TY - JOUR
T1 - Harm! foul! How acute kidney injury SHReDDs patient futures
AU - Hebert, Jessica F.
AU - Funahashi, Yoshio
AU - Hutchens, Michael P.
N1 - Publisher Copyright:
© 2023 Lippincott Williams and Wilkins. All rights reserved.
PY - 2023/3/1
Y1 - 2023/3/1
N2 - Purpose of reviewTransition from acute kidney injury (AKI) to chronic kidney disease (CKD) is increasingly accepted. Less well recognized, but supported by very similar data, is development of disease of other organ systems after AKI. Awareness of other-organ sequelae of AKI may inform efforts to improve the care of patients after AKI.Recent findingsStroke, hypertension, reproductive risk, dementia, and death (SHReDD) are sequelae, which occur with increased risk relative to that of non-AKI within 6 months-3 years after AKI diagnosis, and which are supported by preclinical/mechanistic study. Adjusted hazard ratios for these sequelae are strikingly similar to that of AKI-CKD, ranging from 1.2 to 3.0. Mechanistic studies suggest kidney-centric mechanisms including sodium regulation, volume status regulation, and the renin-angiotensin system are drivers of long-term, extra-renal, change.SummaryFurther clinical characterization and mechanistic insight is necessary, and may have considerable translational impact. Programs which screen or follow post-AKI patients may increase clinical utility if focus is expanded to include the SHReDD complications.
AB - Purpose of reviewTransition from acute kidney injury (AKI) to chronic kidney disease (CKD) is increasingly accepted. Less well recognized, but supported by very similar data, is development of disease of other organ systems after AKI. Awareness of other-organ sequelae of AKI may inform efforts to improve the care of patients after AKI.Recent findingsStroke, hypertension, reproductive risk, dementia, and death (SHReDD) are sequelae, which occur with increased risk relative to that of non-AKI within 6 months-3 years after AKI diagnosis, and which are supported by preclinical/mechanistic study. Adjusted hazard ratios for these sequelae are strikingly similar to that of AKI-CKD, ranging from 1.2 to 3.0. Mechanistic studies suggest kidney-centric mechanisms including sodium regulation, volume status regulation, and the renin-angiotensin system are drivers of long-term, extra-renal, change.SummaryFurther clinical characterization and mechanistic insight is necessary, and may have considerable translational impact. Programs which screen or follow post-AKI patients may increase clinical utility if focus is expanded to include the SHReDD complications.
KW - acute kidney injury sequelae
KW - cardiovascular sequelae of acute kidney injury
KW - post- acute kidney injury screening
KW - reproductive sequelae of acute kidney injury
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U2 - 10.1097/MNH.0000000000000864
DO - 10.1097/MNH.0000000000000864
M3 - Review article
C2 - 36683541
AN - SCOPUS:85146617239
SN - 1062-4821
VL - 32
SP - 165
EP - 171
JO - Current opinion in nephrology and hypertension
JF - Current opinion in nephrology and hypertension
IS - 2
ER -