While SGLT-2 inhibitors increase UTI risk, discontinuing them may unleash a pro-inflammatory state that promotes deleterious cardiorenal effects.
Discontinuing SGLT-2i after UTI may worsen cardiorenal outcomes; leaves optimal management open in Level 5 data.
SGLT-2i-associated UTI and cardiorenal risk. The graphical abstract shows that use of SGLT-2i promotes an increased risk of urinary tract infections (UTI), which in turn are associated with a higher incidence of cardiorenal events. However, these outcomes are also negatively affected by a discontinuation of SGLT-2i. On one hand, we have the SGLT-2i-induced glycosuria as a driving force for the occurrence of UTI, which may trigger low-grade inflammation underlying the higher cardiorenal risk in this setting. On the other hand, the combination of UTI and subsequent SGLT-2i discontinuation may leave unleash a pro-inflammatory state that promote a range of deleterious effects in the heart and kidney.
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Cosentino et al. (2025) studied this question.
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