Table 11.3-1. Classification, etiologies, and clinical features of glomerulopathies


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


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


– 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.