It turns out they are not that “reno-protective” after all
According to this study performed on mice and humans, medications that are used to inhibit the renin-angiotensin system (ACEi or ARBs) can lead to hypertrophy (overgrowth) in the small arteries inside the kidneys.
In essence, with time the renin-producing cells transform from endocrine cells to matrix-producing cells. They end up surrounding the vessel walls and inducing the accumulation of adjacent smooth muscle cells and extracellular matrix, resulting in blood flow obstruction, focal ischemia, and fibrosis.
So do these medications protect the kidneys?
Vitamin C deficiency causes epigenetic changes in the renal tubules
In this study performed on mice who are dependent on dietary vitamin C, researchers used the sophisticated single-cell RNA sequencing to map out the DNA/RNA methylation in the renal cells.
They found that vitamin C deficiency can cause acute tubular injury (ATN) by causing epigenetic modifications of DNA/RNA in these cells.
The oxidation-resistant vitamin C derivative, ascorbyl phosphate magnesium, promoted DNA demethylation and prevented the progression of cisplatin-induced ATN.
The effects of SGLT-2 inhibitors on electrolytes
This is a meta-analysis that aimed to look at the comparative effects of various SGLT-2 inhibitors on electrolyte balances in diabetes.
The study found that all SGLT-2 inhibitors can lead to a mild increase in magnesium and phosphate levels. Dapagliflozin was associated with the highest increase in magnesium.
Interestingly, the study did not find any effects on other electrolytes. Other studies have demonstrated that SGLT-2 inhibitors can:
1. Increase magnesium level
2. Increase potassium level
3. Lower sodium level
4. Increase phosphate level
5. Lower uric acid level
We still don’t know their effects on other micronutrients such as zinc and others.
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