Bilateral Renal Artery Thrombosis in a Patient With COVID-19

Shamy, Osama El; Munoz-Casablanca, Nitzy; Coca, Steven G.; Sharma, Shuchita; Lookstein, R.; Uribarri, Jaime

doi:10.1016/j.xkme.2020.07.010

Cited by 18 publications

(24 citation statements)

References 19 publications

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“…Neutrophils and neutrophil extracellular traps — frequently aggregating with platelets — have been observed in many organs including the kidneys, despite the sporadic presence of virus on histology, suggesting a role of inflammation in the development of intravascular thrombi 71 . Cases of renal artery thrombosis have also been anecdotally reported 72 , 73 . Finally, patients with severe COVID-19 often present with complications associated with chronic endothelial dysfunction, such as hypertension or diabetes, which are themselves associated with decreased endothelial nitric oxide synthase activity and bioavailability of nitric oxide — a major vasodilator and antithrombotic factor 74 .…”

Section: Pathophysiology Of Covid-19 Akimentioning

confidence: 99%

Pathophysiology of COVID-19-associated acute kidney injury

et al. 2021

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Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidney involvement is also common. Available evidence supports a number of potential pathophysiological pathways through which acute kidney injury (AKI) can develop in the context of SARS-CoV-2 infection. Histopathological findings have highlighted both similarities and differences between AKI in patients with COVID-19 and in those with AKI in non-COVID-related sepsis. Acute tubular injury is common, although it is often mild, despite markedly reduced kidney function. Systemic haemodynamic instability very likely contributes to tubular injury. Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome with causes other than COVID-19. Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury, as might endothelial injury and microvascular thrombi. Findings of high viral load in patients who have died with AKI suggest a contribution of viral invasion in the kidneys, although the issue of renal tropism remains controversial. An impaired type I interferon response has also been reported in patients with severe COVID-19. In light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide insights into therapeutic strategies.

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Section: Pathophysiology Of Covid-19 Akimentioning

confidence: 99%

Pathophysiology of COVID-19-associated acute kidney injury

et al. 2021

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“…88 Renal artery thrombosis and renal vein thrombosis have both been documented, including cases with associated renal infarction; however, these are likely rare events. [88][89][90][91][92]…”

Section: Micro or Macrovascular Injury/endothelial Activation Contributing To Ckd Riskmentioning

confidence: 99%

COVID-19 Survival and its impact on chronic kidney disease

Long

Strohbehn

Sawtell

et al. 2022

Translational Research

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“…1, другим важным бассейном, который наиболее часто вовлекается при COVID-19, является верхняя брыжеечная артерия. В литературе также описаны случаи поражения и других артериальных бассейнов, в частности дуги и грудного отдела аорты, почечной [36] и селезёночной артерий [14] и даже глазничной артерии [37].…”

Section: Covid19: факторы риска и сопутствующие заболеванияunclassified