New Drug Being Tested To Reverse Kidney Damage

[okarol]

New Drug Being Tested To Reverse Kidney Damage

POSTED: 12:20 pm CDT July 9, 2008

SAN ANTONIO -- Marcelo Jimenez is among thousands of San Antonians who suffer from kidney problems due to diabetes.

Every time he visited his doctor, he was told his kidneys were getting worse and he would need to undergo dialysis.

But his kidneys seem to be improving thanks to a new drug being tested at the Diabetes and Glandular Disease Clinic in San Antonio.
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Dr. Sherwyn Schwartz said the drug, which doesn't have a name yet, is the first medication that shows sign of reversing kidney damage.

The drug has helped Jimenez so much that he no longer has to start dialysis.

For some people, participating in a brand new drug study can be a risky endeavor, but in Jimenez's case it proved worthwhile.

"I mean, there's gotta be someone who will try it out or else we won't succeed," said Schwartz.

Researchers are looking for more participants who have kidney disease and are at risk of undergoing dialysis treatment, but have not yet received the treatment.

For more information on participating in the study, call 210-615-5555.

http://www.ksat.com/health/16833033/detail.html?rss=ant&psp=news

[stauffenberg]

Since this drug seems to be focused on diabetics, I wonder if it is an immunosuppressant?  I say this because some interesting research has demonstrated the presence of antibodies in a subset of diabetes to nephrin, a protein found in the lining of capillaries, in the beta cells of the pancreas, and in the kidneys.  The hypothesis advanced by some authors is that 1) since the three sites in the body where this protein are found also correspond to three sites of the body targeted by diabetic complications; and 2) since the nephrin antibodies are found in 30% of type 1 diabetics tested, which is about the same percentage of type 1 diabetics who go on to suffer renal failure; and 3) since the autoimmune process causing type 1 diabetes is known to continue throughout the lifetime of the patient; and 4) since it is common for autoimmune diseases (such as lupus, Henoch-Schoenlein purpura, Wegener's vasculitis, Goodpasture Syndrome, etc.) to attack several organs, not just one as diabetes has long been assumed to do, we can hypothesize that it is this antibody to nephrin, which plays a vital role in renal health, which is in fact causing diabetic renal failure, and not hyperglycemia per se.  The fact that diabetics seldom develop renal failure more than 20 years after onset of diabetes  if they have not already developed it by then, no matter how high their blood sugars go, reinforces this suspicion that a slow autoimmune process is operative here, not hyperglycemia.

[Zach]

Since this drug seems to be focused on diabetics, I wonder if it is an immunosuppressant?  I say this because some interesting research has demonstrated the presence of antibodies in a subset of diabetes to nephrin, a protein found in the lining of capillaries, in the beta cells of the pancreas, and in the kidneys.  The hypothesis advanced by some authors is that 1) since the three sites in the body where this protein are found also correspond to three sites of the body targeted by diabetic complications; and 2) since the nephrin antibodies are found in 30% of type 1 diabetics tested, which is about the same percentage of type 1 diabetics who go on to suffer renal failure; and 3) since the autoimmune process causing type 1 diabetes is known to continue throughout the lifetime of the patient; and 4) since it is common for autoimmune diseases (such as lupus, Henoch-Schoenlein purpura, Wegener's vasculitis, Goodpasture Syndrome, etc.) to attack several organs, not just one as diabetes has long been assumed to do, we can hypothesize that it is this antibody to nephrin, which plays a vital role in renal health, which is in fact causing diabetic renal failure, and not hyperglycemia per se.  The fact that diabetics seldom develop renal failure more than 20 years after onset of diabetes  if they have not already developed it by then, no matter how high their blood sugars go, reinforces this suspicion that a slow autoimmune process is operative here, not hyperglycemia.

Would this be true with Type 2 Diabetes?

[stauffenberg]

Medicine started out by viewing type 1 and type 2 diabetes as essentially the same, and then by the late 1960s the theory developed that they were in fact quite different, with the former being an autoimmune disease, while the latter was a disease of insulin resistance and gradual exhaustion of the pancreas' capacity to deal with that resistance by putting out extra insulin.  Now things are going the other way again, and more and more evidence is emerging that both type 1 and type 2 diabetes have a large genetic component, that insulin resistance can play a role in both conditions, that c-peptide, thought to play a role in the development of complications, is lacking in type 1 and poorly utilized in type 2, and that high antibody levels (especially GAD antibodies) are present in both diseases.  So yes, in theory, there could be some role for immunological attack on the kidneys even in type 2.

Another interesting recent discovery is that neuropathy in type 1 diabetics is being caused by auto-immune processes, at least in part, although previously it was believed that only hyperglycemia had a causal role in this process.  Experiments have also shown that normoglycemic serum from type 1 diabetics is neurotoxic in vitro.  There have also been reports (Kidney International, 1986 Supplement) of some patients presenting with diabetic complications but without diabetes, suggesting that they may just have had the auto-immune component of the disease but not the characteristic hyperglycemia.  Finally, if autoimmunity is causing diabetic complications, this might explain why some patients develop complications rapidly despite good blood sugar control, while others never do despite very poor control.

Dr. Denise Faustman at Harvard showed a few years ago that in type 1 diabetics the auto-immune attack never stops, even decades after it has destroyed the beta cells of the pancreas.  It has always seemed to me to be counter-intuitive that all the complications of this continuing auto-immune disease should be due just to one side-effect of the disease, high blood sugar, and not to the persistence of the original disease itself.  If this were to turn out to be the case, at a time when the nearly universal consensus in the medical community is that complications are caused solely by high blood sugar, and at a time when the daily lives of diabetics are being burdened by strict control, multiple blood sugar testing, and repeated insulin injections, often causing serious trauma or even death from hypoglycemia, then this would be a truly revolutionary discovery.

An interesting topic for a documentary, some might say!