Journal
PHYSIOLOGICAL REPORTS
Volume 5, Issue 7, Pages -Publisher
WILEY
DOI: 10.14814/phy2.13228
Keywords
Crystal; diabetic nephropathy; glomerulosclerosis; progression
Categories
Funding
- Deutsche Forschungsgemeinschaft [AN372/16-1, AN372/20-1, STE2437/2-1]
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Sodium glucose transporter (SGLT)-2 inhibition has renoprotective effects in diabetic kidney disease. Whether similar effects can be achieved also in non-diabetic kidney disease is speculative. Chronic kidney disease was induced in C57BL/6N mice by feeding an oxalate-rich diet for 14days, known to induce nephrocalcinosis-related tubular atrophy and interstitial fibrosis without directly affecting the glomerular compartment. Empagliflozin treatment started from day 0 of oxalate feeding had no effect on the decline of glomerular filtration rate, crystal deposition, blood urea nitrogen or serum creatinine levels on day 7 and 14. Tissue morphometry of tubular injury and kidney mRNA levels of kidney injury molecule-1 or tissue inhibitor of metalloproteinase-2 were comparable between empagliflozin- and vehicle-treated mice with oxalate nephropathy on day 7 and 14. Similarly, empagliflozin did not affect markers of interstitial fibrosis, including silver, alpha smooth muscle actin (alpha SMA) and collagen 1 staining, and mRNA levels of fibronectin-1, collagen 1 alpha 1, fibroblast-specific protein-1, and transforming growth factor (TGF)-beta 2 on day 7 and 14. Thus, the specific renoprotective mechanisms-of-action of SGLT2 inhibition in diabetic kidney disease do not apply to chronic oxalosis, a non-diabetic form of chronic kidney disease.
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