Search Results (7)

Background: Fluid overload (FO) is a frequent ICU complication and an important predictor of adverse outcomes. While classically attributed to resuscitative fluids, recent data emphasize the contribution of non-therapeutic “fluid creep” from medication diluents and carrier infusions. This study examined associations between fluid creep, FO, acute kidney injury (AKI), and mortality, and explored the predictive value of the modified Renal Angina Index (mRAI) for AKI risk stratification and FO; Methods: A retrospective cohort of 250 critically ill adults (ICU stay ≥72 h) admitted to a mixed medical–surgical ICU between May 2021 and November 2024 was analyzed. All fluids administered during the first 72 h were categorized and indexed to ideal body weight. Fluid creep included drug diluents, carriers, and flushes. FO% was calculated as [(Cumulative Fluid Balance)/IBW] × 100; Results: Fluid creep was higher in non-survivors (5183 ± 2541 vs. 4354 ± 2171 mL; p = 0.008) and correlated with FO, cumulative balance, and total input (r = 0.41 to 0.43; p < 0.001). Creep and FO independently predicted ICU mortality. Abnormal mRAI scores were associated with FO and early AKI; Conclusions: Fluid creep and FO were independent mortality predictors. Routine monitoring and minimization of creep, along with structured de-resuscitation protocols, may improve outcomes in critically ill adults. Full article

Acute kidney injury (AKI) is a frequent and severe complication in trauma patients, affecting up to 28% of intensive care unit (ICU) admissions and contributing significantly to morbidity, mortality, and long-term renal impairment. Trauma-related AKI (TRAKI) arises from diverse mechanisms, including hemorrhagic shock, ischemia–reperfusion injury, systemic inflammation, rhabdomyolysis, nephrotoxicity, and complex organ crosstalk involving the brain, lungs, and abdomen. Pathophysiologically, TRAKI involves early disruption of the glomerular filtration barrier, tubular epithelial injury, and renal microvascular dysfunction. Inflammatory cascades, oxidative stress, immune thrombosis, and maladaptive repair mechanisms mediate these injuries. Trauma-related rhabdomyolysis and exposure to contrast agents or nephrotoxic drugs further exacerbate renal stress, particularly in patients with pre-existing comorbidities. Traditional markers such as serum creatinine (sCr) are late indicators of kidney damage and lack specificity. Emerging structural and stress response biomarkers—such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), C-C motif chemokine ligand 14 (CCL14), Dickkopf-3 (DKK3), and the U.S. Food and Drug Administration (FDA)-approved tissue inhibitor of metalloproteinases-2 × insulin-like growth factor-binding protein 7 (TIMP-2 × IGFBP-7)—allow earlier detection of subclinical AKI and better predict progression and the need for renal replacement therapy. Together, functional indices like urinary sodium and fractional potassium excretion reflect early microcirculatory stress and add clinical value. In parallel, risk stratification tools, including the Renal Angina Index (RAI), the McMahon score, and the Haines model, enable the early identification of high-risk patients and help tailor nephroprotective strategies. Together, these biomarkers and risk models shift from passive AKI recognition to proactive, personalized management. A new paradigm that integrates biomarker-guided diagnostics and dynamic clinical scoring into trauma care promises to reduce AKI burden and improve renal outcomes in this critically ill population. Full article

Fluid overload significantly increases morbidity and mortality in critically ill children. Following hematopoietic cell transplant (HCT), children are at a high risk of fluid accumulation due to essential increased fluid intake for nutrition, blood products, and antimicrobials. In addition, many complications predispose these children to capillary leak and fluid overload (FO), such as sinusoidal obstruction syndrome, engraftment syndrome, sepsis, and acute kidney injury (AKI). FO > 10% occurs in nearly half of children following HCT and is associated with a lower PICU survival rate. In addition, in children with acute respiratory failure post HCT, each 1% increase in cumulative fluid balance on d 3 increases the odds of PICU mortality by 3%. Furthermore, FO worsens AKI. Tools such as the renal angina index and urinary biomarkers such as neutrophil gelatinase-associated lipocalin can help identify patients at risk of AKI and FO. Early detection, prevention, and intervention are crucial to improving outcomes in this population. Management strategies include fluid restriction, diuretics, and continuous kidney replacement therapy (CKRT) when FO exceeds 10% and other measures have failed. Full article

