Dataset Information

Urine sediment findings were milder in patients with COVID-19-associated renal injuries than in those with non-COVID-19-associated renal injuries.

ABSTRACT:

Background

Acute renal injury is an important complication of coronavirus disease 2019 (COVID-19). Both COVID-19-specific mechanisms, such as damage to the renal parenchyma by direct infection, and non-specific mechanisms, such as the pre-renal injury factors, have been proposed to be involved in COVID-19-associated renal injuries. In this study, we aimed to elucidate the characteristics of COVID-19-associated renal injuries, focusing mainly on urine sediment findings.

Methods

We compared the urine sediment findings and their associations with renal functions or urinary clinical parameters between subjects with COVID-19 and subjects without COVID-19 with acute renal injuries.

Results

We found that the number of urine sediment particles and the levels of N-acetyl-β-D-glucosaminidase, α1-microglobulin, liver type fatty acid-binding protein, and neutrophil gelatinase-associated lipocalin were associated with the severity of COVID-19. In addition, we observed that the number of granular casts, epithelial casts, waxy casts, and urinary chemical marker levels were lower in the subjects with COVID-19 than subjects without COVID-19 with acute renal injuries when the subjects were classified according to their renal function.

Conclusions

These results suggest that pre-renal injury factors might be largely involved in the pathogenesis of COVID-19-associated renal injuries compared with non-COVID-19-associated renal injuries arising from surgery or sepsis.

SUBMITTER: Morita Y

PROVIDER: S-EPMC8849830 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Urine sediment findings were milder in patients with COVID-19-associated renal injuries than in those with non-COVID-19-associated renal injuries.

Morita Yoshifumi Y Kurano Makoto M Jubishi Daisuke D Ikeda Mahoko M Okamoto Koh K Tanaka Masami M Harada Sohei S Okugawa Shu S Moriya Kyoji K Yatomi Yutaka Y

International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases 20220217

<h4>Background</h4>Acute renal injury is an important complication of coronavirus disease 2019 (COVID-19). Both COVID-19-specific mechanisms, such as damage to the renal parenchyma by direct infection, and non-specific mechanisms, such as the pre-renal injury factors, have been proposed to be involved in COVID-19-associated renal injuries. In this study, we aimed to elucidate the characteristics of COVID-19-associated renal injuries, focusing mainly on urine sediment findings.<h4>Methods</h4>We ...[more]

PMID: 35182739

Similar Datasets

Project description:Background: Coronavirus disease 2019 (COVID-19) is a viral respiratory illness caused by the novel coronavirus SARS-CoV-2. The presence of the pre-existing cardiac disease is associated with an increased likelihood of severe clinical course and mortality in patients with COVID-19. Besides, current evidence indicates that a significant number of patients with COVID-19 also exhibit cardiovascular involvement even in the absence of known cardiac risk factors. Therefore, there is a need to understand the underlying mechanisms and genetic predispositions that explain cardiovascular involvement in COVID-19. Objectives: In silico analysis of publicly available datasets to decipher the molecular basis, potential pathways, and the role of the endothelium in the pathogenesis of cardiac and vascular injuries in COVID-19. Materials and Methods: Consistent significant differentially expressed genes (DEGs) shared by endothelium and peripheral immune cells were identified in five microarray transcriptomic profiling datasets in patients with venous thromboembolism "VTE," acute coronary syndrome, heart failure and/or cardiogenic shock (main cardiovascular injuries related to COVID-19) compared to healthy controls. The identified genes were further examined in the publicly available transcriptomic dataset for cell/tissue specificity in lung tissue, in different ethnicities and in SARS-CoV-2 infected vs. mock-infected lung tissues and cardiomyocytes. Results: We identified 36 DEGs in blood and endothelium known to play key roles in endothelium and vascular biology, regulation of cellular response to stress as well as endothelial cell migration. Some of these genes were upregulated significantly in SARS-CoV-2 infected lung tissues. On the other hand, some genes with cardioprotective functions were downregulated in SARS-CoV-2 infected cardiomyocytes. Conclusion: In conclusion, our findings from the analysis of publicly available transcriptomic datasets identified shared core genes pertinent to cardiac and vascular-related injuries and their probable role in genetic susceptibility to cardiovascular injury in patients with COVID-19.

Project description:BackgroundAmong various complications of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), renal complications, namely COVID-19-associated kidney injuries, are related to the mortality of COVID-19.MethodsIn this retrospective cross-sectional study, we measured the sphingolipids and glycerophospholipids, which have been shown to possess potent biological properties, using liquid chromatography-mass spectrometry in 272 urine samples collected longitudinally from 91 COVID-19 subjects and 95 control subjects without infectious diseases, to elucidate the pathogenesis of COVID-19-associated kidney injuries.ResultsThe urinary levels of C18:0, C18:1, C22:0, and C24:0 ceramides, sphingosine, dihydrosphingosine, phosphatidylcholine, lysophosphatidylcholine, lysophosphatidic acid, and phosphatidylglycerol decreased, while those of phosphatidylserine, lysophosphatidylserine, phosphatidylethanolamine, and lysophosphatidylethanolamine increased in patients with mild COVID-19, especially during the early phase (day 1-3), suggesting that these modulations might reflect the direct effects of infection with SARS-CoV-2. Generally, the urinary levels of sphingomyelin, ceramides, sphingosine, dihydrosphingosine, dihydrosphingosine L-phosphate, phosphatidylcholine, lysophosphatidic acid, phosphatidylserine, lysophosphatidylserine, phosphatidylethanolamine, lysophosphatidylethanolamine, phosphatidylglycerol, lysophosphatidylglycerol, phosphatidylinositol, and lysophosphatidylinositol increased, especially in patients with severe COVID-19 during the later phase, suggesting that their modulations might result from kidney injuries accompanying severe COVID-19.ConclusionsConsidering the biological properties of sphingolipids and glycerophospholipids, an understanding of their urinary modulations in COVID-19 will help us to understand the mechanisms causing COVID-19-associated kidney injuries as well as general acute kidney injuries and may prompt researchers to develop laboratory tests for predicting maximum severity and/or novel reagents to suppress the renal complications of COVID-19.

Dataset Information

Urine sediment findings were milder in patients with COVID-19-associated renal injuries than in those with non-COVID-19-associated renal injuries.

Background

Methods

Results

Conclusions

Publications

Urine sediment findings were milder in patients with COVID-19-associated renal injuries than in those with non-COVID-19-associated renal injuries.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets