1.6.0.0 Acute Kid­ney In­jury

Acute kid­ney in­jury (AKI) is usu­al­ly di­ag­nosed by a rapid in­crease in serum Cr, which is also reflected as a rapid de­crease in eGFR, over a rel­a­tive­ly short pe­ri­od of time. Peo­ple with di­a­betes are at high­er risk of AKI than those with­out di­a­betes (16). Other risk fac­tors for AKI in­clude pre­ex­ist­ing CKD, the use of med­i­ca­tions that cause kid­ney in­jury (e.g., non­s­teroidal anti-‍inflam­ma­to­ry drugs), and the use of med­i­ca­tions that alter renal blood flow and in­trarenal he­mo­dy­na­mics. In par­tic­u­lar, many an­ti­hy­per­ten­sive med­i­ca­tions (e.g., di­uret­ics, ACE in­hibitors, and an­giotensin re­cep­tor block­ers [ARBs]) can re­duce in­travas­cu­lar vol­ume, renal blood flow, and/‍or glomeru­lar filtra­tion. There is a con­cern that sodi­um–glu­cose co­trans­porter 2 (SGLT2) in­hibitors may pro­mote AKI through vol­ume de­ple­tion, par­tic­u­larly when com­bined with di­uret­ics or other med­i­ca­tions that re­duce glomeru­lar filtra­tion. How­ev­er, ex­ist­ing ev­i­dence from clin­i­cal tri­als and ob­ser­va­tion­al stud­ies sug­gests that SGLT2 in­hibitors do not significant­ly in­crease AKI (17-19). Time­ly iden­tification and treat­ment of AKI are im­por­tant be­cause AKI is as­so­ci­at­ed with in­creased risks of pro­gres­sive CKD and other poor health out­comes (20).