Clinical and morphological parallels of lung and kidney damage in COVID-19

2020 ◽  
Vol 24 (5) ◽  
pp. 97-107
Author(s):  
A. S. Litvinov ◽  
A. V. Savin ◽  
A. A. Kukhtina ◽  
D. A. Sitovskaya
Keyword(s):  
Morphological Changes ◽  
Human Kidney ◽  
Pathological Process ◽  
Kidney Damage ◽  
Viral Reservoir ◽  
Target Cells ◽  
Acute Renal Injury ◽  
Target Organs ◽  
Autopsy Data ◽  
Lung And Kidney

This article reviews the available literature on the SARS-Cov-2 virus and its similarities with its predecessors. The mechanisms of infection due to the structure and epidemiology of the virus are described. Based on these data, the pathogenesis of COVID- 19 infection is described. Based on this, the authors suggest probable extrapulmonary target cells and target organs for the virus depending on their expression ofthe vector protein, APF-2. The article describes a classic clinical picture of the disease, possible complications of its course, and the extrapulmonary (cardiac, immunological, renal) manifestations ofthe infection. The authors traced and described the chain of knowledge about the involvement of the kidneys in the pathological process at COVID-19. Based on numerous studies, we are looking at the site of acute renal injury, coagulopathy, systemic inflammatory response in the spectrum of manifestations of COVID-19 relative to kidneys in patients with COVID-19, including those with hemodialysis. The article builds clinical-morphological associations between lung and kidney damage at COVID-19. We present new data on the pathomorphological manifestations of COVID-19 in the lungs, including own autopsy data. Specificsigns of the effects of the virus on alveolocytes and its cytopathic effect are highlighted and described. The article focuses on kidney signs of infection. The authors give new results of their own observations obtained during an autopsy of patients with COVID-19. Detailed morphological changes in kidney structures have been described, proving that the human kidney is a specific target for SARS-Cov-2 infection, and can also serve as a viral reservoir for the pathogen, playing a role in its subsequent persistence.

Contemporary view about the pathogenesis of Hantavirus nephropathy (Literature rewiew)

2021 ◽  
Vol 25 (4) ◽  
pp. 23-32
Author(s):  
V. V. Salukhov ◽  
A. N. Kovalenko ◽  
Yu. V. Rudakov ◽  
V. A. Shelukhin ◽  
O. A. Nagibovich ◽  
...  
Keyword(s):  
Immune Response ◽  
World Literature ◽  
Hemorrhagic Fever ◽  
Pathological Process ◽  
Kidney Damage ◽  
Organ Specificity ◽  
Laboratory Model ◽  
Hantavirus Infection ◽  
Target Cells ◽  
Hantavirus Nephropathy

Hantavirus nephropathy (CVI) is considered to be acute kidney injury (AKI) associated with hantavirus infection (CVI). This infection in the countries of the European and Asian continents causes hemorrhagic fever with renal syndrome (HFRS). However, up to 60% of kidney damage is manifested by pathological changes in urinary sediment without signs of AKI, in connection with which the problems of terminology and diagnosis of kidney damage in HFRS were discussed. A review of the world literature of recent years, devoted to the study of modern data on the pathogenesis of CVI, is presented. The data were revealed that explain the organ specificity of the pathological process in different variants of CVI. The data were revealed that explain the organ specificity of the pathological process in different variants of CVI. The mechanisms related to various aspects of the pathogenesis of hantavirus nephropathy are considered. The factors that alter the functional activity of target cells through the direct action of the virus and the factors mediated by the immune response of the biological host to viral proteins in the form of the action of cytokines ("cytokine storm") causing damage to target organs (indirect factors) are listed. The influence of the hantavirus serotype, genetic factors, and the nature of the immune response of the biological host organism on the severity of renal dysfunction was shown. The concept of "acute damage to podocytes" is disclosed, which explains massive protein uria at the onset of the disease. The molecular and cellular mechanisms of damage to the main compartments of the kidney during hantavirus infection are presented. Disorders of hemostasis and mechanisms of hypercoagulation were demonstrated that underlie glomerular AKI due to acute microvascular syndrome, which is realized in the form of disseminated intravascular coagulation (DIC), hemolytic uremic syndrome (HUS), and thrombotic microangiopathy (TMA). The results of experimental data obtained on a laboratory model of infection and in cell culture, histological studies of autopsy material, and nephrobiopsy specimens from patients with hantavirus nephropathy are demonstrated.

