Is Serum Cystatin C a Predictor of Acute Pulmonary Thromboembolism in Patients With Normal Renal Function?

Tutar, Nuri; Kemik, Nur Aleyna; Yılmaz, İnsu; Büyükoğlan, Hakan; Kanbay, Asiye; Doğan, Ali; Oyak, Fatma Sema; Gülmez, İnci; Demir, Ramazan

doi:10.1177/1076029613512416

Cited by 1 publication

(1 citation statement)

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“…The dysregulation of markers such as calprotectin (S100A8/A9), 16,17 cystatin C (CST3), 18,19 and lipocalin-2 (LCN2) 20,21 is linked with cardiovascular complications including vascular inflammation and VTE and tissue injury. S100A8/A9 is secreted from myeloid cells in response to inflammatory reactions and regulates the pathogenesis of cardiovascular disease.…”

Section: Impact Statementmentioning

confidence: 99%

Lipocalin-2, S100A8/A9, and cystatin C: Potential predictive biomarkers of cardiovascular complications in COVID-19

Gupta

Al-Tamimi

Halwani

et al. 2022

Exp Biol Med (Maywood)

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Severe coronavirus (SARS-COV-2) infection often leads to systemic inflammation accompanied by cardiovascular complications including venous thromboembolism (VTE). However, it is largely undefined if inflammatory markers such as lipocalin-2 (LNC2), calprotectin (S100A8/A9), and cystatin C (CST3), previously linked with VTE, play roles in cardiovascular complications and advancement of COVID-19 severity. To investigate the same, hospitalized moderate and severe (presented pneumonia and required intensive care) COVID-19 patients were recruited. The levels of plasma LNC2, S100A8/A9, CST3, myoglobin, and cardiac Troponin I (cTnI) were assessed through enzyme-linked immunosorbent assay (ELISA). The investigation revealed a significantly upregulated level of plasma LNC2 at the moderate stage of SARS-CoV-2 infection. In contrast, the levels of S100A8/A9 and CST3 in moderate patients were comparable to healthy controls; however, a profound induction was observed only in severe COVID-19 patients. The tissue injury marker myoglobin was unchanged in moderate patients; however, a significantly elevated level was observed in the critically ill COVID-19 patients. In contrast, cTnI level was unchanged both in moderate and severe patients. Analysis revealed a positive correlation between the levels of S100A8/A9 and CST3 with myoglobin in COVID-19. In silico analysis predicted interactions of S100A8/A9 with toll-like receptor 4 (TLR-4), MyD88 LY96, and LCN2 with several other inflammatory mediators including MMP2, MMP9, TIMP1, and interleukins (IL-6, IL-17A, and IL-10). In summary, early induction of LCN2 likely plays a role in advancing the COVID-19 severity. A positive correlation of S100A8/A9 and CST3 with myoglobin suggests that these proteins may serve as predictive biomarkers for thromboembolism and tissue injury in COVID-19.

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