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Cumulative Fluid Balance and Mortality in Septic Patients With or Without Acute Kidney Injury and Chronic Kidney Disease*

Neyra, Javier A. MD, MSCS1,2; Li, Xilong PhD, MS3; Canepa-Escaro, Fabrizio MD4; Adams-Huet, Beverley MS3; Toto, Robert D. MD1; Yee, Jerry MD5; Hedayati, S. Susan MD, MHSc1,6; for the Acute Kidney Injury in Critical Illness Study Group

doi: 10.1097/CCM.0000000000001835
Clinical Investigations
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Objective: Incident acute kidney injury and prevalent chronic kidney disease are commonly encountered in septic patients. We examined the differential effect of acute kidney injury and chronic kidney disease on the association between cumulative fluid balance and hospital mortality in critically ill septic patients.

Design: Retrospective cohort study.

Setting: Urban academic medical center ICU.

Patients: ICU adult patients with severe sepsis or septic shock and serum creatinine measured within 3 months prior to and 72 hours of ICU admission. Patients with estimated glomerular filtration rate less than 15 mL/min/1.73 m2 or receiving chronic dialysis were excluded.

Interventions: None.

Measurements and Main Results: A total of 2,632 patients, 1,211 with chronic kidney disease, were followed up until hospital death or discharge. Acute kidney injury occurred in 1,525 patients (57.9%), of whom 679 (44.5%) had chronic kidney disease. Hospital mortality occurred in 603 patients (22.9%). Every 1-L increase in cumulative fluid balance at 72 hours of ICU admission was independently associated with hospital mortality in all patients (adjusted odds ratio, 1.06 [95% CI] 1.04–1.08; p < 0.001), and in each acute kidney injury/chronic kidney disease subgroup (adjusted odds ratio, 1.06 [1.03–1.09] for acute kidney injury+/chronic kidney disease+; 1.09 [1.05–1.13] for acute kidney injury–/chronic kidney disease+; 1.05 [1.03–1.08] for acute kidney injury+/chronic kidney disease–; and 1.07 [1.02–1.11] for acute kidney injury–/chronic kidney disease–). There was a significant interaction between acute kidney injury and chronic kidney disease on cumulative fluid balance (p =0.005) such that different cumulative fluid balance cut-offs with the best prognostic accuracy for hospital mortality were identified: 5.9 L for acute kidney injury+/chronic kidney disease+; 3.8 L for acute kidney injury–/chronic kidney disease+; 4.3 L for acute kidney injury+/chronic kidney disease–; and 1.5 L for acute kidney injury–/chronic kidney disease–. The addition of cumulative fluid balance to the admission Sequential Organ Failure Assessment score had increased prognostic utility for hospital mortality when compared with Sequential Organ Failure Assessment alone, particularly in patients with acute kidney injury.

Conclusions: Higher cumulative fluid balance at 72 hours of ICU admission was independently associated with hospital mortality regardless of acute kidney injury or chronic kidney disease presence. We characterized cumulative fluid balance cut-offs associated with hospital mortality based on acute kidney injury/chronic kidney disease status, underpinning the heterogeneity of fluid regulation in sepsis and kidney disease.

1Division of Nephrology, University of Texas Southwestern Medical Center, Dallas, TX.

2Division of Nephrology, Bone, and Mineral Metabolism, University of Kentucky, Lexington, KY.

3Division of Biostatistics, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX.

4Department of Internal Medicine, Asante Health System, Grants Pass, OR.

5Division of Nephrology and Hypertension, Henry Ford Hospital, Detroit, MI.

6Renal Section, Medical Service, Veterans Affairs North Texas Health Care System, Dallas, TX.

*See also p. 1945.

Drs. Neyra and Hedayati helped in study concept and design. Drs. Neyra, Li, Canepa-Escaro, and Hedayati, and Ms. Adams-Huet helped in analysis and interpretation of data. Drs. Neyra and Hedayati helped in drafting of the article. Drs. Neyra, Toto, Yee, and Hedayati helped in critical revision of the article for important intellectual content. Dr. Li and Ms. Adams-Huet helped in statistical analysis. Drs. Neyra, Canepa-Escaro, Toto, and Yee helped in administrative, technical, and material support. Dr. Neyra helped in study supervision.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (http://journals.lww.com/ccmjournal).

Supported by the University of Texas Southwestern Medical Center O’Brien Kidney Research Core Center (NIH, P30 DK079328-06), the National Center for Advancing Translational Sciences of the National Institutes of Health (NIH, UL1TR001105), and the Division of Nephrology and Hypertension of Henry Ford Hospital. The content is solely the responsibility of the authors and does not represent the official views of the National Institutes of Health, the University of Texas Southwestern, Henry Ford Hospital, or the Veterans Affairs North Texas Health Care System.

Dr. Neyra was supported by the Ben J. Lipps Research Fellowship Program of American Society of Nephrology Foundation for Kidney Research and the Truelson Fellowship Fund at UT Southwestern Charles and Jane Pak Center of Mineral Metabolism and Clinical Research. Dr. Toto received support for article research from the National Institutes of Health (NIH) and received funding from Boehringer Ingelheim Abbvie Relypsa ZS Pharma, Reata Pharmaceuticals, and Celgene. The remaining authors have disclosed that they do not have any potential conflicts of interest.

For information regarding this article, E-mail: javier.neyralozano@utsouthwestern.edu

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