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. 2018 Feb 15;13(2):e0192592.
doi: 10.1371/journal.pone.0192592. eCollection 2018.

Aggressive fluid accumulation is associated with acute kidney injury and mortality in a cohort of patients with severe pneumonia caused by influenza A H1N1 virus

Gustavo Alejandro Casas-Aparicio  1 , Isabel León-Rodríguez  1 , Rafael de Jesús Hernández-Zenteno  2 , Manuel Castillejos-López  3 , Claudia Alvarado-de la Barrera  1 , Christopher E Ormsby  1 , Gustavo Reyes-Terán  1
Affiliations

Aggressive fluid accumulation is associated with acute kidney injury and mortality in a cohort of patients with severe pneumonia caused by influenza A H1N1 virus

Gustavo Alejandro Casas-Aparicio et al. PLoS One. .

Abstract

Introduction: Fluid accumulation is associated with adverse outcomes such as acute kidney injury (AKI) in critically ill patients. This study aimed to describe the factors associated with AKI in individuals with influenza A H1N1 severe pneumonia, and explore the relation of fluid accumulation with AKI and mortality.

Material and methods: We reviewed medical records of individuals with influenza A H1N1 severe pneumonia and no history of chronic kidney disease, attending a national referral center for respiratory diseases between November 2014 and May 2015. Demographic information, risk factors for AKI, physiologic and laboratory data, outcomes and information on fluid intake and output were recorded. Categorical variables were compared using the chi-square test. Quantitative variables were compared using the Mann-Whitney test. Factors associated with AKI and mortality were identified by binary logistic regression. Linear models of fluid accumulation rates for individuals and groups were estimated using segmented linear regression.

Results: Of 60 patients studied, 43 developed AKI (71.6%). Male gender was protective for AKI (p = 0.019). AKI was associated with nephrotoxic drugs (p = 0.016); PEEP>10 cm H2O on admission (p = 0.031); mortality (p = 0.037); and fluid accumulation ≥10% (fluid overload) at day 7 of hospitalization (p = 0.00026). Mortality was associated with older age (p = 0.009); nephrotoxic drugs (p = 0.034); and higher Pneumonia Severity Index score (112 vs. 76, p = 0.008) on admission. The Deceased-AKI group had a higher rate of fluid accumulation (expressed as ml/kg/body weight) than the Survivors-No AKI group during the study period of 7 days (Survivors-No AKI = 13.31 vs. Deceased-AKI = 22.76, p = 0.019). During the highest phase of fluid accumulation, the Survivors-No AKI group had a slower rate of fluid accumulation than the Survivors-AKI group (14.91 vs. 28.49, p = 0.001).

Conclusions: A high rate of fluid accumulation was associated with AKI and mortality. We support the approach of resuscitation in acute illness, with an early transition to neutral and then negative fluid balances.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Fluid accumulation rate during hospitalization.
(A) Estimated linear model including all study participants during the study period of 7 days. (B) Estimated linear model of one individual during the study period of 7 days.
Fig 2
Fig 2. Fluid accumulation rate per groups.
(A) Estimated linear model in the group of Survivors-No AKI; the Survivors-AKI Group; and the Deceased-AKI group during the study period of 7 days. (B) The different slopes in the group of Survivors-No AKI; the Survivors-AKI group; and the Deceased-AKI group during the study period of 7 days.
Fig 3
Fig 3. Phase I of fluid accumulation rate.
(A) Estimated linear model in the group of Survivors-No AKI; the Survivors-AKI group; and the Deceased-AKI group during Phase I. (B) The different slopes in the group of Survivors-No AKI; the Survivors-AKI group; and the Deceased-AKI group during Phase I.
See this image and copyright information in PMC

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