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Kidney function tests

How do we get this checked?
If you are going to actually see actual renal tubular damage and fibrosis,etc..; I would thing a biopsy would be the only way to really tell.
 
Btw, since this is a kidney thread. I can't stress enough how effective Empagliflozin is on kidney health (and heart health).
yes, SGLT2 inhibitors are a new therapeutic option for CKD, that goes beyond its use for Diabetic nephropathy or even DKD
 
How do we get this checked?
Urinary KIM-1
Urinary beta-2 globulin
Urinary NAG
Urinary NGAL

I want to reiteate that most recent research shows that you can have normal GFR and no albuminuria (albumin filtered by glomeruli), and still have kidney damage from tubulointerstitial dysfunction.

Heck, the glomeruli cannot filter out the globulin protein, that is filtered through tubular secretion instead, so you could only be having non-albuminuria proteinuria, through high beta-2 globulin protein in urine, which wouldn't show up in blood tests for albuminuria, however you would still have proteinuria, simply it would then be from tubular dysfunction, aka tubular proteinuria.
 
I used to stop on the way home from the gym to get my blood drawn. Certainly effects some of the results, kidneys for example. And I was never really fully hydrated 🙁 my bad.

We retested after a few days off and not on my way home from the gym, hydrated and rested and the numbers improved. Still not the best, don’t know why.

Just had them imaged today, should know more in a few days. Fingers crossed.
Test results, all good 👍
 
What is the mechanism of action?
quite a few, obviously main role is originally in DKD and Diabetic nephropathy, they improve tubuloglomerular feedback loop by allowing increased tubular reabsoprton of sodium and glucose.
SGLT2 may ease glomerular hyperfiltration as well, notably by allowing afferent arteriole vasoconstriction (will ease intraglomerular pressure, will lower GFR though).
They also have anti-fibrotic effects at tubulointerstitial levels,...,.
Plenty of benefits overall that go beyond the original intended use in Diabetics (easing renal load by improving glucose reabsorption).

Here's a summary of benefits:

biomedicines-10-02458-g001.png
 
Urinary KIM-1
Urinary beta-2 globulin
Urinary NAG
Urinary NGAL

I want to reiteate that most recent research shows that you can have normal GFR and no albuminuria (albumin filtered by glomeruli), and still have kidney damage from tubulointerstitial dysfunction.

Heck, the glomeruli cannot filter out the globulin protein, that is filtered through tubular secretion instead, so you could only be having non-albuminuria proteinuria, through high beta-2 globulin protein in urine, which wouldn't show up in blood tests for albuminuria, however you would still have proteinuria, simply it would then be from tubular dysfunction, aka tubular proteinuria.
To clarify, these are urine tests? And you're saying that even Cystatin C can't show what these will? Do you have the links for any of the studies that are suggesting these conclusions you speak of?
 
quite a few, obviously main role is originally in DKD and Diabetic nephropathy, they improve tubuloglomerular feedback loop by allowing increased tubular reabsoprton of sodium and glucose.
SGLT2 may ease glomerular hyperfiltration as well, notably by allowing afferent arteriole vasoconstriction (will ease intraglomerular pressure, will lower GFR though).
They also have anti-fibrotic effects at tubulointerstitial levels,...,.
Plenty of benefits overall that go beyond the original intended use in Diabetics (easing renal load by improving glucose reabsorption).

Here's a summary of benefits:

View attachment 172970
I am happy to admit that I'm likely wrong but SGLT2 inhibitors  decrease tubular reabsorption of glucose and Na+. Glucose and Na+ are normally filtered through the glomerulus and then reabsorbed in the tubule. SGLT2 inhibitors decrease this function which leads to the osmotic diuresis, which helps heart failure pts too. I forget the units but the tubules ability to reabsorob glucose taps out around 200 (units?). So if your sugar is less than 200 you're tubules handle reabsorbing it, sugar > 200 spills into urine. The SGLT2 inhibitors lower this capacity.
 
I am happy to admit that I'm likely wrong but SGLT2 inhibitors  decrease tubular reabsorption of glucose and Na+. Glucose and Na+ are normally filtered through the glomerulus and then reabsorbed in the tubule. SGLT2 inhibitors decrease this function which leads to the osmotic diuresis, which helps heart failure pts too. I forget the units but the tubules ability to reabsorob glucose taps out around 200 (units?). So if your sugar is less than 200 you're tubules handle reabsorbing it, sugar > 200 spills into urine. The SGLT2 inhibitors lower this capacity.
they decrease it, yes, we're on the same page here. Can't edit my original post now.

Admittedly I don't know much about the Diabetic side of kidney disease, I'd say diabetic nephropathy is a whole issue on its own, has specific possible therapeutic avenues, that might use similar and different therapeutics from more classical forms of CKD.
 
they decrease it, yes, we're on the same page here. Can't edit my original post now.

Admittedly I don't know much about the Diabetic side of kidney disease, I'd say diabetic nephropathy is a whole issue on its own, has specific possible therapeutic avenues, that might use similar and different therapeutics from more classical forms of CKD.
Good thread and perhaps you can ping a mod to fix your original post with the corrected info.
 

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