Infection (hep B, hep C, syphilis)
Autoimmune diseases (SLE)
Drugs (NSAIDs, penicillamine)
Associations of focal segmental glomerulosclerosis
HIV Heroin use Obesity Sickle cell African America & Hispanics
Most common Nephrotic in adults w/o systemic disease
FSGS
Membranous nephropathy
Compliment levels IgA vs PSGN
PSGN- low C3
IgA- normal
