Acute Kidney Injury (AKI) is an independent risk factor for mortality in hospitalized patients. AKI syndrome leads to fluid overload, electrolyte and acid-base disturbances, immunoparalysis, and propagates multiple organ dysfunction through organ “crosstalk”. Preclinical models suggest AKI causes acute lung injury (ALI), and conversely, mechanical ventilation and ALI cause AKI. In the clinical setting, respiratory complications are a key driver of increased mortality in patients with AKI, highlighting the bidirectional relationship. This article highlights the challenging and complex interactions between the lung and kidney in critically ill patients with AKI and acute respiratory distress syndrome (ARDS) and global implications of AKI. We discuss disease-specific molecular mediators and inflammatory pathways involved in organ crosstalk in the AKI-ARDS construct, and highlight the reciprocal hemodynamic effects of elevated pulmonary vascular resistance and central venous pressure (CVP) leading to renal hypoperfusion and pulmonary edema associated with fluid overload and increased right ventricular afterload. Finally, we discuss the notion of different ARDS “phenotypes” and the response to fluid overload, suggesting differential organ crosstalk in specific pathological states. While the directionality of effect remains challenging to distinguish at the bedside due to lag in diagnosis with conventional renal function markers and lack of tangible damage markers, this review provides a paradigm for understanding kidney-lung interactions in the critically ill patient.
OBJECTIVES: Therapeutic plasma exchange (TPE) has been shown to improve organ dysfunction and survival in patients with thrombotic microangiopathy and thrombocytopenia associated with multiple organ failure. There are no known therapies for the prevention of major adverse kidney events after continuous kidney replacement therapy (CKRT). The primary objective of this study was to evaluate the effect of TPE on the rate of adverse kidney events in children and young adults with thrombocytopenia at the time of CKRT initiation. DESIGN: Retrospective cohort. SETTING: Two large quaternary care pediatric hospitals. PATIENTS: All patients less than or equal to 26 years old who received CKRT between 2014 and 2020. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We defined thrombocytopenia as a platelet count less than or equal to 100,000 (cell/mm 3 ) at the time of CKRT initiation. We ascertained major adverse kidney events at 90 days (MAKE90) after CKRT initiation as the composite of death, need for kidney replacement therapy, or a greater than or equal to 25% decline in estimated glomerular filtration rate from baseline. We performed multivariable logistic regression and propensity score weighting to analyze the relationship between the use of TPE and MAKE90. After excluding patients with a diagnosis of thrombotic thrombocytopenia purpura and atypical hemolytic uremic syndrome ( n = 6) and with thrombocytopenia due to a chronic illness ( n = 2), 284 of 413 total patients (68.8%) had thrombocytopenia at CKRT initiation (51% female). Of the patients with thrombocytopenia, the median (interquartile range) age was 69 months (13–128 mo). MAKE90 occurred in 69.0% and 41.5% received TPE. The use of TPE was independently associated with reduced MAKE90 by multivariable analysis (odds ratio [OR], 0.35; 95% CI, 0.20–0.60) and by propensity score weighting (adjusted OR, 0.31; 95% CI, 0.16–0.59). CONCLUSIONS: Thrombocytopenia is common in children and young adults at CKRT initiation and is associated with increased MAKE90. In this subset of patients, our data show benefit of TPE in reducing the rate of MAKE90.
