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Augmented renal proximal tubular sodium-glucose cotransport-2 (SGLT2) activity promotes
hyperfiltration, due to diminished sodium (Na+) delivery at the macula densa (MD),
leading to afferent arteriolar vasodilatation and hyperfiltration. While experimental
models have shown that reduced MD-derived adenosine causes afferent vasodilatation,
the role of adenosine in humans is unknown. Our aims were to 1) develop a urine adenosine
assay in humans with type 1 diabetes (T1D); 2) to determine if the SGLT2 inhibitor
(SGLT2i) empagliflozin, which reduces hyperfiltration through increased Na+ delivery
to the MD, increases urinary adenosine excretion. In this post-hoc analysis, urine
adenosine corrected for creatinine was measured using liquid chromatography with tandem
mass spectrometry (LC-MS/MS) in 40 patients with T1D who participated in an 8-week
study examining the effect of SGLT2i on renal function. The operating characteristics
for the novel LC-MS/MS adenosine assay were excellent. In response to SGLT2i, urine
adenosine increased under clamped hyperglycemic conditions (p=0.0005, Figure 1). Urine adenosine can be detected in patients with T1D using LC-MS/MS. SGLT2i increases
urine adenosine excretion—an effect that may contribute to the regulation of renal
hemodynamic function.
Figure 1Urinary adenosine excretion within type 1 diabetes patients under clamped hyperglycemic
and euglycemic conditions, pre- and post-SGLT2 inhibition treatment. Significant adenosine
release was observed under the hyperglycemic context (p=0.0005), with a similar effect
observed under euglycemia. V3, pre-SGLT2i euglycemic day; V4, pre-SGLT2i hyperglycemic
day; V12, post-SGLT2i euglycemic day; V13, post-SGLT2i hyperglycemic day].
