Renal Biomarkers in AKI and COVID-19
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT04517630|
Recruitment Status : Recruiting
First Posted : August 18, 2020
Last Update Posted : August 20, 2020
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.
|Condition or disease||Intervention/treatment|
|Coronavirus Infection Covid19 SARS (Severe Acute Respiratory Syndrome) AKI||Diagnostic Test: urinary NGAL, TIMP-2, IGFBP7, IL-6, viral load and metabolomic|
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
|Study Type :||Observational [Patient Registry]|
|Estimated Enrollment :||90 participants|
|Target Follow-Up Duration:||3 Months|
|Official Title:||Acute Kidney Injury In Subjects With Severe Acute Respiratory Syndrome Due to SARS-CoV2 Infection|
|Actual Study Start Date :||June 1, 2020|
|Estimated Primary Completion Date :||September 30, 2020|
|Estimated Study Completion Date :||September 30, 2020|
Evaluate the progression to AKI during first 30 days of recruitment
Diagnostic Test: urinary NGAL, TIMP-2, IGFBP7, IL-6, viral load and metabolomic
Determine the evolution of NGAL, TIMP-2, IGFBP7, IL-6, viral load and metabolomic at basal, and the 3 , 5 and 7 days after recruitment
- Urinary levels of renal biomarkers [ Time Frame: Seven days ]To estimate the strength of association between the elevation of urinary levels of NGAL, TIMP-2, IGFBP7 and IL-6 and the development of AKI associated with SARS-CoV-2 pneumonia
- Incidence of AKI [ Time Frame: One month ]Describe the incidence of AKI in critically ill patients with severe COVID-19 pneumonia
- Urinary levels of renal biomarkers and mortality [ Time Frame: 30 days ]Estimate the strength of association of elevated urinary levels of NGAL, TIMP-2, IGFBP7 and IL-6 with mortality
- Urinary levels of renal biomarkers and severity of the disease. [ Time Frame: 30 days ]Estimate the strength of association of elevated urinary levels of NGAL, TIMP-2, IGFBP7 and IL-6 with teh severity of the disease.
- Risk factors for AKI in severe COVID-19 [ Time Frame: 30 days ]Identify possible risk factors (epidemiological, clinical, paraclinical, use of nephrotoxic agents) for the development of AKI in critically ill patients with COVID-19 pneumonia.
- Evolution renal biomarkers [ Time Frame: 7 days ]Compare the evolution over time of renal function markers (NGAL, TIMP-2 and IGFBP7) in patients with and without kidney injury.
- Evolution of viral load [ Time Frame: 7 days ]Compare the evolution over time of the SARS-CoV-2 viral load in patients with and without acute kidney injury.
- Evolution of complement pathway [ Time Frame: seven days ]Analyze the complement pathway in urine and compare its evolution over time in patients with and without acute kidney injury and SARS-CoV-2 infection.
- Metabolomic profile [ Time Frame: 7 days ]Analyze the metabolomic profile in urine in patients with and without acute kidney injury with SARS-CoV-2 infection.
- Respiratory changes [ Time Frame: 30 days ]Describe partial arterial oxygen concentration/inspired oxygen faction (PaO2/FiO2) ratio and radiologic evolution in patients with severe SARS COV2 pneumonia.
- Nosocomial Infections [ Time Frame: 30 days ]Stablish the nosocomial infections in subjects with or without AKI
Biospecimen Retention: Samples With DNA
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04517630
|Contact: Santiago Ávila Ríos, PhD||56667985 ext email@example.com|
|Contact: Amy B. Peralta Prado, MD||56667985 ext firstname.lastname@example.org|
|Centro de Investigacion en Enfermedades Infecciosas||Recruiting|
|Mexico City, Mexico, 14060|
|Contact: Santiago Avila Ríos, PhD +52 (55)56667985 ext 150 email@example.com|
|Contact: Amy B. Peralta Prado, MD +52 (55)56667985 ext 100 firstname.lastname@example.org|
|Principal Investigator:||Santiago Avila Rios, PhD||Instituto Nacional de Enfermedades Respiratorias|