Renal artery thrombosis in SARS-CoV-2 infection: a case report.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is identified as the pneumonia and acute respiratory distress syndrome caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2). The intravascular thrombotic phenomena related to the COVID-19 are emerging as an important complication that contribute to significant mortality. CASE PRESENTATION: We present a 62-year-old man with severe COVID-19 and type 2 diabetes. After symptomatic and supportive treatment, the respiratory function was gradually improved. However, the patient suddenly developed abdominal pain, and the enhanced CT scan revealed renal artery thrombosis. Given the risk of surgery and the duration of the disease, clopidogrel and heparin sodium were included in the subsequent treatment. The patient recovered and remained stable upon follow-up. CONCLUSIONS: Thrombosis is at a high risk in patients with severe COVID-19 pneumonia because of hypercoagulable state, blood stasis and endothelial injury. Thrombotic events caused by hypercoagulation status secondary to vascular endothelial injury deserves our attention. Because timely anticoagulation can reduce the risk of early complications, as illustrated in this case report.

Spontaneous Multiple Arterial Dissection in a COVID-19-Positive Decedent.

ABSTRACT: Spontaneous multiple arterial dissection (SMAD) is a rarely reported phenomenon and has been previously linked to connective tissue diseases and specifically the genetic mutations in SMAD3 and COL3A1. Herein we describe a case of SMAD with scattered thrombi in a COVID-19-positive patient with a history of unspecified mitochondrial myopathy. Vasculopathy involved the splenic artery, inferior mesenteric artery, internal mammary arteries, omental arteries, mesenteric arteries, and small renal arteries. Dissections were confirmed by histology in the splenic artery, inferior mesenteric artery, and bilateral renal medullary arteries. Genetic studies were done to rule out SMAD3 and COL3A1 mutations. Because the Smad3 protein has been previously implicated in COVID-19-associated tissue fibrosis, it may play a role in endothelial dysfunction as well.

Endovascular Treatment of Renal Artery Thrombosis in Living-Donor Kidney Transplant Recipient With Severe COVID-19 Disease.

PURPOSE: Coronavirus disease 2019 (COVID-19) patients have a higher prevalence of micro-and macrovascular thrombotic events. However, the underlying mechanism for the increased thrombotic risk is not completely understood. Solid organ transplant recipients infected with SARS-CoV-2 may have an exponential increase in thrombotic risk and the best management strategy is unknown. CASE REPORT: A female kidney transplant recipient presented with allograft's renal artery thrombosis after a recent COVID-19 infection. Due to the risk of kidney failure or exclusion, catheter directed thrombolysis was performed. Residual thrombus was excluded using an endoprosthesis with an excellent result. There were no adverse events and kidney function improved. CONCLUSION: This paper reports the endovascular treatment of renal artery thrombosis in a living-donor kidney transplant recipient with severe COVID-19 disease.

Adverse Maternal and Fetal Outcomes in a Novel Experimental Model of Pregnancy after Recovery from Renal Ischemia-Reperfusion Injury.

BACKGROUND: Recent clinical studies report that women with a history of AKI have an increased incidence of maternal and fetal adverse outcomes during pregnancy, despite fully recovering renal function prior to conception. The mechanisms contributing to such adverse outcomes in pregnancy after AKI are not yet understood. METHODS: To develop a rodent model to investigate fetal and maternal outcomes in female animals with a history of AKI, we used ischemia-reperfusion injury as an experimental model of AKI in female Sprague Dawley rats. The 12-week-old animals underwent warm bilateral ischemia-reperfusion surgery involving clamping of both renal arteries for 45 minutes or sham surgery (control). Rats were allowed to recover for 1 month prior to mating. Recovery from ischemia-reperfusion injury was confirmed by measurements of plasma creatinine and urinary protein excretion. We assessed maternal and fetal outcomes during late pregnancy on gestational day 20. RESULTS: After recovery from ischemia-reperfusion injury, compared with healthy sham-surgery controls, dams exhibited pregnancy-induced renal insufficiency with increases in plasma creatinine and urea, along with increased urinary protein excretion. Additionally, recovered ischemia-reperfusion dams experienced worse fetal outcomes compared with controls, with intrauterine growth restriction leading to higher rates of fetal demise and smaller pups. CONCLUSIONS: In this rat model, despite biochemical resolution of ischemia-reperfusion injury, subsequent pregnancy resulted in maternal renal insufficiency and significant impairments in fetal growth. This mirrors findings in recent reports in the clinical population, indicating that this model may be a useful tool to further explore the alterations in kidney function after AKI in women.

