From what I’m researching (because my Uric acid level is very low, due to the empagliflozin) its actually not a bad thing …
Here is ChatGPT:
What happens to the body if your uric acid levels are low, due to using an SGLT2 inhibitor?
When uric acid levels are low due to the use of SGLT2 inhibitors (like empagliflozin, dapagliflozin, or canagliflozin), the effect on the body is usually neutral to beneficial, but here’s a breakdown of what can happen:
Mechanism
SGLT2 inhibitors:
- Cause glucosuria (loss of glucose in urine).
- Increase uric acid excretion in urine by altering kidney tubule transport (especially via GLUT9 and URAT1 transporters).
- This leads to lower serum uric acid levels.
Potential Benefits of Lower Uric Acid
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Reduced gout risk: Lower uric acid reduces the likelihood of urate crystal deposition in joints.
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Less inflammation: Uric acid is pro-inflammatory in some tissues; lowering it may reduce systemic inflammation.
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Improved cardiovascular profile: High uric acid is associated with hypertension, insulin resistance, and heart disease—so lowering it may help.
Potential (Rare) Effects or Concerns
While hypouricemia is rarely harmful, especially when caused by medications, very low levels or certain contexts could lead to:
1. Kidney stone risk
- Increased uric acid in urine (uricosuria) can increase stone formation, particularly if the urine is acidic.
2. Loss of antioxidant protection
- Uric acid is an antioxidant in plasma. Very low levels might slightly reduce protection against oxidative stress, though this is not clearly harmful.
3. Marker of other renal effects
- Significant hypouricemia might reflect proximal tubule dysfunction (e.g., Fanconi-like syndrome), but SGLT2 inhibitors alone rarely cause this unless combined with other insults.
4. Potential for electrolyte disturbances
- Because SGLT2 inhibitors also cause osmotic diuresis, mild dehydration and changes in sodium or potassium levels may accompany the uricosuria, but these are separate effects.
Bottom Line:
Low uric acid due to SGLT2 inhibitors is generally beneficial or neutral. It reduces gout risk and may support metabolic and cardiovascular health. However, extremely low levels or symptoms like kidney pain or frequent stones might warrant further evaluation.
Would you like to know what a “low” uric acid level typically means numerically (in mg/dL), or how to monitor for potential issues?
My father just got his first kidney stone last week.
It’s probably due to the SGLT2I.
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Guess what helps with kidney stones (hint a tricarboxylate)
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Can you recommend a good tricarboxylate? 
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I go for a mix of … wait for it … citrate salts
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I’m not sure it’s the SGLT2i that’s responsible. I’ve posted studies showing these agents being protective against kidney stones, but I’m assuming he’s taking empagliflozin? If so, empa shows possible 40% lower risk, at least in diabetics, and there is no reason to think it’s different in nondiabetics.
Empagliflozin and Decreased Risk of Nephrolithiasis: A Potential New Role for SGLT2 Inhibition?
That doesn’t prove empa - or any SGLT2i - didn’t cause his kidney stone, but there’s no indication that it’s more likely.
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Tim
#47
Allipurinol made me faint and dizzy. I had to hold onto something solid to regain my balance. Febuxostat, on the other hand, does a good job of decreasing uric acid and has a lower side-effect profile. As a bonus, it eliminated the pedema caused by amlodipine.
I’m in jardiance 25mg every morning. After taking it for a month my uric acid went from 0.55 to 0.39. (0.44 is the max level). I’m getting tested again in 3 weeks. Hopefully it will be lower. I almost didn’t have any gout attack since.
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