A CLINICAL CASE OF SARS-CoV-2 INFECTION COMPLICATED BY NEPHROGENIC PULMONARY EDEMA AND COVID-ASSOCIATED PNEUMONITIS, ALVEOLITIS.

COVID-19 is a highly transmissible disease with severe course especially in patients with nephrogenic hypertensive disease and chronic kidney disease due to a higher incidence of all-type infections than in the general population. The aim of the study is to describe a clinical case of SARS-CoV-2 infection complicated by nephrogenic pulmonary edema and COVID-associated pneumonitis, alveolitis. Description of the case. Patient K.S., born in 1975, was hospitalized 24 hours after symptom onset at emergency hospital due to complaints of increased blood pressure up to 180-200/110-120 mm Hg, temperature up to 38.7degreeC, dry cough, feeling of heaviness in the chest, change in urine color. PCR smear for SARS-CoV-2 was positive. Computed tomography revealed a pattern of bilateral COVID-associated pneumonitis, alveolitis, with 75% involvement. The electrocardiogram revealed signs of left ventricular myocardial hypertrophy. Ultrasound examination showed numerous cysts in the kidneys. Urinalysis at admission: leukocytes - 499, erythrocytes - 386. Glomerular filtration rate (CKD-EPI: 29 ml/min/1.73 m2) and corresponds to stage IV of chronic kidney disease. Coagulogram: fibrinogen: 32.3 (1.6-4.0) g/l, D-dimer: 663 (0-250). Despite the treatment, the patient's condition worsened, the phenomena of cardiopulmonary and renal insufficiency increased, which led to a fatal outcome. During a virological study of sectional material: SARS-CoV-2 coronavirus RNA was found in the lung and kidneys. Signs of bilateral COVID-associated pneumonitis, alveolitis with diffuse cellular infiltrates in combination with changes in the alveolar apparatus, signs of pulmonary edema were revealed. Heart-related signs - swelling of the interstitium, fragmented muscle fibers, some of them hypertrophied, a wave-like deformation of cardiomyocytes, blurring of the transverse striation. Arteries with thickened sclerosed walls. In the kidneys - diffuse damage to the proximal tubules of the nephron with areas of cortical and proximal necronephrosis, areas of fibrinoid swelling. Conclusion. The cause of death of a 45-year-old patient was a severe course of bilateral COVID-associated pneumonitis, alveolitis, which contributed to the development of renal medullary hypoxia and type 1 cardiorenal syndrome, which led to early nephrogenic pulmonary edema.Copyright © 2023 Saint Petersburg Pasteur Institute. All rights reserved.

Recent Developments in the Evaluation and Management of Cardiorenal Syndrome: A Comprehensive Review.

Cardiorenal syndrome (CRS) is increasingly recognized diagnostic entity associated with high morbidity and mortality among acutely ill heart failure (HF) patients with acute and/ or chronic kidney diseases (CKD). While traditionally viewed as a state of decline in glomerular filtration rate (GFR) due to decreased renal perfusion, mainly due to therapeutic interventions to relieve congestive in HF, Recent insights into the underlying pathophysiologic mechanisms of CRS led to a broader definition and further classification of CRS into five distinct types. In this comprehensive review, we discuss the classification of CRS, highlighting the underlying common pathogenetic pathways of heart failure and kidney injury, including increased congestion, neurohormonal dysregulation, oxidative stress as well as inflammation, and cytokine storm that are particularly evident in COVID-19 patients with multiorgan failure and also in those with other disorders including sepsis, systemic lupus erythematosus and amyloidosis. In this review we also present the recent advances in the diagnostic strategies of CRS including cardiac and renal biomarkers as well as advanced cardiac and renal imaging techniques that are available to aid in the diagnosis as well as in the prognostication of this disorder. Finally, we discuss the various therapeutic options available to-date, including fluid optimization, hemofiltration, renal replacement therapy as well as the role of SGLT2 inhibitors in light of recent data from RCTs. It is important to note that, CRS population are either excluded or underrepresented, at best, in major RCTs and therefore, therapeutic recommendations are largely extrapolated from FH and CKD clinical trials.