TOXICOLOGICAL AND HYGIENE CHARACTERIZATION OF SOME METAL-CONTAINING NANOPARTICLES AT VARIOUS EXPOSITION METHODS: BIOACCUMULATION AND MORPHOFUNCTIONAL EXPOSURE FEATURES

2017 ◽  
pp. 27-34
Author(s):  
N. V. Zaitsevа ◽  
M. A. Zemlianova ◽  
N. N. Zvezdin ◽  
A. A. Dovbysh
Keyword(s):  
Morphological Changes ◽  
Inhalation Exposure ◽  
Circulatory System ◽  
Pathological Process ◽  
Critical Systems ◽  
Target Organs ◽  
Blood Circulatory System ◽  
Size Of Particles ◽  
Dose Dependent

Bioaccumulation and morphofunctional disorders induced by metal-containing nanoparticles were investigated on the example of potentially hazardous to health nanodispersed manganese and nickel oxides under various exposition conditions (particles size of 15-29 and 17-45 nanometers respectively). As a comparison, micro dimensional analogs which particles size was 300- to 1300- fold bigger were used. It was established that metalcontaining nanoparticles at intragastric and inhalation exposure had higher penetration power and low removal efficiency from the organism (14- to 39-fold lower); the profile of «critical» organs includes brain, liver, spleen, lungs; metal-containing NPs cause functional disorders in critical systems and target organs (in the form of disrupted balance in indicators of oxidative and antioxidant processes and neurotransmitters under effect of nano dispersed MnO), these disorders having dose-dependent character. A great degree of expressiveness of morphological changes in the blood circulatory system, macrophagal and lymphoid systems, and also the presence of changes in the tissue of liver, brain and heart not revealed under exposition to microdespersed analogs prove a big damaging ability of metal-containing nanoparticles and dependence of expressiveness degree of pathological process on the size of particles.

Characteristics of the course of nephritis associated with Iga-vasculitis Henoch-Schoenlein in children

2020 ◽  
Vol 24 (3) ◽  
pp. 64-71
Author(s):  
A. V. Sukalo ◽  
I. A. Kazyra
Keyword(s):  
Clinical Laboratory ◽  
Morphological Changes ◽  
Pediatric Nephrology ◽  
Morphological Characteristics ◽  
Lymphocyte Activation ◽  
Renal Tissue ◽  
Kidney Damage ◽  
Iga Vasculitis ◽  
Factors Affecting ◽  
Treatment Regimens

INTRODUCTION. Among systemic vasopathies in children, IgA vasculitis Henoch Schoenlein (HS) is the most common, according to various authors, kidney damage is noted in 25-80 % and usually determines the prognosis of the disease.THE AIM of the study was to analyze clinical, laboratory, immunological, morphological characteristics, features of the course and treatment of nephritis associated with IgA vasculitis HS in children, as well as factors affecting the prognosis.PATIENTS AND METHODS. The study included 31 patients with morphologically verified nephritis due to IgA vasculitis HS (18 – boys, 13 – girls) aged 3 to 17 years, who were monitored at the Nephrology Department of the "2nd Children's City Clinical Hospital" of the National Center for Pediatric Nephrology and Renal Replacement therapy in Minsk from 2010 to 2019 yrs.The following parameters were analyzed: the clinical variant of kidney damage, laboratory tests (including the study of BAFF, RANTES lymphocyte activation molecules, pro-inflammatory IL1β, caspase1, TNFα, growth factors VEGF, TGF), 24 hours monitoring and office blood pressure measurements, ECHO cardiography with indicescalculation, ultrasound of the carotid arteries with the thickness of intima-media complex, morphological changes in the renal tissue, as well as treatment regimens.RESULTS. The contribution of deGal-IgA1, markers of T and B lymphocytes activation, pro-inflammatory and profibrotic molecules in the development of the disease is shown. Arterial hypertension was registered in 42 % of children, signs of heart remodeling according to the calculated indices in 19,3 %. Decrease level of adiponectin, vitamin D, leptin, increase concentration of obestatin, Pro-BNP, hs-CRP, and TSAT indicator classify patients with nephritis due to IgA vasculitis HS at moderate risk for the developmentof cardio-vascular disorders, which suggests the need for timely correction.CONCLUSION. In most cases, nephritis with IgA vasculitis HS has a benign course with rare relapses and progression to the end stage of chronic kidney disease (6,5 %).

scholarly journals The impact of fluid status and decremental PEEP strategy on cardiac function and lung and kidney damage in mild-moderate experimental acute respiratory distress syndrome

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Nazareth N. Rocha ◽  
Cynthia S. Samary ◽  
Mariana A. Antunes ◽  
Milena V. Oliveira ◽  
Matheus R. Hemerly ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Epithelial Cell ◽  
Distress Syndrome ◽  
Cell Damage ◽  
Kidney Injury ◽  
Fluid Administration ◽  
Kidney Damage ◽  
Fluid Status ◽  
Pulmonary Arterial ◽  
Lung And Kidney

