@article{e3fba86a99b54ee7bed619b20998e7ee,
title = "Acute kidney injury in non-severe pneumonia is associated with an increased immune response and lower survival",
abstract = "While sepsis is a leading cause of acute kidney injury in critically ill patients, the relationship between immune response and acute kidney injury in less severely ill patients with infection is not known. Here we studied the epidemiology, 1-year mortality, and immune response associated with acute kidney injury in 1836 hospitalized patients with community-acquired severe and non-severe pneumonia. Acute kidney injury developed in 631 patients of whom 329 had severe and 302 had non-severe sepsis. Depending on the subgroup classification, 16-25% of the patients with non-severe pneumonia also developed acute kidney injury. In general, patients with acute kidney injury were older, had more comorbidity, and had higher biomarker concentrations (interleukin-6, tumor necrosis factor, D-dimer) even among patients without severe sepsis. The risk of death associated with acute kidney injury varied when assessed by Gray's survival model and after adjusting for differences in age, gender, ethnicity, and comorbidity. This risk was significantly higher immediately after hospitalization but gradually fell over time in the overall cohort and in those with non-severe pneumonia. A significantly higher risk of death (hazard ratio 1.29) was also present in those never admitted to an intensive care unit. Hence acute kidney injury is common even among patients with non-severe pneumonia and is associated with higher immune response and an increased risk of death.",
keywords = "Acute kidney injury, Inflammation, Mortality, Pneumonia, Severe sepsis, Severity",
author = "Raghavan Murugan and Vijay Karajala-Subramanyam and Minjae Lee and Sachin Yende and Lan Kong and Melinda Carter and Angus, {Derek C.} and Kellum, {John A.}",
note = "Funding Information: The GenIMS Study was funded by the National Institute of General Medical Sciences (R01 GM61992) with additional support from GlaxoSmithKline (Philadelphia, PA, USA) for enrollment and clinical data collection, and from Diagnostic Products Corporation (Los Angeles, CA, USA) for the cytokine and coagulation assays. The agencies had no role in the design and conduct of the study; the collection, analysis, and interpretation of the data; or the preparation, or approval of the paper. We thank the nurses, respiratory therapists, phlebotomists, physicians, and other health care professionals who participated in GenIMS, as well as the patients and their families who supported this study. Source of support: GenIMS was funded by NIGMS R01 GM61992, with additional support from GlaxoSmithKline for cytokine assays. This publication was made possible by grant KL2 RR024154 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and the NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. Information on NCRR is available at http://www.ncrr.nih.gov/ . Information on Re-engineering the Clinical Research Enterprise can be obtained from http://nihroadmap.nih.gov/clinicalresearch/overview-translational.asp . This publication was also supported in part by career development grant K23GM83215 from NIGMS. ",
year = "2010",
month = mar,
doi = "10.1038/ki.2009.502",
language = "English (US)",
volume = "77",
pages = "527--535",
journal = "Kidney international",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "6",
}