DILATED CARDIOMYOPATHY WITH CARDIOGENIC SHOCK SECONDARY TO COVID-19 INFECTION

SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Acute myocarditis from COVID-19 has been well documented, but there are few cases of COVID -19 patients developing dilated cardiomyopathy (3). We present a case of COVID-19 induced dilated cardiomyopathy leading to cardiogenic shock. CASE PRESENTATION: A 49-year-old African-American female presented to the emergency department (ED) with shortness of breath. She was diagnosed with COVID-19 infection four weeks prior to presentation, and since that time she experienced continuously worsening dyspnea, congestion, and weakness. In the ED, the patient was found to have pulmonary edema and bilateral pleural effusions on chest x-ray, as well as acute kidney injury with a creatinine level of 2.85 mg/dL. An echocardiogram revealed a new diagnosis of dilated cardiomyopathy with reduced ejection fraction of 10-15% with a large left ventricular thrombus. Heparin infusion was initiated and intravenous furosemide was administered for diuresis. Her renal function continued to worsen, which was attributed to cardiorenal syndrome. She became hypotensive and was found to be in cardiogenic shock, which required intensive care unit admission with the initiation of continuous renal replacement therapy (CRRT). The patient improved with CRRT, however her renal function did not recover and she continued to require hemodialysis. She was able to be transferred out of the intensive care unit, and the heparin was bridged to warfarin. Goal-directed medical therapy was initiated for her heart failure. She was eventually discharged home with an external cardioverter-defibrillator vest. A follow-up echocardiogram three months later revealed the left ventricular thrombus had resolved, however, her ejection fraction had improved to only 15-20% despite medication compliance. An implantable cardioverter-defibrillator (ICD) was placed and the patient continues to be followed closely by cardiology. DISCUSSION: Viral infection is a well-documented cause of myocarditis with some patients developing dilated cardiomyopathy (1). Inflammatory dilated cardiomyopathy occurs most commonly in patients infected with Coxsackie B virus, Human Parvovirus B19, Adenovirus, Human Immunodeficiency Virus, Hepatitis C Virus, Cytomegalovirus, Epstein-Barr Virus, and Human Herpes Virus 6 (1). The proposed mechanism of inflammatory cardiomyopathy includes infection of the myocytes, incomplete viral elimination, and persistent retained viral components in the myocytes(2). This may cause direct viral injury or chronic myocardial inflammation leading to remodeling (2). It is documented in the literature that COVID-19 can lead to myocarditis and various types of acute cardiomyopathy (3). However, there have been only a few reported cases of COVID - 19 induced dilated cardiomyopathy (3). CONCLUSIONS: While rarely reported thus far, it should be established that COVID-19 alone can cause dilated cardiomyopathy and lead to heart failure (3). Reference #1: Schultheiss H-P, Baumeier C, Pietsch H, Bock C-T, Poller W, Escher F. Cardiovascular consequences of viral infections: from COVID to other viral diseases. Cardiovascular Research. Published online October 5, 2021. doi:10.1093/cvr/cvab315 Reference #2: Kühl U, Pauschinger M, Seeberg B, et al. Viral Persistence in the Myocardium Is Associated With Progressive Cardiac Dysfunction. Circulation. 2005;(13):1965-1970. doi:10.1161/circulationaha.105.548156 Reference #3: Komiyama M, Hasegawa K, Matsumori A. Dilated Cardiomyopathy Risk in Patients with Coronavirus Disease 2019: How to Identify and Characterise it Early? European Cardiology Review. Published online May 27, 2020. doi:10.15420/ecr.2020.17 DISCLOSURES: No relevant relationships by Amanda Cecchini No relevant relationships by Austin Richardson No relevant relationships by Krupa Solanki

A Case of Acute Decompensated Heart Failure Complicated by Cardiorenal Syndrome Treated With Ultrafiltration.

The standard of care of treatment for acute decompensated heart failure (ADHF) complicated by cardiorenal syndrome (CRS) is diuretics. This case report is an example of how the institution of ultrafiltration early in the course of ADHF complicated by CRS for volume removal can be an alternative approach rather than escalation of the diuretic regimen when the initial diuretic regimen is ineffective and, in turn, yielding a good clinical course.

Cardiorenal Syndrome in COVID-19 Patients: A Systematic Review.

Aims: To perform a systematic review assessing the clinical manifestations and outcomes of cardiorenal syndrome or the presence of both cardiac and renal complications in the 2019 coronavirus disease (COVID-19) patients. Methods: All relevant studies about cardiorenal syndrome or both cardiac and renal complications in COVID-19 patients were retrieved on PUBMED, MEDLINE, and EMBASE from December 1, 2019 to February 20, 2022. Results: Our search identified 15 studies including 637 patients with a diagnosis of cardiorenal syndrome or evidence of both cardiac and renal complications followingSARS-CoV-2 infection. They were male predominant (66.2%, 422/637), with a mean age of 58 years old. Cardiac complications included myocardial injury (13 studies), heart failure (7 studies), arrhythmias (5 studies), or myocarditis and cardiomyopathy (2 studies). Renal complications manifested as acute kidney injury with or without oliguria. Patients with cardiorenal injury were often associated with significantly elevated levels of inflammatory markers (CRP, PCT, IL-6). Patients with a diagnosis of cardiorenal syndrome or evidence of both cardiac and renal complications had more severe disease and poorer prognosis (9 studies). Conclusion: The presence of either cardiorenal syndrome or concurrent cardiac and renal complications had a significant impact on the severity of the disease and the mortality rate among patients with COVID-19 infection. Therefore, careful assessment and management of potential cardiac and renal complications in patients with COVID-19 infection are important to improve their outcomes.

