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Review
. 2021 Jan;7(1):e06008.
doi: 10.1016/j.heliyon.2021.e06008. Epub 2021 Jan 20.

Kidney diseases and COVID-19 infection: causes and effect, supportive therapeutics and nutritional perspectives

Affiliations
Review

Kidney diseases and COVID-19 infection: causes and effect, supportive therapeutics and nutritional perspectives

Hassan Askari et al. Heliyon. 2021 Jan.

Abstract

Recently, the novel coronavirus disease 2019 (COVID-19), has attracted the attention of scientists where it has a high mortality rate among older adults and individuals suffering from chronic diseases, such as chronic kidney diseases (CKD). It is important to elucidate molecular mechanisms by which COVID-19 affects the kidneys and accordingly develop proper nutritional and pharmacological strategies. Although numerous studies have recently recommended several approaches for the management of COVID-19 in CKD, its impact on patients with renal diseases remains the biggest challenge worldwide. In this paper, we review the most recent evidence regarding causality, potential nutritional supplements, therapeutic options, and management of COVID-19 infection in vulnerable individuals and patients with CKD. To date, there is no effective treatment for COVID-19-induced kidney dysfunction, and current treatments are yet limited to anti-inflammatory (e.g. ibuprofen) and anti-viral medications (e.g. Remdesivir, and Chloroquine/Hydroxychloroquine) that may increase the chance of treatment. In conclusion, the knowledge about kidney damage in COVID-19 is very limited, and this review improves our ability to introduce novel approaches for future clinical trials for this contiguous disease.

Keywords: COVID-19; Kidney diseases; Multi-organ failure; Nutritional supplements.

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Figures

Figure 1
Figure 1
Renal insufficiency following SARS-COV-2 infections, causes and potential mechanisms. Kidney infections by viruses can be caused in a variety of ways. Excessive activation of Toll-like receptors results in renal dysfunction. Abbreviations: SARS-COV-2: Severe acute respiratory syndrome coronavirus 2; GFR: Glomerular filtration rate; ESRD: End-stage renal disease; AKI: Acute kidney injury.
Figure 2
Figure 2
Patients with COVID-19 outcomes as well as underlying disorders can lead to an elevated risk of acute kidney injury and its consequences. Recommendations on the management of the COVID-19 with acute kidney injury are suggested at the bottom of the figure. Abbreviations: COVID-19: Coronavirus disease 2019; CRRT: Continuous renal replacement therapy; hrsACE2: Human recombinant soluble angiotensin-converting enzyme 2; SARS-COV-2: Severe acute respiratory syndrome coronavirus 2.
Figure 3
Figure 3
The possible effect of interaction between medications, food, supplement, medical condition, specialized medical equipment and supplies in the care of coronavirus disease 2019 (COVID-19) patients with acute kidney injury. Abbreviation: SARS-COV-2: Severe acute respiratory syndrome coronavirus 2.
Figure 4
Figure 4
Immune dysregulation and renal insufficiency following SARS-COV-2 infections in Vit D deficiency cases. Immune responses may be decreased due to cathelicidin and some β-defensins reduction which lead to proteinuria, albuminuria, and progression to end-stage renal disease (ESRD) by renin-angiotensin system activation and inducing the oxidative stress and secretion of inflammatory cytokines. Abbreviations: COVID-19: Coronavirus disease 2019; CKD: Chronic kidney disease; ESRD: End-stage renal disease; IFNγ: Interferon Gamma; VDR: Vitamin D Receptor.
Figure 5
Figure 5
Protective effect of melatonin against kidney injury induced by SARS-COV-2. Melatonin could be improved sepsis-induced renal injury by suppressing Toll-Like Receptors, proinflammatory cytokines. Abbreviation: SARS-COV-2: Severe acute respiratory syndrome coronavirus 2. MLT: Melatonin; ACE2: Angiotensin-converting enzyme 2; NLRP3: NOD-, LRR- and pyrin domain-containing protein 3; TLR: Toll-Like Receptors; MYD88: Myeloid differentiation primary response protein; TNFR: Tumor Necrosis Factor Receptor; ROS: Reactive oxygen species; IKK: IkappaB Kinase; NF-κB: Nuclear factor kappa B.

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