The effects of SGLT2 inhibitors to increase hematocrit and decrease body weight and circulating natriuretic peptides ( 6, 7) have been linked by some investigators to an effect of diuresis to contract plasma and extracellular volume ( 11–13). Sodium retention in patients with heart failure is related to increased sodium reabsorption in the proximal tubule ( 8), and by attenuating the sodium reabsorption at this site, SGLT2 inhibitors may potentiate the effect of diuretic agents acting at the loop of Henle ( 2, 9, 10). The action of sodium-glucose cotransporter 2 (SGLT2) inhibitors to promote natriuresis and osmotic diuresis ( 1–4) has been proposed as a central mechanism by which these drugs reduce heart failure hospitalizations in large-scale trials ( 5–7). Changes in body weight, hematocrit, and natriuretic peptides (each potentially indicative of a diuretic action of SGLT2 inhibitors) did not track each other closely in their time course or in individual patients.
Patients with recent volume overload were more likely to have been hospitalized for heart failure and to have received an intravenous diuretic agent in an outpatient setting in the previous 12 months, and to experience a heart failure event following randomization, even though they were more likely to be treated with high doses of a loop diuretic agent as an outpatient (all p 0.05).
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