Immune paralysis in paediatric patients with multisystem inflammatory syndrome associated with COVID-19

Background: Paediatric SARS-CoV-2 infection is usually mild and often asymptomatic. Multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19 is a complication that occurs 4 to 6 weeks after primary infection. Typical symptoms are high fever, organ dysfunction and strongly elevated markers of inflammation. The immunopathology includes T-lymphocyte paralysis that is characterised by severely reduced circulating T-cells that have dysregulated activation and differentiation mechanisms, mainly CD4+ T-lymphocytes. Immune paralysis is defined as increased expression of PD-1 and TIM-3. The pathogenesis is unclear but has overlapping features with Kawasaki disease suggestive of vasculitis and a likely autoimmune etiology. Method: We present 3 paediatric patients (2 males, 1 female) with MIS-C aged 11 to 13 years admitted to paediatric intensive care unit in our University teaching hospital in Martin. Immunological parameters were measured after the admission to the hospital and continuously evaluated during the treatment. Results: In all patients we detected in immunological profile significant signs of immune paralysis of T-lymphocytes, both CD4+ and CD8+ T-lymphocytes. One patient had increased expression of PD-1 and TIM-3, other two patients had increased expression of PD-1. In two patients we detected depletion of NK cells. All patients had lymphopenia (moderate to severe) and highly elevated inflammatory markers (CRP, IL-6, ferritin) and procoagulant factors (fibrinogen, D-dimers). They were treated according to the protocol with combined immunomodulatory and anti-inflammatory therapies (intravenous immunoglobulins, corticosteroids, one patient with anakinra) with positive effect on immune profile and also on clinical condition. Conclusion: Children with MIS-C show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal. It is poorly understood how T-cell dysregulation can contribute to the pathogenesis, but hyperactivation of CD4+ T-lymphocytes and immune paralysis that promote further viral infection can drive pulmonary damage, cardiorenal syndrome and organ failure. Understanding of the immunopathology in MIS-C can help in development of better immune intervention therapies to prevent serious long-term effect of COVID-19 infection also in paediatric patients.

Cardio-Pulmonary-Renal Consequences of Severe COVID-19.

Severe acute respiratory syndrome coronavirus 2 has rapidly spread worldwide and resulted in the coronavirus disease 2019 (COVID-19) pandemic. The disease raised an unprecedented demand for intensive care support due to severe pulmonary dysfunction and multiorgan failure. Although the pulmonary system is the potential target of the COVID-19, recent reports have demonstrated that COVID-19 profoundly influences the cardiovascular system and the kidneys. Research studies on cadavers have shown that direct heart and kidney injury can be frequently seen in patients deceased due to COVID-19 infection. On the other hand, functional or structural dysfunction of the heart may deteriorate the renal function and vice versa. This concept is already known as the cardiorenal syndrome and may play a role in COVID-19. Proactive monitoring of micro- and macrohemodynamics could allow prompt correction of circulatory dysfunction and can be of pivotal importance in the prevention of acute kidney injury. Moreover, type and amount of fluid therapy and vasoactive drug support could help manage these patients either with or without mechanical ventilator support. This brief review outlines the current evidence regarding the COVID-19-related renal and cardiorenal complications and discusses potential hemodynamic management strategies.

A brand-new cardiorenal syndrome in the COVID-19 setting.

Coronaviruses are a major pathogen for adults, causing up to one-third of community-acquired respiratory tract infections in adults during epidemics. Although the pandemic outbreak of coronavirus disease-2019 (COVID-19) targets preferentially patient's lungs, recent data have documented that COVID-19 causes myocarditis, acute myocardial infarction, exacerbation of heart failure and acute kidney injury. Studies show that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), similar to its predecessor SARS-CoV, engages angiotensin-converting enzyme 2 (ACE2) as the entry receptor. ACE2 is also expressed in the heart, providing a link between coronaviruses and the cardiovascular system.

Slow Recovery from Critical Coronavirus Disease 2019 Pneumonia in an Immunosuppressed Renal Transplant Recipient with Early Acute Cardiorenal Syndrome.

With the global spread of SARS-Cov-2 infections, increasing numbers of COVID-19 cases have been reported in transplant recipients. However, reports are lacking concerning the treatment and prognosis of COVID-19 pneumonia in renal transplant recipients with acute cardiorenal syndrome. We report here the complete clinical course of a renal transplant recipient with critical COVID-19 pneumonia. In the early phase of SARS-Cov-2 infection, the patient exhibited extensive lung lesions and significant acute kidney and heart injuries, which required treatment in the ICU. After correcting the arrhythmia and heart failure, the patient recovered quickly from the acute kidney injury with a treatment of intensive diuresis and strict control of fluid intake. Without cessation of oral immunosuppressive agents, the patient presented a delayed and low antibody response against SARS-Cov-2 and reappeared positive for the virus twice after being discharged. Nevertheless, the patient's pneumonia continued to improve and he fully recovered in 69 days. This effectively treated case may be meaningful and referable for the treatment of COVID-19 pneumonia in other transplant recipients with acute cardiorenal syndrome.