Urinary Syndecan-1 and acute kidney injury after pediatric cardiac surgery

Ferrer, Natalia Monte Benevides; Cavalcante, Candice Torres de Melo Bezerra; Branco, Klébia Magalhães Castelo; Júnior, Valdester Cavalcante Pinto; Meneses, Gdayllon Cavalcante; Neves, Fernanda Macedo de Oliveira; Souza, Nayana Maria Gomes de; LourençoPenaforte, Kiarelle; Martins, Alice Maria Costa; Libório, Alexandre Braga

doi:10.1016/j.cca.2018.06.033

Cited by 13 publications

(11 citation statements)

References 26 publications

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“…Rehm et al provided the first evidence in humans to the shedding of the endothelial glycocalyx during global or regional ischemia/reperfusion (I/R) procedures in major vascular surgery ( 7 ). Studies have shown that elevated serum and urinary SDC-1 is a potential biomarker in predicting renal dysfunction and mortality in patients with AKI after cardiac surgery ( 8 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

Association Between Syndecan-1, Fluid Overload, and Progressive Acute Kidney Injury After Adult Cardiac Surgery

Jiang

Yang

et al. 2021

Front. Med.

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Background: Acute kidney injury (AKI) is a common complication after cardiac surgery and the prognosis of AKI worsens with the increase in AKI severity. Syndecan-1(SDC-1) is a biomarker of endothelial glycocalyx degradation. Fluid overload (FO) is associated with poor outcomes in AKI patients and may be related to the damage of endothelial function. This study aimed at demonstrating the association between elevated SDC-1, FO, and AKI progression.Methods: In this prospective study, we screened patients who underwent cardiac surgery and enrolled patients who experienced an AKI within 48 h after surgery from December 1, 2018 to January 31, 2019. Blood and urine samples were collected at the time of AKI diagnosis for plasma SDC-1 (pSDC-1) and urine SDC-1 (uSDC-1) measurements. Fluid balance (FB) = accumulated [fluid intake (L) - fluid output (L)]/body weight (kg) × 100%. FO was defined as FB > 5%. The primary endpoint was progressive AKI, defined as AKI progression from a lower to a higher stage. The patients were divided into progressive AKI group vs. non-progressive AKI group.Results: The quartiles of pSDC-1 concentration (117.3 [67.4, 242.3] ng/mL) showed a graded association with the incidence of progressive AKI, ranging from 5.0, 11.9, 32.6 to 52.4% (p for trend < 0.001). Multivariate logistic regression showed that increased pSDC-1 was an independent risk factor for progressive AKI. The AUC-ROC area of pSDC-1 concentration in predicting AKI progression was 0.847. Linear regression showed a positive correlation between FB and pSDC-1 concentration (R2 = 0.384, p < 0.001). In patients with FO, the progressive AKI incidence was significantly higher in the high pSDC-1 (≥117.3 ng/mL) subgroup than in the low pSDC-1 subgroup (58.3 vs. 17.6%, OR = 9.167, P = 0.005). In patients without FO, the progressive AKI incidence was also significantly higher in the high pSDC-1 subgroup with a lower odds ratio (30.4 vs. 7.4%, OR = 6.714, P = 0.002).Conclusion: Elevated pSDC-1 concentration was associated with progressive AKI after cardiac surgery and showed good predictive ability for progressive AKI. FB was related to the increase of pSDC-1. The interaction between pSDC-1 and FB may further aggravate the progression of AKI.

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Section: Introductionmentioning

confidence: 99%

Association Between Syndecan-1, Fluid Overload, and Progressive Acute Kidney Injury After Adult Cardiac Surgery

Jiang

Yang

et al. 2021

Front. Med.

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“…143 The postoperative urinary syndecan-1 levels were significantly higher in pediatric patients with severe AKI after cardiac surgery. 144 Similarly, in adult patients with acute decompensated heart failure, plasma syndecan-1 level was a good predictor of risk of impending renal failure and mortality. 145 High plasma syndecan-1 level also predicted renal failure in kidney transplant patients.…”

Section: Heparanase/shed Syndecan-1 In Kidney Diseasementioning

confidence: 95%

Heparanase-enhanced Shedding of Syndecan-1 and Its Role in Driving Disease Pathogenesis and Progression

Rangarajan¹,

Richter²,

Richter³

et al. 2020

J Histochem Cytochem.

