Stopping kidney protection in the elderly following acute kidney injury: think mortality

Chronic kidney disease (CKD) is projected to become the fifth most common global cause of death by 2040. This illustrates a key consequence of CKD, i.e. premature mortality. Since nephroprotective drugs such as renin–angiotensin system (RAS) blockers and sodium–glucose transport protein 2 (SGLT2) inhibitors decrease glomerular hyperfiltration, they may be stopped following an episode of acute kidney injury (AKI). This may theoretically modify the risks of subsequent events, ranging from hyperkalaemia to CKD progression to cardiovascular events, but the evidence so far has been inconsistent. Roemer et al. have now addressed the shortcomings of prior studies. In a population of mostly elderly (median age 78 years) prevalent users of RAS blockers with an indication for this therapy and who survived for at least 3 months after discharge following a hospitalization characterized by moderate to severe AKI, roughly 50% had stopped RAS blockade at 3 months. Stopping RAS blockade was associated with an increased risk of a primary composite outcome of death, myocardial infarction and stroke, of which a large majority (80%) of events were deaths. In contrast, the risk of hyperkalaemia was reduced and the risk of repeated AKI, CKD progression or heart failure hospitalization was unchanged in patients who stopped RAS blockers. These findings call for a re-evaluation of the practice of stopping RAS blockers in the long-term following AKI and suggest that studies are needed regarding similar practices for SGLT2 inhibitors.