We are the combination of four hospitals: the General Hospital, the Children’s Hospital, the Women’s Hospital and the Traumatology, Rehabilitation and Burns Hospital. We are part of the Vall d’Hebron Barcelona Hospital Campus: a world-leading health park where healthcare plays a crucial role.
Below we will list the departments and units that form part of Vall d’Hebron Hospital and the main diseases that we treat. We will also make recommendations based on advice backed up by scientific evidence that has been shown to be effective in guaranteeing well-being and quality of life.
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Researchers recommend including renal makers in clinical course studies of patients with COVID-19.
Dr. María José Soler, nephrologist at the Nephrology Service of Vall d’Hebron University Hospital and member of the NephJC. The Coronavirus Conundrum: ACE2 and Hypertension edition group has participated in a positioning study on acute kidney injury as one of the serious complications that COVID-19 can entail. The study has been published in the Journal of the American Society of Nephrology.
Until now, the most common complications for the admission in the intensive care unit of patients with severe COVID-19 infection are respiratory failure requiring mechanical ventilation and hypotension requiring vasopressor support. “With this study we wanted to highlight the importance of evaluating and reporting about the incidence and evolution of cases with acute kidney injury (AKI), as there is currently a lack of information and the little information that exists points that it could be a serious complication of COVID-19”, says Dr. Soler.
Although there is no evidence so far that SARS-CoV-2 RNA has been detected in the kidneys, researchers analyzed different studies to know better how coronavirus infection affects this organ. It needs to be pointed out that the main binding point for SARS-CoV-2 is angiotensin-converting enzyme 2 (ACE2), which is expressed in the kidney in a greater proportion than in the lungs.
One of the studies indicate that the virus could directly infect human renal tubules and induce cytoplasmic renal tubular inclusions, a feature that has been observed in other virus-associated nephropaties. Therefore, although acute kidney injury can be attributed to hypotension and the decrease of renal perfusion secondary to hemodynamic or hemostatic factors or associated sepsis, it must be taken into account that renal viral infection with viral replication directly in renal parenchyma can also play a role.
On the other hand, some studies have demonstrated that COVID-19 is also associated with an increase of myocardial injury that mimics myocardial infarction, possibly by myocarditis and microangiopathy. Therefore, they point out that hypercoagulable stage seems to be a characteristic complication of severe COVID-19 and, in some cases, it could promote the evolution of acute tubular necrosis to cortical necrosis and, therefore, to irreversible renal failure.
Finally, a single cell transcriptome analysis in human kidney samples compared the proportion of renal cells that express ACE2, the binding point of SARS-CoV-2 and the TMPRSS family proteases between Western and Asian individuals. Interestingly, the expression of ACE2 and renal disease-related genes was higher in Western donors in comparison with Asian donors. That would suggest that the susceptibility to renal injury by coronavirus infection could be higher in individuals of Western than Asian descent. Nevertheless, we don’t have any knowledge of data that confirm this possibility.
Despite the little information on kidney affectation in COVID-19, AKI seems to involve a complex process promoted by a virus-driven injury, cytokine storm, activation of AngII (angiotensin II) pathway, complement dysregulation, hypercoagulation and microangiopathy that interact with common and known AKI risk factors. There is lack of data regarding clinical and lab features of AKI in patients with COVID-19 and that is why “we urge that other studies that describe and analyze clinical course of COVID-19 patients include appropriate renal function and AKI diagnostics indexes in their analysis, including renal injury markers, urinary sediment, quantified urine protein, urine production and urine electrolytes”, Dr. María José Soler insists. Markers of macrophage activation, coagulation, microangiopathy and complement activation, as well as kidney imaging and the need for renal replacement therapy (with relevant details), are needed data to deepen our understanding of COVID-19 associated AKI physiopathology. It is also recommended that they report the reversibility taxes or partial improvement of renal function and any result of renal biopsy (including immunofluorescence and electron microscopy). Finally, “we are committed to a complete and standardized evaluation of clinical and lab expression because the preventive and therapeutic strategies for AKI in COVID-19 patients can be properly designed and implemented”, the specialist concludes.
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