ABSTRACT
Background@#The development of acute kidney injury (AKI) in patients with coronavirus disease 2019 (COVID-19) is associated with a high risk of death. Published data demonstrate the possibility of severe kidney injury in patients suffering from COVID-19. However, these data are still controversial. @*Methods@#A total of 1,280 patients with a proven diagnosis of COVID-19 were included in our study. COVID-19 was confirmed in all patients using reverse transcriptase polymerase chain reaction test of a nasopharyngeal swab, and based on the typical computed tomography findings. Demographic data, underlying comorbidities, and laboratory blood tests were assessed. We assessed the incidence of AKI and its associated mortality defined by survival status at discharge. @*Results@#Proteinuria was identified with 648 patients (50.6%) with COVID-19. AKI was identified in 371 patients (29.0%). Ten of these patients (2.7%) required dialysis. The risk factors for AKI included age of > 65 years, augmentation of C-reactive protein, ferritin and an increase in values of activated partial thromboplastin time. Overall, 162 of the 1,280 hospitalized patients (12.7%) and 111 of the 371 patients (29.9%) with AKI did not survive. The hazard ratio (HR) for mortality was 3.96 (95% confidence interval, 2.83–5.54) for patients with AKI vs. no AKI. @*Conclusion@#AKI was a relatively common finding among patients with COVID-19. The risk factors for AKI in COVID-19 included old age, the inflammatory response, the severity of lung involvement, and disseminated intravascular coagulation. These same factors, in addition to arterial hypertension, were found to increase the risk of mortality.
ABSTRACT
Background@#The development of acute kidney injury (AKI) in patients with coronavirus disease 2019 (COVID-19) is associated with a high risk of death. Published data demonstrate the possibility of severe kidney injury in patients suffering from COVID-19. However, these data are still controversial. @*Methods@#A total of 1,280 patients with a proven diagnosis of COVID-19 were included in our study. COVID-19 was confirmed in all patients using reverse transcriptase polymerase chain reaction test of a nasopharyngeal swab, and based on the typical computed tomography findings. Demographic data, underlying comorbidities, and laboratory blood tests were assessed. We assessed the incidence of AKI and its associated mortality defined by survival status at discharge. @*Results@#Proteinuria was identified with 648 patients (50.6%) with COVID-19. AKI was identified in 371 patients (29.0%). Ten of these patients (2.7%) required dialysis. The risk factors for AKI included age of > 65 years, augmentation of C-reactive protein, ferritin and an increase in values of activated partial thromboplastin time. Overall, 162 of the 1,280 hospitalized patients (12.7%) and 111 of the 371 patients (29.9%) with AKI did not survive. The hazard ratio (HR) for mortality was 3.96 (95% confidence interval, 2.83–5.54) for patients with AKI vs. no AKI. @*Conclusion@#AKI was a relatively common finding among patients with COVID-19. The risk factors for AKI in COVID-19 included old age, the inflammatory response, the severity of lung involvement, and disseminated intravascular coagulation. These same factors, in addition to arterial hypertension, were found to increase the risk of mortality.
ABSTRACT
BACKGROUND AND OBJECTIVES: Autosomal dominant polycystic kidney disease is a pathology mainly characterized by the progressive development and enlargement of cysts in each kidneys. Such as many adult epithelial tissue, renal tubule replaces damaged or death cells through the presence of stem/progenitor cells CD133+CD24+ Obviously, in ADPKD the repair of damages is insufficient to block the disease, but renal stem cells could have a role in the pathology. In this study we investigate the localization and the involvement of cells CD133+CD24+ in ADPKD progression. METHODS AND RESULTS: Two normal kidneys and two ADPKD kidneys were examined. CD133 and CD24 expression was investigated by confocal microscopy and immunoblotting. Renal tissue and cells were analyzed. CD133 and CD24 have the same localization in ADPKD tissues and in normal kidneys: a subset of epithelial cells (PEC) of Bowman's capsule and luminal side of tubules. It is interesting that CD133+CD24+ cells are statistically more represented in ADPKD tubules (p<0.001) and in healthy glomeruli (p=0.0016). Cysts express CD133 and CD24. CONCLUSIONS: Renal epithelial progenitors demonstrate to be involved in ADPKD pathogenesis but their role will have to be clarified and possibly managed to obtain improvement, or at least stabilization, of disease.