DR without DKD is common. DKD without DR is rare. Accurate?

For type 1’s? What I mean to say is, the eyes are more sensitive to BG levels than the Kidneys.

The marker of microalbumin should be seen as suspect IF there is no evidence of retinopathy.

I don’t know a lot technically about this. But the eyes and kidneys are the most likely to show damage because of the small vessels involved. Diabetes causes thicker blood so small vessels are the easiest to have damage. That can show up first in the kidneys or the eyes or both…or the heart or who knows??? It is just more likely to hit the kidneys or the eyes and any sign of either one not being normal should not be ignored. But there is no guarantee which it will show up in, if at all or if it will show up somewhere else first. Higher BG levels, thicker blood…damage probable.

One might get it in the eyes first and another in the kidneys. One is just a little more likely to get it first maybe.

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I think they are independent, but common.
If your kidneys are not filtering what it should be, I would want it rechecked regardless of retinopathy.

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What a bunch of nonsense. Look these are separate systems. Yes it might be that once you have kidney failure or eye disease or vice versa. I am fortunate to have neither and shades of both. So which happens first? The one that happens first happens. There is not generally A or B or C or any of the rest. It is as much likely to be C as A or B or D.

From my own experience I’ve had problems with my eyes for years now, no detected problems in the microalbumin area. My retinopathy does seem to be highly dependent on my blood glucose over the previous few months, exactly like my HbA1C. My eye doctor said, “no need to see you for 6 months” four months ago, but then winter came (my HbA1C invariably goes up in winter, as my exercise goes down).

So my own conclusion, based on observation not science (although, science is based on observation other things are too), is that my retinopathy is reflective of my bg over the last few months. Meanwhile I suspect microalbumin might be reflective of long term damage, but I’m not an endo; I just have one without the other.

It isn’t really nonsense if you consider the mechanisms are similar and the small vessels in the eye vs the more robust kidneys.

From what i’ve read it seems there is a high correlation between the two. Especially those with microalbumin and above having retinopathy as well…but there are many with retinopathy whom have no microalbumin.

I did not have retinopathy until this last fall after having been a type 1 for 62 yrs. My kidneys seem to be fine. Almost all of my A1c’s have been between 4.6 to 5.4 in the last 16 yrs. I had one 5.8. When I was dx with retinopathy my A1c was 5.1.

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In both kidneys and retina, a similar disease process occurs from life long high sugars.
High sugars cause inflammation and in the smaller vessels in kidney and eyes are more susceptible.
The organs will lose blood flow. Your body to compensate will grow new blood vessels, which are more fragile than the ones you grew when you were a fetus.

Those are susceptible to rupture from high blood pressure and just plain getting older.
Once they rupture, the area surrounding dies and eventually enough die to render them useless.

They are different enough. Your capillaries in eyes are just there to feed and nourish your retina. In your kidneys the capillaries are there to filter the blood.

Both totally different but are being assaulted by the same mechanism.

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Ive no doubt that the two mechanisms are the same. But to make such a blanket statement makes no sense to me. Organ damage, organ systems make up, and other factors also play into the issue of damage.

Here is where i am coming from, I do not have heart disease because of diabetes, instead I have a structural abnormality. That caused some issues in my kidneys over the years and in September I had to have a kidney removed, it had been denied adequate blood flow during my formative years.

So now I am in stage 2 (not too far along) kidney disease. Yet no eye issues. It originated in the heart had nothing to do with eyes and yet I am a PWD with kidney issues.

My tart answer relates the fact that there are often many factors. A does not mean B and C is completely different than D which is caused by B.

It is simply too far out to make specific statements.

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I totally understand, Phil.

Where I am coming from is, my eyes are 100% clear and always have been, but I had one positive microalbumin test which was highly questionable (to me) 7 years ago.

The positive was never duplicated since then (which I think invalidates it as a one off) My doctor has even said I definitively do not have kidney damage from diabetes. But it still weirds me out and i’ve seen many sources online that say there is something like an 80% plus correlation if you have microalbumin and retinopathy… in fact i’ve even seen kidney health sites say that if there is no retinopathy present, look for potential other causes of microalbumin in the patient like exercise or another health issue, a false positive, etc.

Cristoph. One more thing. No one test shows you have kidney failure. It takes at least two in a row, at least 30 days apart to demonstrate that there is even something to check out. Dehydration, exercise, to much hydration can cause a funky result. As you say it was a one off 8 years ago. Stop worrying about this and instead focus on life.

There is also a persistent belief that you will have retinopathy by the time you reach 20 years with type1.

It’s clearly false.

I get retinal,photographs taken for 20 years. On the little card you fill out they ask how many years since diagnosis.
At my 20 year photo it came back that I have increased blood vessel growth, which puts me at high risk of retinopathy

I went to a specialist who told me my eyes are perfectly normal.
I’m now at 34 years and I still don’t have any sign of retinopathy so far.
But I’m certain that 20 year remark was made just because it was 20 years.

My first eye damage was noted around the 20 year mark, 35+ years ago. First lasers at 25 years, surgery after that. But still see quite well for an oldie T1D.
Back then it was highly probable damage by 20 years.

Just a reminder that c-peptide is supposed to protect small blood vessels from diabetic damage. Is c-peptide added to our insulin? No! In the long-ago past when animal insulin was in use, there was c-peptide and other hormones in the “poorly” purified mixture. I believe that is why those old enough to have used animal insulins or those of us who came down with T1 later in life and still produce some of our own insulin have little to no damage to small blood vessels in eyes and kidneys.

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I don’t think it is as simple as that. The function of c- peptide is not clear. There are some who think it protects us.
If it were that simple then people with Type2 would not get eye and kidney disease. But they not only get those diseases, they get them in higher numbers than type 1.
According to the data I read from 2 different studies. Granted they were old, from the 80 s but it still valuable.

I’ve often wondered if there is a c peptide resistance which might explain it

Its also possible you just have a very long lasting LADA progression.

@MM1, of course that is a possibility. However, I was not speaking of myself. I have retinitis pigmentosa (which I am told is a genetic condition) which counteracts the possibility of the prolification of small blood vessels in the eye. RP shrivels the retinal vessels and, of course, causes loss of vision by another means. But a prolonged progression of LADA would do the same in keeping the small blood vessels healthy for longer. But would it not make sense to add c-peptide to the insulin we all use?

Interesting question. C-peptide is the leftover part that comes from conversion of native (pancreas) pro-insulin into 2 chains. The c-peptide does nothing, but indicate it came from pancreas, not injection. So just adding it to vial human insulin wouldn’t do much.

Lots of longterm PWD claim that their complications didn’t happen until they started using human insulins which didn’t have c-peptide like the animal insulins did. I would also argue it was just how long they had had diabetes as much as the absence of c-peptide. I for sure don’t know whether c-peptide provided protective factors. I used animal insulins in the 1970’s and have used all of the subsequent generations of insulin. No complications after 45 years but many of the other people advocating for c-peptides are in the 50-75 years range with T1 diabetes.

I know you can get c peptide for injection.
And it makes perfect sense that it has some function. Just not nailed down yet. It’s a gigantic protein. Makes no sense that so much would go into a waste product.
And a waste product that has a very long lifespan.
I would take it I’d my doctor would prescribe it.