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There is a chunk of immune system research (p53 related) going on already.Booch wrote:I feel awkward requesting for research on my disease, IgA Nephropathy, because I feel selfish and because of all the work you do already but hey... its worth a shot right
Possibly; I am kindly petitioning to see if it might.7im wrote:Folding@home studies protein folding, the mis-folding of proteins, and diseases that result from mis-folding. Is IgA Nephropathy a result of mis-folding proteins?
Quoted from: http://www.igan.ca/id36.htmCauses of IgAN
General. At this writing, nobody really knows what causes a person to develop IgAN. Our immune system produces a number of different immunoglobulin complexes to fight off infections, allergens, etc. Among these are IgE, IgM, IgG and IgA. In the case of IgAN, something appears to go wrong with either the form of the IgA immune complex itself, or with their production and clearance within the body, or both. There may also be abnormal deposits of IgM or IgG, although with IgAN, the IgA proteins are the predominant ones.
IgA proteins. IgA stands for immunoglobulin A. We all have IgA proteins circulating in our blood at all times. IgA proteins (also referred to as IgA complexes) are produced at various sites in the body, such as the bone marrow and mucousal tissues in the tonsils, lungs and the intestines. While it may be logical to think that lowering the amount of these IgA proteins that circulate in the blood might slow the progression of IgAN, research as shown that this is not the case. For one thing, the amount of IgA that somehow sticks in the kidneys is tiny in comparison to the overall number of IgA proteins that are in the circulation, doing their job of fighting infection.
Mechanism of injury. The short explanation for IgAN is that some of these large IgA proteins are deposited in the glomeruli, where they remain to cause inflammation and to eventually choke off (or clog) the glomeruli so that blood cannot flow through them. Commonly, they are deposited and accumulate in the portion of glomeruli called the mesangium, until eventually, the tiny blood vessels which form the glomeruli are deprived of blood flow. When glomeruli become damaged through inflammation and loss of blood flow, they become scarred. This is referred to as glomerulosclerosis. Most adult patients already have some degree of glomerulosclerosis by the time a biopsy is performed. Ultimately, it is the glomerulosclerosis which causes permanent loss of kidney function.
Progressive chronic renal failure. Since there are about a million glomeruli in each kidney, there is an ample reserve of kidney function, and a person can go many years or even decades without feeling the effects of renal failure. However, once a glomerulus is damaged, it cannot be repaired. IgAN progressively destroys these glomeruli. As more and more glomeruli become scarred and non-functional, the remaining ones start working harder (a process called hyperfiltration), and eventually, as more and more of them fail at an increasingly faster rate, the kidneys no longer have enough function left to perform their task of filtering waste products from the blood. When this happens, the person is said to have reached end-stage renal disease (ESRD). At that point, some form of renal replacement therapy is required to sustain life (dialysis or a kidney transplant).