ABSTRACT
The novel coronavirus disease 19 (nCoV19) is universally known as Covid-19, which is caused by severe acute respiratory coronavirus 2 (SARS-CoV-2), and affects diverse range of organs, presenting with pulmonary manifestations as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), and extra-pulmonary manifestations like acute kidney injury (AKI). AKI is regarded as a poor prognostic factor in patients with severe Covid-19, thus early detection and management of this critical status may reduce the risk of complications and mortality. We present the case of a 30 years old man with moderate Covid-19 presenting with haematuria and eventually diagnosed as AKI. The patient was managed compared with a Covid-19 patient as control. The patient recovered within three weeks of supportive and standard care therapy. Reversible AKI and associated haematuria can be the presenting features of Covid-19 and are linked with mild-moderate SARS-CoV-2 infection.
Subject(s)
Acute Kidney Injury , COVID-19 , Respiratory Distress Syndrome , Acute Kidney Injury/diagnosis , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , Adult , Humans , Lung , Male , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , SARS-CoV-2ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a causative virus in the development of coronavirus disease 2019 (Covid-19) pandemic. Respiratory manifestations of SARS-CoV-2 infection such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) leads to hypoxia, oxidative stress, and sympatho-activation and in severe cases leads to sympathetic storm (SS). On the other hand, an exaggerated immune response to the SARS-CoV-2 invasion may lead to uncontrolled release of pro-inflammatory cytokine development of cytokine storm (CS). In Covid-19, there are interactive interactions between CS and SS in the development of multi-organ failure (MOF). Interestingly, cutting the bridge between CS and SS by anti-inflammatory and anti-adrenergic agents may mitigate complications that are induced by SARS-CoV-2 infection in severely affected Covid-19 patients. The potential mechanisms of SS in Covid-19 are through different pathways such as hypoxia, which activate the central sympathetic center through carotid bodies chemosensory input and induced pro-inflammatory cytokines, which cross the blood-brain barrier and activation of the sympathetic center. ß2-receptors signaling pathway play a crucial role in the production of pro-inflammatory cytokines, macrophage activation, and B-cells for the production of antibodies with inflammation exacerbation. ß-blockers have anti-inflammatory effects through reduction release of pro-inflammatory cytokines with inhibition of NF-κB. In conclusion, ß-blockers interrupt this interaction through inhibition of several mediators of CS and SS with prevention development of neural-cytokine loop in SARS-CoV-2 infection. Evidence from this study triggers an idea for future prospective studies to confirm the potential role of ß-blockers in the management of Covid-19.