Covid19 Clinical Trial
Official title:
Acute Kidney Injury In Subjects With Severe Acute Respiratory Syndrome Due to SARS-CoV2 Infection
Severe pneumoniae related to Coronavirus Disease (COVID-19), had a high in-hospital mortality; this condition are worst in subjects with acute kidney disease (AKI); conditioning increased mortality, days of assisted mechanical ventilation (AMV), increased nosocomial infections and high costs. We need many studies for determinated the risk factors for AKI in subjects with COVID-19. This study pretends identify the incidence of AKI in subjects with severe pneumoniae by COVID-19, describe the role of some biomarkers in the physiopathology of AKI-COVID-19; and determine the evolution of urinary biomarkers during hospitalization, like neutrophil gelatinase-associated lipocalin (NGAL), tissue inhibitor of metalloproteinases-2 (TIMP-2), insulin-like growth factor binding protein-7 (IGFBP7), and interleukin-6 (IL-6) and the progression of viruria of Severe Acute Respiratory Syndrome (SARS) related to CoronaVirus 2 (CoV2) in subjects with or without AKI.
The usefulness of urinary NGAL levels and the platelet / lymphocyte index as predictive markers of AKI in the context of COVID-19 will be studied. These results will allow to propose more appropriate strategies for the prevention, diagnosis and timely management of patients with severe pneumonia due to COVID-19 and AKI. Knowing the viral load in urine and its evolution in patients with and without AKI will allow us to explore associations between the presence of the virus at the local level and the presence of kidney damage. Likewise, the presence of viral load in urine and its possible relationship with the local activation of the complement system, together with the detection of biomarkers of kidney damage, like NGAL, TIMP-2, IGFBP7, and IL-6, will allow us to better understand the pathophysiology of these alterations in the context of COVID-19; additionally, some patients received tocilizumab, an IL-6 inhibitor as a compassionate measure, which may reduce urinary levels of interleukins and other inflammatory markers. Finally, the study of possible differences in the metabolome in urine in patients with and without acute kidney injury could favor the discovery of new markers to identify patients with SARS-CoV-2 infection susceptible to the development of AKI. Determine the evolution of NGAL, TIMP-2, IGFBP7, IL-6, viral load and metabolomic basal, and the days 3 , 5 and 7 after recruitment ;
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