IgA nephropathy is a condition that is considered to be of unknown cause (“idiopathic” in medical terminology) that causes kidney damage. Over time, this condition can get worse and the kidneys can suffer varying degrees of damage (though some people get better even without treatment). The condition is common in North America, though much more common in the Mediterranean region and Asia.
Most often, IgA nephropathy is detected incidentally in a routine urine test when blood or protein is found. Sometimes it is first noted after a cold or flu episode that leads to blood in the urine. Very rarely the condition starts out as acute failure of the kidneys.
Naturopathic medicine offers a unique ability to work with the totality of your situation. We can help you assess and monitor your condition, help figure out some of the possible underlying causes and treat those, as well as offering natural supportive and corrective treatments. We can work with and even prescribe most of your medications if necessary. We can work with your other providers to determine if some medications might not be needed or doses reduced.
What Causes IgA Nephropathy?
IgA nephropathy is a classic example of a condition in which someone with a genetic predisposition only develops a problem when exposed to one of several potential environmental triggers (thus a “two-hit” condition). It is now known that people who develop IgA nephropathy have a genetic problem with attaching certain sugars to their A type immunoglobulins (antibodies), or IgA, subtype 1. IgA1 antibodies are very unusual in humans for being blood proteins that have so-called O-linked sugars. The enzymes that control which sugars are attached to the IgA1 are mutated in such a way that not very many galactose sugars are attached. The results if the IgA1 don’t work very well. This is only an issue if the body calls out for production of a lot of IgA1: the environmental trigger.
Many studies point to the fact that people with IgA nephropathy have allergic reactions to food (Kovacs, et al. 1996; Coppo, et al. 1991). A particular problem is a reaction to wheat, which is different than celiac disease (Almroth, et al. 2006; Laurent, et al. 1987). These reactions are one of the potential environmental triggers that stimulates lots of IgA1 to be made. They stick onto food proteins but don’t do anything useful. The resulting immune complex (IgA1-antigen complex) then floats through the blood and ends up sticking in the kidneys, provoking inflammation and damage.
Not all patients with IgA nephropathy have food allergies. As noted above, infections are also a common trigger of IgA1 production and thus provoking IgA nephropathy. Getting blood in the urine during an acute infection is known technically as “synpharyngitic hematuria” and is a major hallmark of this condition not seen in most other diseases. Anyhow, it is critically important that the possibility of food reactions be investigated and any problem foods removed to prevent the condition from progressing. The process of determining the foods that we use at Northwest Naturopathic Urology is called an elimination-challenge diet, but if for some reason that can’t be done then there are some much less reliable tests that can be done. Testing for antibodies to gliadin, the compound in wheat that most often triggers an allergic reaction damaging the kidneys, is usually done to help decide whether to remove wheat from the diet.
The way the elimination-challenge diet is done is very important. It is critical to realize that many food reactions are delayed, and also there is no predicting for any single patient what food or foods will be a problem, so just avoiding common antigens (like wheat, gluten, or dairy) is not sufficient. Short eliminations without challenges are also a problem because many reactions are delayed, and there may be no noticeable symptoms (so using urine protein testing is critical to monitor the process). Speaking with Dr. Yarnell about how to properly do an elimination/challenge diet is advised.
Another part of the problem that often underlies IgA nephropathy is known as leaky gut syndrome. In this case, food molecules are absorbed that shouldn’t be, which can trigger the reactions that damage the kidney. A simple urine test is done to determine if this is a problem and whether natural treatments such as glutamine are indicated to help fix the leakiness.
Other Natural Treatments
Several studies have shown that high-doses of fish oil can help decrease the severity of the disease (Hogg, et al. 2006). Most people who treat themselves use far too little to make a difference. We can help you figure out the optimal dose for your body size.
A number of herbal medicines have been used effectively in our practice to help prevent and even reverse some of the kidney damage that occurs in people with IgA nephropathy. Some of the most important herbs of this type include Lespedeza capitata (round-head lespedeza) leaf and flower, Rheum palmatum (rhubarb) root (used at a low-dose to prevent diarrhea), and Parietaria judaica (pellitory-of-the-wall) herb. These herbs are extremely safe. We generally develop an individualized herbal formula to address your condition and help protect your kidneys.
There are several natural therapies, including magnesium and the powerful herb Rauvolfia serpentina (Indian snakeroot), that can help us manage any high blood pressure you may have naturally, Sometimes this allows patients to avoid medications for blood pressure, and sometimes they are used in combination for optimal effects.
Some vitamins may also be helpful for your situation, though this requires analysis of your symptoms and how long you have had the condition to determine.
Does It Work?
We have had four IgA nephropathy patient in 2009. Three of them had relatively mild or early disease, without symptoms other than protein or blood in the urine. Urine protein levels declined or became normal in all three after elimination-challenge diet and with high-dose fish oil and herbal medicines (and occasionally a couple of other supplements). No one has developed any complications attributable to treatment or IgA nephropathy.
One patient seen initially in 2006 has been followed up for years. She had severe disease (present for over 20 years, with high blood pressure and significantly reduce kidney function). She was able to maintain at a functional level for those entire three years until finally she had to go on dialysis. Conventional doctors all said there was nothing she could do but wait until she had to go on dialysis, then get a transplant. Though ultimately in her case this was not prevented, it was at least delayed significantly. Who knows what might have happened if she had seen a naturopathic doctor before the condition got completely out of control.
As of 2004, Dr. Yarnell has worked with 37 patients with a definitive diagnosis of IgA nephropathy, ranging from teenagers to adults. A compilation of their results is still ongoing. Nine with food follow-up definitely had significant improvement; one (described above) improved despite having advanced disease but ultimately had to go on dialysis and then get a transplant. Four did not undertake treatment and did not follow-up, so their outcomes are unknown. At least one patient already on dialysis did not have much improvement, not surprisingly. One patient who already had a transplant due to IgA nephropathy and was showing some signs of rejection has stabilized and stayed stable working with Dr. Yarnell for the past three years.
Almroth G, Axelsson T, Müssener E, et al. (2006) “Increased prevalence of anti-gliadin IgA-antibodies with aberrant duodenal histopathological findings in patients with IgA-nephropathy and related disorders” Uppsala J Med Sci 111(3):339–52.
Coppo R, Amore A, Roccatello D, et al. (1991) “Role of food antigens and alcohol in idiopathic nephritis with IgA deposits” Minerva Urol Nefrol 43(3):171-4 [in Italian].
Hogg RJ, Fitzgibbons L, Atkins C, et al. (2006) “Efficacy of omega-3 fatty acids in children and adults with IgA Nephropathy is dosage- and size-dependent” Clin J Am Soc Nephrol 1: 1167–72.
Jenkins DA, Bell GM, Ferguson A, Lambie AT (1988) "Intestinal permeability in IgA nephropathy" Nephron 50(4):390.
Kovács T, Kun L, Schmelczer M, et al. (1996) "Do intestinal hyperpermeability and the related food antigens play a role in the progression of IgA nephropathy? I. Study of intestinal permeability" Am J Nephrol 16(6):500–5.
Kovács T, Mette H, Per B, et al. (1996) “Relationship between intestinal permeability and antibodies against food antigens in IgA nephropathy” Orv Hetil 137(2):65-9 [in Hungarian].
Laurent J, Branellec A, Heslan JM, et al. (1987) “An increase in circulating IgA antibodies to gliadin in IgA mesangial glomerulonephritis” Am J Nephrol 7(3):178-83.