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b In the Hayes et al. (1989) study, ill controls had lower respiratory tract illnesses that did not require hospitalization.
These patients are classified as AI and compared to critically ill control patients with sepsis and without sepsis who have a high hemoglobin level (Hb).
In this cross-sectional case series, we report for the first time that critically ill patients with AKI due to causes other than rhabdomyolysis have elevated FGF-23 levels compared with critically ill controls.
However, Kropski et al. showed that levels of CC-16 in plasma or edema fluid were lower in ARDS than in critically ill controls with cardiogenic pulmonary edema [68].
Serum from 16 patients with the severest AKI (KDIGO 3, not yet on renal replacement, highest fold-change in serum creatinine) was compared to that of 15 critically ill controls without AKI.
FGF-23 levels were significantly higher in critically ill AKI cases compared with critically ill non-AKI subjects, with a median FGF-23 level of 1948 RU/mL (IQR, 437-4369) in AKI cases compared with 252 RU/mL (IQR, 65-533) in critically ill controls (p = 0.01; Figure 1B).
Therefore, we conducted a comprehensive investigation of plasma profiles of PI3, SLPI, and HNE in ARDS patients and at-risk, critically ill controls.
Characteristics of critically ill control patients (n = 16).
Among the 15 nonseptic critically ill control patients there were no deaths.
Global and neurocognitive functioning over the duration of treatment was comparable to never ill controls.
Fifteen nonseptic critically ill patients at the same ICU during the study period were enrolled randomly as the critically ill control group.
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