Serum and Urinary Biomarkers in COVID-19 Patients with or without Baseline Chronic Kidney Disease

Filev, Rumen; Lyubomirova, Mila; Hristova, Julieta; Bogov, Б.; Kalinov, Krassimir; Sviranov, Dobrin; Rostaing, Lionel

doi:10.3390/jpm13030382

Cited by 3 publications

(2 citation statements)

References 40 publications

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“…Further, soluble programmed cell-death receptor-1 (sPDL-1), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular adhesion molecule-1 (sVCAM-1) were also found to be associated with severe AKI and ARF. Additionally, the levels of CCL-2, CCL-3, CCL-4, CXCL-8, CXCL-10, IFN-γ, IL-2, IL-6, TNF-α, IL-1Ra, IL-10, and VEGF were also found to be significantly higher in AKI patients [60][61][62][63][64][65][66]. The role of inflammatory cytokines as biomarkers is supported by the fact that inflammatory cytokines are increased during cytokine storm, which is associated with AKI [67].…”

Section: Biomarkers Of Kidney Injury In Covid-19mentioning

confidence: 94%

“…The pandemic has taught us that the earlier the diagnosis of AKI, the greater the probability of a better outcome for these patients because AKI and CKD are associated with higher mortality in COVID-19 patients. Table 1 summarizes the common possible biomarkers for AKI in COVID-19 patients, as reported in various studies [60][61][62][63][64][65][66]. IL-6 was found to have a moderate accuracy of prediction, while cystatin C, KIM-1, urine-Klotho, TIMP-2, and IL-6 had poor accuracy for predicting the incidence of AKI.…”

Section: Biomarkers Of Kidney Injury In Covid-19mentioning

confidence: 99%

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COVID-19 and Kidney: The Importance of Follow-Up and Long-Term Screening

Rai

2023

Life

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Renal involvement and kidney injury are common in COVID-19 patients, and the symptoms are more severe if the patient already has renal impairment. Renal involvement in COVID-19 is multifactorial, and the renal tubule is mainly affected, along with podocyte injury during SARS-CoV-2 infection. Inflammation, complement activation, hypercoagulation, and crosstalk between the kidney and lungs, brain, and heart are contributory factors. Kidney injury during the acute phase, termed acute kidney injury (AKI), may proceed to chronic kidney disease if the patient is discharged with renal impairment. Both AKI and chronic kidney disease (CKD) increase mortality in COVID-19 patients. Further, COVID-19 infection in patients suffering from CKD is more severe and increases the mortality rate. Thus, it is important to address both categories of patients, either developing AKI or CKD after COVID-19 or previously having CKD, with proper management and treatment. This review discusses the pathophysiology involved in AKI and CKD in COVID-19 infection, followed by management and treatment of AKI and CKD. This is followed by a discussion of the importance of screening and treatment of CKD patients infected with COVID-19 and future perspectives to improve treatment in such patients.

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Section: Biomarkers Of Kidney Injury In Covid-19mentioning

confidence: 94%

Section: Biomarkers Of Kidney Injury In Covid-19mentioning

confidence: 99%

COVID-19 and Kidney: The Importance of Follow-Up and Long-Term Screening

Rai

2023

Life

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Novel mechanism of the COVID-19 associated coagulopathy (CAC) and vascular thromboembolism

