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The concept of pyrexia as a protective physiological response to aid in host defence has been challenged with the awareness of the severe metabolic stress induced by pyrexia. The host response to pyrexia varies, however, according to the disease profile and severity and, as such, the management of pyrexia should differ; for example, temperature control is safe and effective in septic shock but remains controversial in sepsis. From the reported findings discussed in this review, treating pyrexia appears to be beneficial in septic shock, out of hospital cardiac arrest and acute brain injury.Multiple therapeutic options are available for managing pyrexia, with precise targeted temperature management now possible. Notably, the use of pharmacotherapy versus surface cooling has not been shown to be advantageous. The importance of avoiding hypothermia in any treatment strategy is not to be understated.Whilst a great deal of progress has been made regarding optimal temperature management in recent years, further studies will be needed to determine which patients would benefit the most from control of pyrexia and by which means this should be implemented. This narrative review is part of a series on the pathophysiology and management of pyrexia.

Introduction: Several factors, including diuretic use and sepsis, interfere with the fractional excretion of sodium, which is used to distinguish transient from persistent acute kidney injury (AKI). These factors do not affect the fractional excretion of urea (FeUrea). However, there are conflicting data on the diagnostic accuracy of FeUrea., Methods: We conducted an observational, prospective, multicenter study at three ICUs in university hospitals. Unselected patients, except those with obstructive AKI, were admitted to the participating ICUs during a six-month period. Transient AKI was defined as AKI caused by renal hypoperfusion and reversal within three days. The results are reported as medians (interquartile ranges)., Results: A total of 203 patients were included. According to our definitions, 67 had no AKI, 54 had transient AKI and 82 had persistent AKI. FeUrea was 39% (28 to 40) in the no-AKI group, 41% (29 to 54) in the transient AKI group and 32% (22 to 51) in the persistent AKI group (P = 0.12). FeUrea was of little help in distinguishing transient AKI from persistent AKI, with the area under the receiver operating characteristic curve being 0.59 (95% confidence interval, 0.49 to 0.70; P = 0.06). Sensitivity was 63% and specificity was 54% with a cutoff of 35%. In the subgroup of patients receiving diuretics, the results were similar., Conclusions: FeUrea may be of little help in distinguishing transient AKI from persistent AKI in critically ill patients, including those receiving diuretic therapy. Additional studies are needed to evaluate alternative markers or strategies to differentiate transient from persistent AKI.

Fluid resuscitation is widely used, and many patients are therefore exposed to plasma volume expanders. Among these, colloids, particularly hydroxyethyl starches, have been shown in recent experiments and clinical studies to induce acute kidney injury. The mechanisms of colloid-induced acute kidney injury remain incompletely elucidated. The risks associated with colloid osmotic pressure elevation in vivo and the high incidence of osmotic nephrosis lesions in experimental models and clinical studies indicate that hydroxyethyl starches can no longer be considered safe.