Fluid Overload Precedes and Masks Cryptic Kidney Injury in Pediatric Acute Respiratory Distress Syndrome OBJECTIVES: Given the complex interrelatedness of fluid overload (FO), creatinine, acute kidney injury (AKI), and clinical outcomes, the association of AKI with poor outcomes in critically ill children may be underestimated due to definitions used. We aimed to disentangle these temporal relationships in a large cohort of children with acute respiratory distress syndrome (ARDS).DESIGN: Retrospective cohort study. SETTING: Quaternary care PICU. PATIENTS:Seven hundred twenty intubated children with ARDS between 2011 and 2019. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS:Daily fluid balance, urine output (UOP), and creatinine for days 1-7 of ARDS were retrospectively abstracted. A subset of patients had angiopoietin 2 (ANGPT2) quantified on days 1, 3, and 7. Patients were classified as AKI by Kidney Disease Improving Global Outcomes (KDIGO) stage 2/3 then grouped by timing of AKI onset (early if days 1-3 of ARDS, late if days 4-7 of ARDS, persistent if both) for comparison of PICU mortality and ventilator-free days (VFDs). A final category of "Cryptic AKI" was used to identify subjects who met KDIGO stage 2/3 criteria only when creatinine was adjusted for FO. Outcomes were compared between those who had Cryptic AKI identified by FO-adjusted creatinine versus those who had no AKI. Conventionally defined AKI occurred in 26% of patients (early 10%, late 3%, persistent 13%). AKI was associated with higher mortality and fewer VFDs, with no differences according to timing of onset. The Cryptic AKI group (6% of those labeled no AKI) had higher mortality and fewer VFDs than patients who did not meet AKI with FO-adjusted creatinine. FO, FO-adjusted creatinine, and ANGPT2 increased 1 day prior to meeting AKI criteria in the late AKI group.CONCLUSIONS: AKI was associated with higher mortality and fewer VFDs in pediatric ARDS, irrespective of timing. FO-adjusted creatinine captures a group of patients with Cryptic AKI with outcomes approaching those who meet AKI by traditional criteria. Increases in FO, FO-adjusted creatinine, and ANGPT2 occur prior to meeting conventional AKI criteria.
An integrated multi-dimensional model for the digital follow up of mothers and neonates exposed to Sars-Cov-2 A. Creation of individual networks based on data from different dimensions, clinical, biological, social, and behavioral characteristics that define the risk of both mother and child. The circles represent signs, symptoms and factors related to the domains of data collection B. Development of dynamic networks to monitor change over time in network organization and connectivity aimed at identifying windows of vulnerability and resilience. C. Dynamic network analysis. D. Digital phenotyping over time (green, blue, and purple). The red lines represent the connections among signs, symptoms, and factors; Letters and colors refer to those shown in the figure.
BACKGROUND AND AIM:Progressive multi organ dysfunction (PMODS) leads to high mortality in pediatric intensive care unit (ICU) patients. Acute kidney injury (AKI) is common in PMODS, but evolution of MODS in AKI requiring continuous renal replacement therapy (CRRT) and associations with short-term outcomes have not been well described. METHOD:Multicenter study of pediatric CRRT (2/2014 to 2/2020). Chronic kidney disease patients were excluded. Pediatric Logistic Organ Dysfunction 2 (PELOD-2) scores and organ sub-scores were used to categorize MODS at two time points; PMODS was defined as increase in PELOD-2 score from ICU admission to CRRT start. The primary outcome was Major Adverse Kidney Events at 30 days (MAKE 30); secondary outcome was CRRT-free days.RESULTS: 373 patients (median age 84 months (IQR 16-172)) received CRRT for 9 days (IQR 3-20). Most common admission reason and co-morbidity were septic shock (23%) and hematological/oncological (22%), respectively. Median CRRT-free days was 21 (IQR 10-27). 71% met MAKE 30.PELOD-2 increased from admission 6 (IQR 3-9) to CRRT start 9 (IQR 7-12) (p<0.001). 62% had PMODS, number of organ failures increased from 3 (IQR 2-4) at admission to 4 (IQR 3-5) at CRRT start. The most common new organ dysfunction at CRRT start was respiratory. PMODS was associated with MAKE 30 (OR 1.06 (1.00 -1.12) and CRRTfree days (β -0.35 (-0.65 --0.06). CONCLUSIONS:PMODS is common in the pediatric CRRT population and is associated with MAKE 30 and fewer CRRTfree days. Future studies need to explore drivers of PMODS before CRRT and its association with patient outcomes.
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