Singh,

Pushpakumar,

Zheng

et al. 2023

npj Viruses

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Previous studies from our laboratory revealed that SARS-CoV-2 spike protein (SP) administration to a genetically engineered model expressing the human angiotensin-converting enzyme 2; ACE2 receptor (i.e., hACE2 humanized mouse) mimicked the coronavirus disease-19 (COVID-19) pathology. In humans the cause of high morbidity, and mortality is due to ‘cytokine-storm’ led thromboembolism; however, the exact mechanisms of COVID-19 associated coagulopathy (CAC) have yet to be discovered. Current knowledge suggests that CAC is distinct from the standard coagulopathy, in that the intrinsic and extrinsic thrombin-dependent coagulation factors, and the pathway(s) that are common to coagulopathy, are not recruited by SARS-CoV-2. Findings from patients revealed that there is little change in their partial thromboplastin, or the prothrombin time coupled with a significant decline in platelets. Further, there appears to be an endothelial dysfunction during COVID-19 suggesting an interaction of the endothelia with immune cells including neutrophils. There are also reports that inflammatory NGAL is elevated during COVID-19. Furthermore, the levels of NPT are also increased indicating an increase in inflammatory M1 macrophage iNOS which sequesters BH4; an essential enzyme co-factor that acts as a potent antioxidant thus causing damage to endothelia. SARS-CoV-2 entry into the host cells is facilitated by a co-operative action between TMPRSS2 and the main ACE2 receptor. Interestingly, after infection ADAMTS13; a von Willebrand factor; VWF cleaving enzyme is found to be decreased. Based on these facts, we hypothesize that vascular thromboembolism is associated with serine and metalloproteinase, and in that context, we opine that inhibition of iNOS might help mitigate COVID-19 harmful effects. To test this hypothesis, we administered SP to the hACE2 mice that were subsequently treated with amino guanidine (AG; a potent inhibitor of glycoxidation, lipoxidation and oxidative vicious cycles). Our results revealed increase in TMPRSS2, and NGAL by SP but treatment with AG mitigated their levels. Similarly, levels of MMP-2, and -9 were increased; however, AG treatment normalized these levels. Our findings suggest that occurrence of CAC is influenced by TMPRSS2, ADAMTS13, NGAL and MMP- 2, and -9 factors, and an intervention with iNOS blocker helped mitigate the CAC condition in experimental settings.

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Urinary Neutrophil Gelatinase-Associated Lipocalin as a Predictor of COVID-19 Mortality in Hospitalized Patients

Švitek,

Zlosa,

Grubišić

et al. 2024

AMH

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Neutrophil gelatinase-associated lipocalin (NGAL) is a protein secreted by activated neutrophils and certain tissues. The aim of this study was to investigate the prognostic role of urinary neutrophil gelatinase-associated lipocalin (uNGAL) in hospitalized COVID-19 patients with regard to mortality. The prospective observational cohort study involved 86 hospitalized adult COVID-19 patients. Patients’ urine samples were collected upon admission and 48–72 h after admission. General anamnesis and clinical status information were obtained from medical records. Within 24 h of sample collection, urine aliquots were centrifuged, the supernatant was separated, and samples were frozen at −80 °C until uNGAL concentration measurement, which was performed within two years of sample collection. The patients were categorized into groups based on disease outcome (survived/deceased). Data analysis was performed to identify predictive factors and diagnostic indicators for the unfavorable outcome group using logistic regression and ROC curve methods. Logistic regression associated age, cardiomyopathy, invasive mechanical ventilation, and uNGAL concentration (follow-up sampling) with mortality. ROC analysis identified uNGAL concentration (follow-up sampling) as an indicator of mortality, with a cut-off value of >23.8 ng/mL. This study concludes that there is an association between disease outcome and uNGAL concentration in COVID-19 patients. However, understanding the dynamics of uNGAL concentration during COVID-19 remains limited, which is crucial for its effective clinical application.

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Serum and Urinary Biomarkers in COVID-19 Patients with or without Baseline Chronic Kidney Disease

Cited by 3 publications

References 40 publications

COVID-19 and Kidney: The Importance of Follow-Up and Long-Term Screening

COVID-19 and Kidney: The Importance of Follow-Up and Long-Term Screening

Novel mechanism of the COVID-19 associated coagulopathy (CAC) and vascular thromboembolism

Urinary Neutrophil Gelatinase-Associated Lipocalin as a Predictor of COVID-19 Mortality in Hospitalized Patients

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