Long-Term Effects of Renal Artery Denervation.

Background and Objectives: Renal artery denervation (RDN) procedure is a broadly discussed method in the treatment of resistant hypertension. Many studies report short-term (3-12 months) results for blood pressure and arterial stiffness. The primary endpoints were changes in 24 h mean systolic blood pressure (BP) and office systolic BP 48 months after RDN. The secondary endpoints were changes in aortic pulse wave velocity and impact of polypharmacy on these variables. Materials and Methods: Renal artery denervation was performed in 73 patients treated for resistant hypertension; 49 patients remained in final analysis. Patient examination was carried out before the procedure, and subsequently at 3, 6, 12, 24, and 48 months later. Patients' antihypertensive and overall medication regimens were carefully analysed. Results: Mean 24 h arterial blood pressure lowered and was sustained at lower levels for up to 48 months; median (interequartile range-IQR) from 158(23.5)/100(14.2) to 140(26.5)/86(16.2) mmHg. Mean reduction in 24 h ambulatory systolic BP was -11 ± 25 mmHg (95% CI, -20 to -2; p < 0.001), while office systolic BP reduced by -7 ± 23 mmHg (95%CI, -24 to -1; p < 0.02). A significant reduction in median aortic pulse wave velocity 12 months after the procedure (drop from baseline 11.2 [3.15] m/s (95%CI 6.1 to 16.2) to 9.8 [2.1] m/s (95%CI 6.1 to 13.7; p = 0.002)). After 48 months, there was no worsening compared to the baseline level of 10.3 [4.0] m/s (95% CI 6.9 to 17.8) (p > 0.05). The total mean number of antihypertensive drugs remained unchanged: 5.97(±1.1) vs. 5.24 (±1.45). A higher number of pills after 48 months was associated with higher aortic pulse wave velocity (1-5 pill group: 8.1 ± 1.6 m/s; 6-10 pill group: 10.9 ± 1.8 m/s; >11 pill group: 15.1 ± 2.6 m/s) (p = 0.003). Conclusions: Antihypertensive effect after renal denervation lasts up to 48 months with no worsening of arterial stiffness compared to baseline. In our study, polypharmacy was associated with increased arterial stiffness 48 months after the procedure.

Value of renal resistive index in covid-19 ARDS patients: an early inflammation alert for the lung-kidney cross-talk?

We analysed RRI and other hemodynamic, re-spiratory and inflammation parameters in critically ill pa-tients affected by severe covid-19 with acute distress respi-ratory syndrome (ARDS) aiming at verifying their modifica-tions during supine and prone positioning and any mutual correlation or interplay with RRI.

COVID-19 as the cause of thrombosis: recognising COVID-19 infection in apparently asymptomatic patients.

COVID-19 has serious thrombotic complications in critically ill patients; however, thrombus is not a typical presenting symptom. This case report describes a patient with no respiratory symptoms who presented to the emergency department with abdominal pain. The pain was attributed to renal thrombosis, but the patient was found to have no risk factors for thrombotic disease and subsequent hypercoagulable work-up was unremarkable. Pulmonary manifestations of COVID-19 infection were detected incidentally on the abdominal CT scan and confirmed via PCR test. The patient was isolated and went on to develop mild respiratory failure secondary to COVID-19 infection. This case suggests that unexplained thrombus in otherwise asymptomatic patients can be a direct result of COVID-19 infection, and serves as a call to action for emergency department clinicians to treat unexplained thrombotic events as evidence of COVID-19.

Case Report: COVID-19 Associated Renal Infarction and Ascending Aortic Thrombosis.

Following its discovery in Wuhan, China, in December 2019, COVID-19 has attained pandemic status in mere months. It is caused by SARS-CoV-2, an enveloped beta coronavirus. This infection causes a prothrombogenic state by interplay of inflammatory mediators, and endothelial, microvascular, and possible hepatic damage and tissue tropism of the virus. This leads to frequent pulmonary and cerebral thromboembolism as well as occasional involvement of other organs. We present a 71-year-old man who initially presented with 2 weeks of fever, cough, and shortness of breath and was diagnosed with COVID-19 pneumonia. He required readmission due to worsened hypoxia and was later found to have left renal artery thrombosis with left kidney infarction, associated with an ascending aortic thrombus. He was anticoagulated and recovered uneventfully. We suggest that physicians have a high degree of suspicion to diagnose and manage the novel manifestations of this disease.