par Gleeson, Patrick James;Crippa, Ilaria Alice
;Sannier, Aurélie;Koopmansch, Caroline
;Bienfait, Lucie
;Allard, Justine
;Sexton, Donal D.J.;Fontana, Vito;Rorive, Sandrine
;Vincent, Jean Louis
;Creteur, Jacques
;Taccone, Fabio ![](/vufind/images/ULB/publications_list.png)
Référence Clinical Kidney Journal, 16, 10, page (1664-1673)
Publication Publié, 2023-10
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Référence Clinical Kidney Journal, 16, 10, page (1664-1673)
Publication Publié, 2023-10
Article révisé par les pairs
Résumé : | Background. Acute kidney injury (AKI) requiring renal replacement therapy (RRT) in the intensive care unit (ICU) portends a poor prognosis. We aimed to better characterize predictors of survival and the mechanism of kidney failure in these patients. Methods. This was a retrospective observational study using clinical and radiological electronic health records, analysed by univariable and multivariable binary logistic regression. Histopathological examination of post-mortem renal tissue was performed. Results. Among 157 patients with AKI requiring RRT, higher serum creatinine at RRT initiation associated with increased ICU survival [odds ratio (OR) 0.33, 95% confidence interval (CI) 0.17–0.62, P = .001]; however, muscle mass (a marker of frailty) interacted with creatinine (P = .02) and superseded creatinine as a predictor of survival (OR 0.26, 95% CI 0.08–0.82; P = .02). Achieving lower cumulative fluid balance (mL/kg) predicted ICU survival (OR 1.01, 95% CI 1.00–1.01, P < .001), as supported by sensitivity analyses showing improved ICU survival with the use of furosemide (OR 0.40, 95% CI 0.18–0.87, P = .02) and increasing net ultrafiltration (OR 0.97, 95% CI 0.95–0.99, P = .02). A urine output of >500 mL/24 h strongly predicted successful liberation from RRT (OR 0.125, 95% CI 0.05–0.35, P < .001). Post-mortem reports were available for 32 patients; clinically unrecognized renal findings were described in 6 patients, 1 of whom had interstitial nephritis. Experimental staining of renal tissue from patients with sepsis-associated AKI (S-AKI) showed glomerular loss of synaptopodin (P = .02). Conclusions. Confounding of creatinine by muscle mass undermines its use as a marker of AKI severity in clinical studies. Volume management and urine output are key determinants of outcome. Loss of synaptopodin implicates glomerular injury in the pathogenesis of S-AKI. |