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Sodium glucose transporter-2 inhibition has no renoprotective effects on non-diabetic chronic kidney disease

Qiuyue Ma1, Stefanie Steiger1, Hans-Joachim Anders2

  • 1Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Munich, Germany.

Physiological Reports
|April 2, 2017
PubMed

Insights

Sodium glucose transporter (SGLT)-2 inhibitors do not protect against non-diabetic kidney disease caused by oxalate nephropathy in mice. Their renoprotective effects seen in diabetic kidney disease do not translate to this condition.

Area of Science:

  • Nephrology
  • Pharmacology
  • Toxicology

Background:

  • Sodium glucose transporter (SGLT)-2 inhibition demonstrates renoprotective effects in diabetic kidney disease.
  • The efficacy of SGLT2 inhibition in non-diabetic kidney diseases remains largely speculative.
  • Oxalate nephropathy is a non-diabetic kidney disease model characterized by tubular injury and fibrosis.

Purpose of the Study:

  • To investigate the renoprotective effects of SGLT2 inhibition in a non-diabetic kidney disease model.
  • To determine if empagliflozin confers benefits in oxalate-induced nephropathy.
  • To explore the applicability of SGLT2 inhibitor mechanisms beyond diabetic kidney disease.

Main Methods:

  • Chronic kidney disease was induced in C57BL/6N mice using an oxalate-rich diet for 14 days.
  • Empagliflozin treatment was administered from day 0 of oxalate feeding.
  • Kidney function (GFR, BUN, creatinine), crystal deposition, tubular injury, and fibrosis markers were assessed on days 7 and 14.

Main Results:

  • Empagliflozin did not improve glomerular filtration rate, reduce crystal deposition, or alter blood urea nitrogen and serum creatinine levels.
  • Tissue analysis showed no significant differences in tubular injury markers (Kidney Injury Molecule-1, tissue inhibitor of metalloproteinase-2) between treated and control groups.
  • Empagliflozin did not attenuate markers of interstitial fibrosis, including alpha-smooth muscle actin and collagen 1, nor related gene expression.

Conclusions:

  • The renoprotective mechanisms of SGLT2 inhibition observed in diabetic kidney disease are not applicable to chronic oxalosis.
  • Empagliflozin does not offer protection against oxalate-induced kidney injury and fibrosis in this non-diabetic model.
  • Further research is needed to understand the specific pathways involved in SGLT2 inhibitor efficacy in different kidney disease contexts.
Keywords:
Crystaldiabetic nephropathyglomerulosclerosisprogression

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