Cytokine and Chemokine Retention Profile in COVID-19 Patients with Chronic Kidney Disease

Toxins (Basel). 2022 Sep 28;14(10):673. doi: 10.3390/toxins14100673.

Abstract

Chronic kidney disease (CKD) patients are more susceptible to infections compared to the general population. SARS-CoV-2 virus pathology is characterized by a cytokine storm responsible for the systemic inflammation typical of the COVID-19 disease. Since CKD patients have a reduced renal clearance, we decided to investigate whether they accumulate harmful mediators during the COVID-19 disease. We conducted a retrospective study on 77 COVID-19 hospitalized subjects in the acute phase of the illness. Thirteen different cytokines were assessed in plasma collected upon hospitalization. The patients were divided into three groups according to their estimated glomerular filtration rate, eGFR < 30 (n = 23), 30 < eGFR < 60 (n = 33), eGFR > 60 mL/min (n = 21). We found that Tumor Necrosis Factor α and its receptors I and II, Interleukin-7, Leukemia Inhibitory Factor, FAS receptor, Chitinase 3-like I, and the Vascular Endothelial Growth Factor showed an increased accumulation that negatively correlate with eGFR. Moreover, non-survivor patients with an impaired kidney function have significantly more elevated levels of the same mediators. In conclusion, there is a tendency in COVID-19 ESRD patients to accumulate harmful cytokines. The accumulation seems to associate with mortality outcomes and may be due to reduced clearance but also to increased biosynthesis in most severe cases.

Keywords: CKD; COVID-19; eGFR; mortality.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • COVID-19*
  • Chemokines
  • Chitinases*
  • Cytokines / immunology
  • Glomerular Filtration Rate / physiology
  • Humans
  • Interleukin-7
  • Leukemia Inhibitory Factor
  • Renal Insufficiency*
  • Renal Insufficiency, Chronic*
  • Retrospective Studies
  • SARS-CoV-2
  • Tumor Necrosis Factor-alpha
  • Vascular Endothelial Growth Factor A
  • fas Receptor

Substances

  • Chemokines
  • Chitinases
  • fas Receptor
  • Interleukin-7
  • Leukemia Inhibitory Factor
  • Tumor Necrosis Factor-alpha
  • Vascular Endothelial Growth Factor A
  • Cytokines

Grants and funding

Part of this study was supported by “Piano di Sostegno alla Ricerca-Linea 2-Dotazione annuale”, by Department of Health Sciences University of Milan.