Thirteen Things About IgA Nephropathy & Me, 8th

1. IgA Nephropathy or Berger’s (”burrjays”) disease is the most common non-diabetic kidney disease.
2. It results when IgA (immunoglobulin A), a normal component of the blood, collects in the kidney as damaging deposits. These deposits are an immune system defect, hence IgAN is considered an autoimmune disease.
3. 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.
4. One of the first signs of IgAN in adults is hematuria (blood in the urine), which I have had show up on lab-work for years but doctors haven’t followed up on.
5. While I was actively pursing a fibromyalgia diagnosis last year, one of the clues that led the doctors to suspect IgAN was excessively high levels of C-reactive protein in my blood.
6. A kidney biopsy is necessary to confirm the diagnosis. A long thin needle was inserted into my back 8 times to attempt to collect a small sample of my kidney — they missed 6 of those times. The doctor told my mother they only inserted the needle 2 times. They did not anesthetize me for this. I was only given Tylenol for the pain. Afterward, I had to remain in the hospital for 24 hours unable to move from the reclining position, not even to pee, while they made certain that I wasn’t bleeding internally from the procedure. It was a very long day.
7. A side effect of kidney disease is hypertension or high blood pressure, which I have mysteriously suffered from since my early 30’s. Even when I lost 55lbs in 2002, my blood pressure remained unchanged. (I’ve since gained it back without affecting my blood pressure.)
8. 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.
9. I am currently taking 20mg/day of Lisinopril in an effort to keep my blood pressure normal and reduce my C-reactive Protein levels, which remain high.
10. The heavy use of some analgesics, medicines that help to control pain and reduce fever, such as aspirin, acetaminophen (Tylenol), ibuprofen (Advil, Motrin), ketoprofen (Orudis, Oruvail) and naproxen sodium (Alleve), can damage the kidneys. Acetaminophen remains the drug of choice for occasional use in patients with kidney disease because of bleeding complications that may occur when these patients use aspirin. Unfortunately, I also have a fibromyalgia diagnosis and acetaminophen no longer helps the pain because it does nothing to reduce the inflammation like ibuprofen or naproxen sodium would, but it’s a catch-22.
11. 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).
12. At present, there is no cure for IgAN. Some people have mild cases which progress very slowly, with long periods of relative stability (which may even be perceived as a “remission”), and some have more aggressive cases which progress to chronic renal insufficiency and to end-stage renal disease more rapidly.
13. Currently, my prognosis is good. My doctor has assured me that my kidneys are functioning at pretty much 100% and as long as I lower my C-reative Protein,keep working to improve my overall health, and stick with my diet of no red meat or poultry among other minor adjustments, I shouldn’t have to worry for a long time about ESRD.

Sources: IgA Nephropathy Home Page, Wikipedia: IgA Nephropathy, The Foundation for IgA Nephropathy, National Kidney Foundation
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