ABSTRACT
INTRODUCTION: The recent Sars-Cov-2 pandemic (COVID-19) has led to growing research to explain the poor clinical prognosis in some patients. EVIDENCE ACQUISITION: While early observational studies highlighted the role of the virus in lung failure, in a second moment thrombosis emerged as a possible explanation of the worse clinical course in some patients. Despite initial difficulties in management of such patients, the constant increase of literature in the field is to date clarifying some questions from clinicians. However, several other questions need answer. EVIDENCE SYNTHESIS: A novel disease (Covid-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection was responsible for thousands of hospitalizations for severe acute respiratory syndrome, with several cases of thrombotic complications due to excessive inflammation, platelet activation, endothelial dysfunction, and stasis. Covid-19 and hospitalizations for Covid-19 may carry several potential risk factors for thrombosis. Severe coagulation abnormalities may occur in almost all of the severe and critical ill COVID-19 cases. CONCLUSIONS: Despite a strong pathophysiological rationale, the evidences in literature are not enough to recommend an aggressive antithrombotic therapy in COVID- 19. However, it is our opinion that an early use, even at home at the beginning of the disease, could improve the clinical course.
ABSTRACT
In a WSO review the risk of stroke during Covid-19 infection is about 5%;in a significant percentage of cases the symptoms of infection are not present at the admission. A 76-year-old woman came to ED for neck pain, vertigo, balance instability for 48 hours. Cerebral CT Scan showed cerebellar ischemic hypodense area of 2 cm. On EKG sinus rhythm, elevation of the anterolateral ST segment. No chest pain or palpitation. Normal C-reactive protein, troponin 222 pg / ml, D-Dimer 1053 ng / ml. TE: left ventricle of normal size, akinesia of the apex. Chest CT scan: normal aorta, no thrombo-embolic defects, ground glass thickening in the lingula site. Molecular test for Covid-19 positive. EGA pO2 79 mmHg, Sat02 96% in air. Stroke unit consult: no indication for revascularization therapy by time window, prescription therapy with 125 mg aspirin, no recommendation against use of anticoagulant if indicated for infectious therapy. Troponin in reduction in 3rd day. EKG evolution with negative T wave in the anterior area. After 48 hours stable brain ischemic injury, improvement of ventricular wall motion. Enoxaparin was added. Sat02 98% with O2 at low flows. Cerebral MRI: paramedian cerebellar area with hemorrhagic infarction, regular intracranial arterial circulation. Cardiac MRI: hypokinesia of the apical segments, edema of the ventricular myocardium in the mid-apical planes, increased image values in T1 and T2 mapping, no defects of perfusion. The clinical course was regular. Viral infections induce a pro-thrombotic state and can cause stroke by increasing the cardio-embolic risk or through the formation of arterial thrombi. D-dimer was elevated, no antiphospholipid antibodies were measured. We cannot exclude asymptomatic atrial fibrillation. The mechanism of stroke in the patient is unclear, no cardiac thrombotic formations were documented. Stress induced by stroke symptoms and the delayed access to treatment due to fear of going to hospital because of Covid-19 infection was probably the cause of stress cardiomyopathy. The incidence of Tako-Tsubo cardiomyopathy increased worldwide during the pandemic.
