Background: Candidozyma auris (C. auris) is an emerging multidrug-resistant yeast that has become an important cause of healthcare-associated outbreaks, particularly in intensive care units (ICUs). Colonization frequently precedes invasive infection, yet the epidemiology, progression to candidemia, and mortality among critically ill patients remain incompletely characterized. Methods: We conducted a narrative review of published studies evaluating C. auris colonization and infection in ICU populations. Studies reporting colonization rates, progression to invasive infection, and mortality were synthesized. Descriptive pooled proportions were calculated from aggregated data across eligible observational studies. Results: Colonization rates varied widely according to local epidemiology, ranging from 0.2 to 0.4% in routine surveillance studies to over 50% during outbreaks. Across 17 observational studies including 1879 colonized ICU patients, 616 developed invasive infection, yielding a descriptive pooled incidence of 32.8% (95% CI, 30.7–34.9%), predominantly candidemia. The median interval from ICU admission to candidemia was 25.8 days. Among 13 studies including 1354 colonized and/or infected ICU patients, the descriptive pooled 30-day in-hospital mortality was 36.4% (95% CI, 33.8–39.0%). In 12 studies comprising 396 patients with C. auris candidemia, the descriptive pooled 30-day mortality was 45.9% (95% CI, 41.0–50.8%), significantly higher than that observed in mixed colonized/infected ICU populations. Conclusions: C. auris represents a major threat in ICUs because of its ability to establish persistent colonization, progress to invasive candidemia, and cause high mortality among critically ill patients. Early identification of colonized patients, rigorous infection prevention measures, and prompt antifungal management are essential to reduce transmission and improve clinical outcomes.

Background: Candidozyma auris (C. auris) is an emerging multidrug-resistant yeast that has become an important cause of healthcare-associated outbreaks, particularly in intensive care units (ICUs). Colonization frequently precedes invasive infection, yet the epidemiology, progression to candidemia, and mortality among critically ill patients remain incompletely characterized. Methods: We conducted a narrative review of published studies evaluating C. auris colonization and infection in ICU populations. Studies reporting colonization rates, progression to invasive infection, and mortality were synthesized. Pooled estimates were calculated using aggregated data from eligible observational studies. Results: Colonization rates varied widely according to local epidemiology, ranging from 0.2–0.4% in routine surveillance studies to over 50% during outbreaks. Across 17 observational studies including 1,879 colonized ICU patients, 616 developed invasive infection, yielding a pooled incidence of 32.8%, predominantly candidemia. The median interval from ICU admission to candidemia was 25.8 days. Among 13 studies including 1,354 colonized and/or infected ICU patients, the pooled 30-day in-hospital mortality was 36.4% (95% CI, 33.8–39.0%). In 12 studies comprising 396 patients with C. auris candidemia, pooled 30-day mortality was 45.9% (95% CI, 41.0–50.8%), significantly exceeding that in mixed colonized/infected populations. Conclusions: Candidozyma auris represents a major threat in ICUs because of its ability to establish persistent colonization, progress to invasive candidemia, and cause high mortality among critically ill patients. Early identification of colonized patients, rigorous infection prevention measures, and prompt antifungal management are essential to reduce transmission and improve clinical outcomes.

Background/Objectives: The renal resistive index (RRI) has emerged as an early marker of renal vascular resistance. The purpose of this study was to investigate the association between RRI on intensive care unit (ICU) admission and the development of acute kidney injury (AKI) in a general ICU population, and to assess its predictive accuracy. Methods: This prospective observational study was conducted in a multidisciplinary ICU. Consecutive mechanically ventilated adults were enrolled; RRI was measured within 24 h of admission after hemodynamic stabilization. AKI was defined by Kidney Disease: Improving Global Outcomes (KDIGO) criteria within seven days. Multivariable regression, receiver operating characteristic (ROC), reclassification, and mediation analyses were performed. Results: A total of 181 patients were included. AKI occurred in 36%. Median RRI was 0.73 (0.65–0.80). RRI correlated with age, acute physiology and chronic health evaluation (APACHE) II and sequential organ failure assessment (SOFA) scores, lactate, and glomerular filtration rate (GFR) (all p < 0.001). In multivariable analysis, RRI was the only independent predictor of AKI (OR 2.86 per 0.05 increase, 95% CI 1.64–4.98, p = 0.001). It was also associated with an increased likelihood of presenting with a more severe AKI stage. RRI showed high discriminative ability (AUC = 0.89, 95% CI 0.84–0.94); the optimal cut-off was 0.77 (sensitivity 0.83, specificity 0.82). Adding RRI to a clinical model improved prediction (ΔAUC p = 0.049; net reclassification index (NRI) = 0.52, p < 0.001). Mediation analyses showed that RRI significantly mediated the effects of hypertension and low baseline GFR on AKI risk. Subgroup analyses confirmed consistent predictive performance across age, lactate, and sepsis categories. Conclusions: RRI is an independent early predictor of AKI and its severity, as well as a mediator of both hypertension and low GFR, regarding their effect on AKI development in ICU patients. RRI could serve as an early bedside marker of renal perfusion impairment in critically ill patients, guiding strategies aimed at reducing the risk of AKI.