ABSTRACT
The COVID-19 pandemic is caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2), a respiratory pathogen with neuroinvasive potential. Neurological COVID-19 manifestations include loss of smell and taste, headache, dizziness, stroke, and potentially fatal encephalitis. Several studies found elevated proinflammatory cytokines such as TNF-α, IFN-γ, IL-6 IL-8, IL-10 IL-16, IL-17A, and IL-18 in severely and critically ill COVID-19 patients, which may persist even after apparent recovery from infection. Biomarker studies on CSF and plasma and serum from COVID-19 patients have also shown a high level of IL-6, intrathecal IgG, neurofilament light chain (NFL), glial fibrillary acidic protein (GFAP), and tau protein. Emerging evidence on the matter has established the concept of COVID-19 associated neuroinflammation, in the context of COVID-19 associated cytokine storm. While the short-term implications of this condition are extensively documented, its long-term implications are yet to be understood. The association of the aforementioned cytokines with the pathogenesis of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington disease, and amyotrophic lateral sclerosis, may increase COVID-19 patients' risk to develop neurodegenerative diseases. Analysis of proinflammatory cytokines and CSF biomarkers in patients with COVID-19 can contribute to the early detection of the disease's exacerbation, monitoring the neurological implications of the disease and devising risk scales, and identifying treatment targets.
ABSTRACT
BACKGROUND: The most common extra pulmonary organ dysfunction in acute respiratory distress syndrome is acute kidney injury. Current data so far indicate low incidence of AKI in Covid-19 disease. OBJECTIVE: In this retrospective study, we analysed the clinical features of patients diagnosed with Covid-19 and investigated the effect of Covid-19 on kidney function. METHODS: Ninety-six patients diagnosed with Covid-19 were included in our study. Demographic features (Age, gender, co-morbidities), symptoms, thorax CT findings, Covid-19 PCR results and laboratory findings were recorded. The clinical features of the patients were analysed and kidney function values before Covid-19 diagnosis were compared with kidney function values after Covid-19 diagnosis. RESULTS: Most presenting symptom was fever (51%). Most accompanying co-morbidity was hypertension (56%). According to laboratory findings; ferritin, D-dimer and C-reactive protein levels were statistically significantly higher in ARDS group than severe pneumonia and pneumonia group (P = .002, P = .001 and P < .001, respectively). Also lymphocyte levels were statistically significantly lower in ARDS group than severe pneumonia and pneumonia group (P = .042). According to KDIGO criteria 3 (3.1%) patients had AKI during the hospital stay. For all patients, there was statistically significant difference between basal, 1st, 5th and 10th day BUN and SCr levels (P = .024 and P = .018, respectively). For severe pneumonia group there was statistically significant difference between basal, 1st, 5th and 10th day SCr levels (P = .045). CONCLUSION: Our study demonstrated that Covid-19 can cause renal impairment both with pneumonia and ARDS. A large-scale prospective randomised studies are needed to reach final judgement about this topic.