IgA nephropathy is a fairly common kidney disorder. It is caused by an inflammation (glomerulonephritis) in the network of blood capillaries involved in the filtration of waste products from the blood. More specifically, it manifests itself through the deposit of the antibody immunoglobulin A (IgA) in the mesangial cells, which support the walls of the capillaries. The IgA deposits and accompanying lesions to the capillaries interfere with proper filtration of waste products from the blood.
IgA nephropathy is more common in men than in women and its incidence peaks between the ages of 16 and 35 years. IgA nephropathy is associated with a gradual decline in kidney function leading to end- stage renal disease within 5 to 25 years of diagnosis in 20-40% of patients. The disease is usually diagnosed after blood or excess protein is observed in the urine. Serum creatinine levels are abnormally high in IgA nephropathy because the kidneys are unable to filter creatinine (a waste byproduct of creatine, a protein that supplies energy for muscle contraction) out of the blood and excrete it in the urine. A doubling in serum creatinine level corresponds to a 50% decline in kidney function. There are no pharmaceutical drugs that will slow down or reverse the progression of IgA nephropathy.