With the cardiovascular and kidney protective benefits of medications such as sodium-glucose cotransporter-2 (SGLT2) inhibitors, renin-angiotensin -aldosterone system (RAAS) inhibitors, and mineralocorticoid receptor antagonists (MRAs), there are increased rates of initiation and use of combinations of these agents. The same mechanisms that allow for reduction of glomerular hypertension and blood pressure reduction limit the ability to maintain kidney perfusion in the setting of volume depletion and relative hypotension, and as a result increase the risk of acute kidney injury (AKI) development or severity.