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Right Idea, But Wrong Organ

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I was convinced that Nadir's urinary issues were caused by food allergies that irritated the lining of his bladder similar to inerstitial cystitis in humans. I had no doubts whatsoever that eating certain foods caused his problems. How they affected him was just a guess though. When I brought him to Auburn and explained how his condition was closely linked to certain foods the idea was summarily dismissed and I was given the explanation that symptoms wax and wane. They waxed and waned alright, they waxed when I fed him something he shouldn't eat and waned when I didn't

I learned from his necropsy that it was his kidneys that were affected so I've been searching and reading whatever I can that could give some kind of explanation for the link between the foods he ate and his urinary problems. I found some studies this passed week that align with my conviction that food allergens can affect the organs such as the bladder and the kidneys.

I'm sure no one cares to read the entire thing so I'm just copying and pasting the background, some points that I felt were key (the mention of rice protein as one of the allergens), and the conclusion that was reached.


Gluten sensitivity in patients with IgA nephropathy





Coeliac disease is more frequent in IgA nephropathy (IgAN) patients compared to the healthy population. Several hypotheses postulate that food antigens like gluten may be involved in the onset of IgAN.




IgA nephropathy (IgAN) is the most common glomerulonephritis characterized by circulating immune complexes and deposition of IgA1 and complement C3 in the glomerular mesangium [ 1 ]. An association with infections in the respiratory or gastrointestinal tract with a triggering mucosal immune reaction is commonly observed [ 2 ]. The exact mechanism or antigens involved are,however,not known. In the late 1980s,potential food antigens were suggested as being involved in the onset of IgAN [ 36 ], and several studies have since then been conducted as to which food antigens are responsible,if any,and by which mechanism. Gluten has been proposed as one potential antigen [ 710 ]. Deposition of other food antigens (like soy bean protein,casein and rice protein) has been found in the mesangium of patients with IgAN [ 11 ]. Coppo et al. [ 12 ] have shown that experimental IgAN can be induced by gliadin in mice,and an association between IgAN and coeliac disease has been reported in clinical investigations [ 8 ,13 ]. Approximately 4% of the IgAN patients have coeliac disease,as compared with 0.51% in a healthy population [ 13 ]. Still,a gluten triggering immune response in IgAN is disputable and the mechanism remains unclear.



It is concluded that approximately one-third of our IgAN patients have a rectal mucosal sensitivity to gluten,but without signs of coeliac disease,and we hypothesize that such sub-clinical inflammation to gluten might be involved in the pathogenesis of IgAN in a subgroup of patients.

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That's very interesting and one of the reasons why I only give A2 milk (different - and older - protein to the mutated one in modern Holstein milk) to an elderly relative I look after who, amongst a whole raft of other things, has late stage kidney issues. Chronic Inflammatory responses are always best avoided and likewise unecessary low grade stress.

It is probably also significant that NSAIDs often exacerbate kidney failure. See this if you'd like to find out more..

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I wasn't able to view the article as the link took me to a sign in page. I have no doubts though that NSAIDS use can contribute to kidney failure.


Here's another paper that was written on the subject of food antigens. I can't copy and paste this one as easily so I'll just copy and paste the link from the 1st page for those interested in reading further and the 5th page, which gives the conclusions.


Glomerular deposition of food antigens in IgA nephropathy.


M Sato, H Kojima, K Takayama, and S Koshikawa


Page 1



Page 5



In this study too, it was concluded that food antigens strongly participate in the pathogenesis, the mechanism that causes Iga Nephropathy.

Edited by 4My2Greys
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Looks like I gave you the incorrect link... try this one Still won't work :headwall try looking up 'how nsaids compromise kidney function'


It never ceases to amaze me that the body is actually able to achieve long-term homeostasis.


Having lost 3 dogs over many years to CRF I think we need to know when their kidney function begins to decline so that we can do out best to remove stress.

Edited by JohnF
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Having lost 3 dogs over many years to CRF I think we need to know when their kidney function begins to decline so that we can do out best to remove stress.

I agree. I don't think the standard urinalysis test is enough. I think at a minimum once a year a protein creatinine ratio should be determined even if the urinalysis results don't warrant it. This would test for urinary albumin excretion. According to this next link I'm posting it is an earlier sign of vascular damage and is considered a predictor of worse outcomes for both kidney and heart patients. It also states that cardiovascular and renal risk is elevated even in the high normal range of microalbuminuria.

You'll have to use the link to read the rest of the paper, I've only copied the beginning.


Microalbuminuria, is it so important?


A Koroshi






Microalbuminuria (defined as urinary albumin excretion of 30-300 mg/day, or 20-200 µg/min) is an earlier sign of vascular damage. It is a marker of general vascular dysfunction and nowadays is considered a predictor of worse outcomes for both kidney and heart patients. There is a significant correlation between blood pressure and microalbuminuria. Even high normal blood pressure is associated with significant higher frequency of microalbuminuria and this way may be a biomarker of increased cardiovascular risk. Microalbuminuria could be taken also, as an indicator of insulin resistance and of the increased renal and cardiovascular risk associated with metabolic syndrome. Renal involvement is a pivotal development in diabetes and microalbuminuria is generally the first clinical sign of renal dysfunction in diabetics. It is demonstrated that cardiovascular and renal risk is elevated even in the high normal range of microalbuminuria (below 30 mg/day). There is no doubt that therapies that prevent or delay the development of microalbuminuria and all measures that reduce it, may help to prevent or delay end organ damage

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