ABSTRACT
Background: COVID19 caused by novel Coronavirus SARS-COV-2 initially presenting primarily as a respiratory illness, is now known to affect several organ systems as part of multiorgan failure including acute kidny injury (AKI), some cases also manifesting nephrotic range proteinuria or syndrome. Methods: 10 renal biopsies from 6 institutions (1 transplant) performed in April-May 2020 were processed for light microscopy, immunostaining (IS) and electron microscopy (EM) for clinco-pathologic analysis. Results: The 10 patients ranged from 25-73 years (Mean 43), male:female 5:5, 8 African American, 1 Hispanic, 1 Asian Indian, having pre-existing co-morbidities of hypertension (7), Diabetes mellitus (5), obesity (9), presenting with AKI (10), nephrotic syndrome (9), proteinuria ranging from 1.5-25g/24hrs, lung symptoms or pneumonia (7), fever (5). SARS-COV-2 RT-PCR positive (7), IgG antibody positive (2), both negative (1). All kidney biopsies showed widespread acute tubular injury with focal necrosis, 9 with typical features of segmental/global collapsing glomerulopathy in 10-53% of glomeruli, global glomerulosclerosis (0-35%), focal tubular microcystic changes (8), patchy (7) or diffuse (2) active tubulointerstitial inflammation and scarring (10-40%), focal & diffuse peritubular capillary inflammation, moderate vascular sclerosis anddiabetic kidney disease in 2. No immune deposits were localized by IS. By EM, varied glomerular capillary wall wrinkling and collapse with segmental or global loss of patency (7), total foot process effacement (7), with hyperplastic and vacuolated epithelial cells having protein droplets are noted. The endothelial cells are variably swollen, with tubuloreticular inclusions in 2. Viral particles are identified within cells of glomeruli and tubulointerstitium, scattered or in clustesr in the cytoplasm and endoplasmic reticulum vesicles, confirmed by IS. Conclusions: The constellation of typical glomerular collapsing features with tubulointerstitial findings and localization of virus by EM, suggests a distinct viral associated nephropathy, reminicent of HIV associated nephropathy. A role for viral cytopathic effect, cytokines and underlying APOL1 gene variants could be considered.
ABSTRACT
Background: Patients infected with the novel coronavirus 2019 (COVID19) have a wide spectrum of symptoms ranging from asymptomatic carriers to multisystem organ failure and death. While 20-40% of critically ill patients develop acute kidney injury (AKI) during the course of the disease, only few are biopsied. The most severely affected patients, frequently with multiple co-morbidities, provide insight into renal disease at autopsy. Methods: 30 of 34 autopsies performed on COVID patients had kidneys available for routine evaluation. Clinicopathologic features are presented. Results: The 34 patients range in age from 30-100 years (mean 68.5), 24 males and 10 females, 13 Caucasian, 10 Hispanic, 5 African American, 3 Indian, 3 Asian. All cases were positive by RT PCR nasal swab for SARS-CoV-2 except 3 (presumed false negative). All had on average 3.4 comorbidities (range: 0-7, hypertension (HTN), diabetes (DM), obesity, COPD, asthma, stroke, dementia, cancer), frequently HTN (20) and DM (20), 11 required intubation. 18 patients had AKI (53%), 2 previously ESRD, and 5 required renal replacement therapy. Presenting Cr ranged from 0.7-9.6 mg/dl (mean 1.7). Renal pathology included diabetic nephropathy (14, 47%), with tubulointerstitial scarring ranging from <25% (60%), 25-50% (23%), to >50% (17%), and moderate (40%) or severe (40%) chronic vascular sclerosis. Other findings: obesity related glomerulopathy (2), atheroemboli (1), bilateral infarction (1), papillary necrosis (2), and thrombotic microangiopathy (2). No collapsing glomerulopathy was seen. Tubular autolysis prevents complete assessment of ATN. Platelet thrombi were seen by CD61 staining in 43% of cases to involve >20% of glomeruli and peritubular capillaries. C5b-9 staining was strong, 2-3+ arteriolar in 67% and glomeruli in 20%, suggesting localized complement activation. By electron microscopy, viral particles were identified within cells of glomeruli and tubulo-interstitium. Conclusions: Pathology in autopsy kidneys from 30 patients with COVID display pre-existing chronic disease correlating with co-morbidities, presenting with AKI or ESRD (59%). Despite varied tissue autolysis and the absence of significant proteinuria, the majority of AKI is presumed to be acute tubular injury due to ischemia and other causes. The viral particles in the renal glomerular and tubular cells may play a role in renal cytopathic injury.