TY - JOUR
T1 - Acute Kidney Injury Associates with Long-Term Increases in Plasma TNFR1, TNFR2, and KIM-1
T2 - Findings from the CRIC study
AU - the Chronic Renal Insufficiency Cohort (CRIC) Study Investigators
AU - McCoy, Ian E.
AU - Hsu, Jesse Y.
AU - Bonventre, Joseph V.
AU - Parikh, Chirag R.
AU - Go, Alan S.
AU - Liu, Kathleen D.
AU - Ricardo, Ana C.
AU - Srivastava, Anand
AU - Cohen, Debbie L.
AU - He, Jiang
AU - Chen, Jing
AU - Rao, Panduranga S.
AU - Hsu, Chi Yuan
AU - Appel, Lawrence J.
AU - Feldman, Harold I.
AU - Lash, James P.
AU - Nelson, Robert G.
AU - Rahman, Mahboob
AU - Shah, Vallabh O.
AU - Unruh, Mark L.
N1 - Publisher Copyright:
Copyright 2022 by ASN
PY - 2022/6
Y1 - 2022/6
N2 - Background Some markers of inflammation—TNF receptors 1 and 2 (TNFR1 and TNFR2)—are independently associated with progressive chronic kidney disease (CKD), as is a marker of proximal tubule injury, kidney injury molecule 1 (KIM-1). However, whether an episode of hospitalized AKI may cause long-term changes in these biomarkers is unknown. Methods Among adult participants in the Chronic Renal Insufficiency Cohort (CRIC) Study, we identified 198 episodes of hospitalized AKI (defined as peak/nadir inpatient serum creatinine values ≥1.5). For each AKI hospitalization, we found the best matched non-AKI hospitalization (unique patients), using prehospitalization characteristics, including estimated glomerular filtration rate and urine protein/creatinine ratio. We measured TNFR1, TNFR2, and KIM-1 in banked plasma samples collected at annual CRIC study visits before and after the hospitalization (a median of 7 months before and 5 months after hospitalization). Results In the AKI and non-AKI groups, we found similar prehospitalization median levels of TNFR1 (1373 pg/mL versus 1371 pg/mL, for AKI and non-AKI, respectively), TNFR2 (47,141 pg/mL versus 46,135 pg/mL, respectively), and KIM-1 (857 pg/mL versus 719 pg/mL, respectively). Compared with matched study participants who did not experience AKI, study participants who did experience AKI had greater increases in TNFR1 (23% versus 10%, p<0.01), TNFR2 (10% versus 3%, p<0.01), and KIM-1 (13% versus -2%, p<0.01) . Conclusions Among patients with CKD, AKI during hospitalization was associated with increases in plasma TNFR1, TNFR2, and KIM-1 several months after their hospitalization. These results highlight a potential mechanism by which AKI may contribute to more rapid loss of kidney function months to years after the acute insult.
AB - Background Some markers of inflammation—TNF receptors 1 and 2 (TNFR1 and TNFR2)—are independently associated with progressive chronic kidney disease (CKD), as is a marker of proximal tubule injury, kidney injury molecule 1 (KIM-1). However, whether an episode of hospitalized AKI may cause long-term changes in these biomarkers is unknown. Methods Among adult participants in the Chronic Renal Insufficiency Cohort (CRIC) Study, we identified 198 episodes of hospitalized AKI (defined as peak/nadir inpatient serum creatinine values ≥1.5). For each AKI hospitalization, we found the best matched non-AKI hospitalization (unique patients), using prehospitalization characteristics, including estimated glomerular filtration rate and urine protein/creatinine ratio. We measured TNFR1, TNFR2, and KIM-1 in banked plasma samples collected at annual CRIC study visits before and after the hospitalization (a median of 7 months before and 5 months after hospitalization). Results In the AKI and non-AKI groups, we found similar prehospitalization median levels of TNFR1 (1373 pg/mL versus 1371 pg/mL, for AKI and non-AKI, respectively), TNFR2 (47,141 pg/mL versus 46,135 pg/mL, respectively), and KIM-1 (857 pg/mL versus 719 pg/mL, respectively). Compared with matched study participants who did not experience AKI, study participants who did experience AKI had greater increases in TNFR1 (23% versus 10%, p<0.01), TNFR2 (10% versus 3%, p<0.01), and KIM-1 (13% versus -2%, p<0.01) . Conclusions Among patients with CKD, AKI during hospitalization was associated with increases in plasma TNFR1, TNFR2, and KIM-1 several months after their hospitalization. These results highlight a potential mechanism by which AKI may contribute to more rapid loss of kidney function months to years after the acute insult.
KW - Biomarkers
KW - Plasma
KW - acute kidney injury
KW - acute renal failure
KW - chronic kidney disease
KW - hospitalization
KW - renal injury
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U2 - 10.1681/ASN.2021111453
DO - 10.1681/ASN.2021111453
M3 - Article
C2 - 35296554
AN - SCOPUS:85129293341
SN - 1046-6673
VL - 33
SP - 1173
EP - 1181
JO - Journal of the American Society of Nephrology
JF - Journal of the American Society of Nephrology
IS - 6
ER -