
To test the hypothesis that the reduction in urinary kidney injury molecule‐1 (KIM‐1) observed with the sodium‐glucose cotransporter‐2 (SGLT2) inhibitor canagliflozin is mediated through its effects on urine albumin to creatinine ratio (UACR) and monocyte chemoattractant protein‐1 (MCP‐1) by assessing the proportion of the effect of canagliflozin on KIM‐1 that is mediated through its effects on MCP‐1 and UACR in patients with type 2 diabetes and albuminuric kidney disease. This post hoc analysis suggests that urinary albumin leakage may lead to tubular inflammation and induction of injury, and provide mechanistic insight for how canagliflozin may ameliorate tubular damage, but further research is required to confirm these findings.
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