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Both heparanase and syndecan-1 are known to be present and active in disease pathobiology. An important feature of syndecan-1 related to its role in pathologies is that it can be shed from the surface of cells as an intact ectodomain composed of the extracellular core protein and attached heparan sulfate and chondroitin sulfate chains. Shed syndecan-1 remains functional and impacts cell behavior both locally and distally from its cell of origin. Shedding of syndecan-1 is initiated by a variety of stimuli and accomplished predominantly by the action of matrix metalloproteinases. The accessibility of these proteases to the core protein of syndecan-1 is enhanced, and shedding facilitated, when the heparan sulfate chains of syndecan-1 have been shortened by the enzymatic activity of heparanase. Interestingly, heparanase also enhances shedding by upregulating the expression of matrix metalloproteinases. Recent studies have revealed that heparanase-induced syndecan-1 shedding contributes to the pathogenesis and progression of cancer and viral infection, as well as other septic and non-septic inflammatory states. This review discusses the heparanase/shed syndecan-1 axis in disease pathogenesis and progression, the potential of targeting this axis therapeutically, and the possibility that this axis is widespread and of influence in many diseases.

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“…Postoperative urinary syndecan-1 was collected within 2 h after surgery and was higher in patients suffering from acute kidney injury in the follow-up. In addition, the prediction of acute kidney injury in a risk-stratified statistical model of clinical outcome was improved after adding urinary syndecan-1 ( Ferrer et al, 2018 ). These data were recently confirmed and expanded by Bangalore et al (2021) , demonstrating an association of the amount of circulating heparan sulfate with metabolic acidosis, renal dysfunction and capillary leak in 27 neonates and infants following cardiopulmonary bypass surgery.…”

Section: Pathology Of the Eg In Acute Childhood Diseases And Chronic Conditions With Childhood-onsetmentioning

confidence: 99%

The Endothelial Glycocalyx: Physiology and Pathology in Neonates, Infants and Children

Puchwein-Schwepcke

Genzel‐Boroviczény²,

Nußbaum³

2021

Front. Cell Dev. Biol.

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The endothelial glycocalyx (EG) as part of the endothelial surface layer (ESL) is an important regulator of vascular function and homeostasis, including permeability, vascular tone, leukocyte recruitment and coagulation. Located at the interface between the endothelium and the blood stream, this highly fragile structure is prone to many disruptive factors such as inflammation and oxidative stress. Shedding of the EG has been described in various acute and chronic diseases characterized by endothelial dysfunction and angiopathy, such as sepsis, trauma, diabetes and cardiovascular disease. Circulating EG components including syndecan-1, hyaluronan and heparan sulfate are being evaluated in animal and clinical studies as diagnostic and prognostic markers in several pathologies, and advances in microscopic techniques have enabled in vivo assessment of the EG. While research regarding the EG in adult physiology and pathology has greatly advanced throughout the last decades, our knowledge of the development of the glycocalyx and its involvement in pathological conditions in the pediatric population is limited. Current evidence suggests that the EG is present early during fetal development and plays a critical role in vessel formation and maturation. Like in adults, EG shedding has been demonstrated in acute inflammatory conditions in infants and children and chronic diseases with childhood-onset. However, the underlying mechanisms and their contribution to disease manifestation and progression still need to be established. In the future, the glycocalyx might serve as a marker to identify pediatric patients at risk for vascular sequelae and as a potential target for early interventions.

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Urinary Syndecan-1 and acute kidney injury after pediatric cardiac surgery

Cited by 13 publications

References 26 publications

Association Between Syndecan-1, Fluid Overload, and Progressive Acute Kidney Injury After Adult Cardiac Surgery

Association Between Syndecan-1, Fluid Overload, and Progressive Acute Kidney Injury After Adult Cardiac Surgery

Heparanase-enhanced Shedding of Syndecan-1 and Its Role in Driving Disease Pathogenesis and Progression

The Endothelial Glycocalyx: Physiology and Pathology in Neonates, Infants and Children

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