Acute kidney injury (AKI) is an acute condition of impaired kidney function with decreased glomerular filtration rate, which results in dysregulation in volume, electrolyte, and acid–base equilibrium. AKI can be a life-threatening condition and can also lead to chronic kidney disease. It is important to diagnose AKI early in the course of the disease or to predict its development, as this can influence therapeutic decisions, outcome, and, consequently, the prognosis. In clinical practice, an elevated serum creatinine concentration remains the most common laboratory indicator for diagnosing AKI. However, due to the delay in its rise, creatinine levels are often insensitive and inaccurate for early diagnosis. Novel biomarkers of kidney tubular injury and the renal angina index have shown promise in predicting AKI earlier and more accurately. Contrast-enhanced ultrasonography (CEUS) and ultra-microangiography (UMA) are radiological methods that can quantify renal microperfusion and may be able to predict the development of AKI. They have not yet been used for quantifying renal perfusion in children with risk factors for developing AKI. Further research is needed to compare these sonographic techniques with the renal angina index and emerging kidney injury biomarkers for predicting acute kidney injury (AKI) in both children and adults. Full article

Acute kidney injury (AKI) occurs frequently in critically ill children, having an incidence of up to 26.9% and is associated with high morbidity and mortality in pediatric intensive care units (PICU). Currently, the decrease in the glomerular filtration rate is calculated using the serum creatinine levels. Nevertheless, there may be a 48 h delay between the renal injury and measurable increase in creatinine. Urinary neutrophil gelatinase-associated lipocalin (uNGAL) has been validated in relation to cardiopulmonary bypass in children, being able to detect AKI before the functional change proven by the rise in serum creatinine. Our aim was to study the utility of using uNGAL in the management of critical pediatric patients admitted to our hospital in a six month period, more specifically, its capacity to predict AKI development, alone and in the association with the renal angina index (RAI). Twenty-eight critically ill children aged from 1 day to 15 years have been included. We found that an increase in uNGAL in day 1 of admission in the PICU was significantly correlated with a decrease in creatinine clearance but not anymore in day 3. However, in our sample uNGAL did not show a significant predictability for AKI development nor the supplementary incorporation of RAI into the prediction model. Therefore, apart from cardiac surgery, the efficacy and utility or uNGAL in the management of critically ill children is still questionable. For the best prediction, we will need to incorporate not only the RAI or other PICU scores, but other biomarkers such as KIM-1, urinary cystatin, and IL 18 in larger samples. Full article

Pediatric acute kidney injury (AKI) is a major cause of morbidity and mortality in children undergoing interventional procedures. The review summarizes current classifications of AKI and acute kidney disease (AKD), as well as systematizes the knowledge on pathophysiology of kidney injury, with a special focus on renal functional reserve and tubuloglomerular feedback. The aim of this review is also to show the state-of-the-art in methods assessing risk and prognosis by discussing the potential role of risk stratification strategies, taking into account both glomerular function and clinical settings conditioned by fluid overload, urine output, or drug nephrotoxicity. The last task is to suggest careful assessment of eGFR as a surrogate marker of renal functional reserve and implementation of point-of-care testing, available in the case of biomarkers like NGAL and [IGFBP-7] × [TIMP-2] product, into everyday practice in patients at risk of AKI due to planned invasive procedures or treatment. Full article

Background: Acute myocardial infarction (AMI) survivors are at risk of major adverse cardiac events and their risk stratification is a prerequisite to tailored therapeutic approaches. Biomarkers could be of great utility in this setting. Methods: We sought to evaluate the utility of the combined assessment of Galectin 3 (Gal-3) and Galectin 3 binding protein (Gal-3bp) for post-AMI risk stratification in a large, consecutive population of AMI patients. The primary outcomes were: Recurrent angina/AMI and all-cause mortality at 12 months after the index event. Results: In total, 469 patients were included. The median Gal-3bp was 9.1 μg/mL (IQR 5.8–13.5 μg/mL), while median Gal-3 was 9.8 ng/mL (IQR 7.8–12.8 ng/mL). During the 12 month follow-up, 34 patients died and 41 had angina pectoris/reinfarction. Gal-3 was associated with all-cause mortality, while Gal-3bp correlated with the risk of angina/myocardial infarction even when corrected for other significant covariates. The final multivariable model for mortality prediction included patients’ age, left ventricular ejection fraction (LVEF), Gal-3, and renal function. The ROC curve estimated for this model has an area under the curve (AUC) of 0.84 (95%CI 0.78–0.9), which was similar to the area under the ROC curve obtained using the GRACE score 1-year mortality. Conclusions: The integrated assessment of Gal-3 and Gal-3bp could be helpful in risk stratification after AMI. Full article