Glomerulopathy |
Etiology/secondary causes |
Clinical features | |
Postinfectious GN |
– Primarily streptococcal and staphylococcal infections – Less commonly gram-negative bacteria, viral, fungal, or protozoal |
Nephritic syndrome ~1-3 weeks after streptococcal infection, 4 weeks after staphylococcal infection | |
IgA nephropathy |
– Seen with Henoch-Schönlein purpura – Associated with cirrhosis, celiac disease, inflammatory bowel disease, HIV, and seronegative arthritis |
Microscopic hematuria, “synpharyngitic” gross hematuria, hypertension, proteinuria | |
Membranoproliferative GN | |||
Immune complex–mediated |
Hepatitis C with cryoglobulinemia, hepatitis B, HIV, endocarditis, shunt nephritis, malaria, schistosomiasis, autoimmune disorders (SLE, Sjögren syndrome), malignancies (dysproteinemias, rarely lymphomas, carcinomas) |
Varied presentation: microscopic hematuria and nonnephrotic proteinuria, nephrotic syndrome, occasionally rapidly progressive renal failure, commonly hypertension | |
Complement-mediated |
C3 nephritic factor, factor H deficiency (inherited or autoimmune) | ||
Minimal change disease |
– Most commonly primary/idiopathic – Secondary causes include NSAIDs, interferon, lithium, gold, lymphoproliferative disorders (Hodgkin lymphoma) |
Nephrotic syndrome | |
Membranous nephropathy |
– Most commonly primary/idiopathic – Secondary causes include autoimmune conditions (primarily SLE), infections (hepatitis B and C), medications (NSAIDs, gold, penicillamine), malignancies |
Nephrotic syndrome | |
FSGS |
– Primary/idiopathic – Secondary causes include HIV, parvovirus B19, CMV, EBV, pamidronate, heroin, lithium, obesity, reflux, sickle cell disease |
Hypertension, proteinuria, and microscopic hematuria; nephrotic syndrome and abrupt development more common in primary/idiopathic FSGS | |
CMV, cytomegalovirus; EBV, Epstein-Barr virus; FSGS, focal segmental glomerulosclerosis; GN, glomerulonephritis; NSAID, nonsteroidal anti-inflammatory drug; SLE, systemic lupus erythematosus. |