A clinical case of SARS-CoV-2 infection complicated by nephrogenic pulmonary edema and COVID-associated pneumonitis, alveolitis

O. Vorobeva, Natalya E. Gimaldinova, L. P. Romanova
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Abstract

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 180200/110120 mm Hg, temperature up to 38.7C, 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 (1.64.0) g/l, D-dimer: 663 (0250). Despite the treatment, the patients 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.
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SARS-CoV-2感染并发肾源性肺水肿合并新冠肺炎、肺泡炎1例
COVID-19是一种高度传染性疾病,特别是肾源性高血压疾病和慢性肾脏疾病患者,由于所有类型感染的发生率高于一般人群,病程严重。本研究描述1例SARS-CoV-2感染并发肾源性肺水肿并与新冠病毒相关的肺炎、肺泡炎的临床病例。案件描述。患者k.s., 1975年出生,因血压升高至180200/110120毫米汞柱,体温高达38.7℃,干咳,胸部感觉沉重,尿色改变,在症状出现24小时后被送往急救医院。SARS-CoV-2 PCR涂片阳性。计算机断层扫描显示双侧冠状病毒相关肺炎,肺泡炎,累及75%。心电图显示左室心肌肥厚征象。超声检查显示肾脏内有大量囊肿。入院时尿检:白细胞499,红细胞386。肾小球滤过率(CKD-EPI: 29 ml/min/1.73 m2),对应慢性肾病IV期。凝血图:纤维蛋白原:32.3 (1.64.0)g/l, d -二聚体:663(0250)。尽管进行了治疗,但患者病情恶化,心肺、肾功能不全现象增多,最终导致死亡。在切片材料的病毒学研究中:在肺和肾脏中发现了SARS-CoV-2冠状病毒RNA。双侧新型冠状病毒肺炎征象、肺泡炎伴弥漫性细胞浸润并肺泡器官改变、肺水肿征象显露。心脏相关征象间质肿胀,肌纤维碎裂,部分肥厚,心肌细胞呈波浪形变形,横纹模糊。动脉壁增厚硬化。肾脏弥漫性损害肾元近端小管伴皮质区和近端坏死区,纤维蛋白样肿胀区。结论。45岁患者的死亡原因是严重的双侧新冠肺炎、肺泡炎,导致肾髓质缺氧和1型心肾综合征的发展,导致早期肾源性肺水肿。
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