Mechanistically, the effects of SGLT-2 inhibition on intraglomerular pressure appear to complement the effects of RAS inhibition (Figure 1) without causing hyperkalaemia or acute kidney injury, so their combination may have the potential to benefit those at risk of hyperfiltration (i.e., those with reduced eGFR and/or albuminuria). Here, SLC5A2 is linked to acute kidney injury.