Only $2.99/month

Terms in this set (32)

Epidemiology: Most common cause of glomerulonephritis worldwide; appears in 2nd to 3rd decade of life; most prominent in Asian and Caucasian populations

Etiology: Environmental antigens trigger a mucosal immune response that forms IgA antibodies. Antigen may be viral, bacterial, or food. The IgA immune complexes are pathogenic.

Pathogenesis: Formation of IgA immune complexes that are abnormally glycosylated and cannot be cleared by the spleen. The complexes are recognized as abnormal by the immune system and a second antibody, IgG, is formed against it (they recognize the abnormal hinge region where the glycosylation occurs). These large macromolecules then deposit in the mesangium of the kidney. Complement is activated.

Diagnosis: Renal biopsy. Serum complement is normal, as the activation occurs locally and not systemically. Mesangial cells proliferate and make more matrix: more so than usual.

Clinical presentation: ~40% have gross hematuria following Upper Respiratory Infection; synpharyngitic hematuria. ~30% have microscopic hematuria and proteinuria discovered incidentally. 5-10% present with acute nephritic syndrome, and some present with rapidly progressing glomerulonephritis (RPGN). May be associated with skin or GI abnormalities; dermatitis herpetiformis, celiac sprue, cirrhosis

Treatment: Prognosis is variable, with 10-40% progressing to chronic renal failure. If renal function is normal and proteinuria is <500 mg, then no treatment. If proteinuria > 1g, then treat with ACE inhibitors or ARBs. Fish oil. Steroids for patients with proteinuria >1g or with progressive disease (ex: prednisone)