|
Items in IgA Nephropathy
Other kidney diseases and IgAN
|
The Foundation for IgA Nephropathy
Other kidney diseases and IgAN
It's still hard to say that definitely, IgAN is or isn't associated with anything else, since nobody knows why IgAN happens. If it is associated with getting or doing something else, it sure isn't an obvious thing that can clearly be identified, because by now, just about everything has been considered.
Post-streptococcal glomerulonephritis (PSGN)
There was a time when post-strep GN and IgAN would have been considered more or less the same thing, but that has long been disproved. At one time, prior to the late 1960's, they might both have been referred to as Bright's disease, with one version simply being more chronic than the other. At that time, medical science had not yet developed the ability to distinguish between the many types of glomerular kidney diseases.
Among parents of children with IgAN, the question often comes up as to whether IgAN is a consequence of PSGN. In presentation, acute PSGN can be very similar to an acute episode (or "flare-up") of IgAN. They can often both happen after an upper respiratory infection, so they can easily be confused initially if no biopsy has been done (we suspect that the IgAN has already been present when that happens, and that the flare-up only brings about more obvious symptoms that then lead to diagnosis). We might suppose it's possible they could also happen simultaneously sometimes, with a PSGN leading to the discovery of already existing but sub-clinical IgAN when a biopsy is done. But post-strep GN isn't a permanent, chronic disease, while IgAN is. While acute IgAN and PSGN share many symptoms, PSGN tends to affect C3 and C4 complements. In IgAN, C3 and C4 are usually not affected. IgAN episodes tend to recur following subsequent upper respiratory infections, while PSGN is usually a one-time event. But if there's any confusion, the biopsy should resolve it, since there is no characteristic deposition of IgA in the glomeruli, as there is with IgAN. Also, in PSGN, there are other distinguishing features on the biopsy. Is IgAN actually caused as a consequence of PSGN? Probably not, since most people who get PSGN at some point do not develop IgAN.
Diabetic nephropathy
Diabetes generally affects the vascular system (blood vessels), and since the glomeruli (the filters in the kidneys) are really just tiny little balls of miniature blood vessels, they are very susceptible to being damaged over time by poorly-controlled diabetes. The result is progressive kidney damage, leading eventually to ESRD. Having diabetes plus IgAN may increase your chances of reaching ESRD, but this has not been studied. There is no relation between diabetes and IgAN.
Hypertensive kidney disease
High blood pressure that is uncontrolled and sustained over a long period of time can lead to ESRD on its own, without the presence of any other kidney disease - hence the great emphasis on controlling high blood pressure if you have any kidney disease, including IgAN.
End-stage renal disease (ESRD)
This is what it's called when you reach the point where dialysis or kidney transplant is needed. ESRD is not a kidney disease as such. While it is treated as one once a person has it, it is really simply what happens when, due to a kidney disease, hypertension, drugs, etc., the person reaches the point where the loss of kidney function is permanent, and renal replacement therapy is required to maintain life. This can be any form of dialysis, or a kidney transplant. Statistics on this are not absolutely clear, but anywhere from 30 to 50% of IgAN patients will reach ESRD within their lifetime. It's a variable statistic, since IgAN typically progresses to ESRD over a decade or two. Many haven't reached ESRD after 20, 25 or even 30-plus years since the initial discovery of blood and/or protein in their urine, while some reach it much sooner. For more information on this, please continue into the Renal Insufficiency Notebook section of the website.
|