Primary/idiopathic 85% of<unk>  cases are classified as primary<unk> —that is to say, the cause of the disease is idiopathic (of unknown origin or cause). This can also be referred to as idiopathic<unk>  nephropathy. One study has identified antibodies to an M-type phospholipase A2 receptor in 70% (26 of 37) cases evaluated. Testing for these anti-PLA2R has revolutionised diagnosis and treatment of this disease in antibody positive patients, and tracking titre level over time allows you to predict risk of disease progression and chance of spontaneous remission In 2014, a second autoantigen was discovered, the thrombospondin type 1 domain-containing 7A (THSD7A) system that might account for an additional 5-10% of<unk>  nephropathy cases, and appears to be associated with malignancies. New studies are identifying novel auto-antigens responsible for causing a<unk>  nephropathy pattern of injury continue to be published, with antibodies against NELL-1 and EXT1/EXT2 in 2019, Semaphorin3B and Protocadherin 7 (PCDH7) in 2020, and serine protease HTRA1 in 2021. Secondary The remainder is secondary due to: * autoimmune conditions (e.g., systemic lupus erythematosus). * infections (e.g., syphilis, malaria, hepatitis B, hepatitis C, HIV). * drugs (e.g., captopril, NSAIDs, penicillamine, probenecid, Bucillamine, Anti-TNF therapy, Tiopronin). * inorganic salts (e.g. gold, mercury). * tumors, frequently solid tumors of the lung and colon; hematological malignancies such as chronic lymphocytic leukemia are less common.
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis
Focal proliferative nephritis
Transplant glomerulopathy
Mesangial proliferative glomerulonephritis
Diffuse proliferative nephritis
Minimal mesangial glomerulonephritis
IgA nephropathy