Abstract Background We evaluated the effects of abrupt versus gradual PEEP decrease, combined with standard versus high-volume fluid administration, on cardiac function, as well as lung and kidney damage in an established model of mild-moderate acute respiratory distress syndrome (ARDS). Methods Wistar rats received endotoxin intratracheally. After 24 h, they were treated with Ringer’s lactate at standard (10 mL/kg/h) or high (30 mL/kg/h) dose. For 30 min, all animals were mechanically ventilated with tidal volume = 6 mL/kg and PEEP = 9 cmH2O (to keep alveoli open), then randomized to undergo abrupt or gradual (0.2 cmH2O/min for 30 min) PEEP decrease from 9 to 3 cmH2O. Animals were then further ventilated for 10 min at PEEP = 3 cmH2O, euthanized, and their lungs and kidneys removed for molecular biology analysis. Results At the end of the experiment, left and right ventricular end-diastolic areas were greater in animals treated with high compared to standard fluid administration, regardless of PEEP decrease rate. However, pulmonary arterial pressure, indicated by the pulmonary acceleration time (PAT)/pulmonary ejection time (PET) ratio, was higher in abrupt compared to gradual PEEP decrease, independent of fluid status. Animals treated with high fluids and abrupt PEEP decrease exhibited greater diffuse alveolar damage and higher expression of interleukin-6 (a pro-inflammatory marker) and vascular endothelial growth factor (a marker of endothelial cell damage) compared to the other groups. The combination of standard fluid administration and gradual PEEP decrease increased zonula occludens-1 expression, suggesting epithelial cell preservation. Expression of club cell-16 protein, an alveolar epithelial cell damage marker, was higher in abrupt compared to gradual PEEP decrease groups, regardless of fluid status. Acute kidney injury score and gene expression of kidney injury molecule-1 were higher in the high versus standard fluid administration groups, regardless of PEEP decrease rate. Conclusion In the ARDS model used herein, decreasing PEEP abruptly increased pulmonary arterial hypertension, independent of fluid status. The combination of abrupt PEEP decrease and high fluid administration led to greater lung and kidney damage. This information adds to the growing body of evidence that supports gradual transitioning of ventilatory patterns and warrants directing additional investigative effort into vascular and deflation issues that impact lung protection.

scholarly journals Evidence of Human Parvovirus B19 Infection in the Post-Mortem Brain Tissue of the Elderly

Viruses ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 582 ◽  
Author(s):  
Sandra Skuja ◽  
Anda Vilmane ◽  
Simons Svirskis ◽  
Valerija Groma ◽  
Modra Murovska
Keyword(s):  
White Matter ◽  
Frontal Lobe ◽  
Brain Tissue ◽  
Morphological Changes ◽  
Structural Characteristics ◽  
Parvovirus B19 ◽  
Elderly Subjects ◽  
Target Cells ◽  
Human Parvovirus B19 ◽  
Pathogenic Potential

After primary exposure, the human parvovirus B19 (B19V) genome may remain in the central nervous system (CNS), establishing a lifelong latency. The structural characteristics and functions of the infected cells are essential for the virus to complete its life cycle. Although B19V has been detected in the brain tissue by sequencing PCR products, little is known about its in vivo cell tropism and pathogenic potential in the CNS. To detect B19V and investigate the distribution of its target cells in the CNS, we studied brain autopsies of elderly subjects using molecular virology, and optical and electron microscopy methods. Our study detected B19V in brain tissue samples from both encephalopathy and control groups, suggesting virus persistence within the CNS throughout the host’s lifetime. It appears that within the CNS, the main target of B19V is oligodendrocytes. The greatest number of B19V-positive oligodendrocytes was found in the white matter of the frontal lobe. The number was significantly lower in the gray matter of the frontal lobe (p = 0.008) and the gray and white matter of the temporal lobes (p < 0.0001). The morphological changes observed in the encephalopathy group, propose a possible B19V involvement in the demyelination process.

scholarly journals HIV-1 uncoating occurs via a series of rapid biomechanical changes in the core related to individual stages of reverse transcription

2021 ◽  
Author(s):  
Sanela Rankovic ◽  
Akshay Deshpande ◽  
Shimon Harel ◽  
Christopher Aiken ◽  
Itay Rousso
Keyword(s):  
Reverse Transcription ◽  
Viral Genome ◽  
Morphological Changes ◽  
Viral Capsid ◽  
Target Cells ◽  
Viral Core ◽  
Successful Infection ◽  
Capsid Shell ◽  
Hiv 1

AbstractThe HIV core consists of the viral genome and associated proteins encased by a cone-shaped protein shell termed the capsid. Successful infection requires reverse transcription of the viral genome and disassembly of the capsid shell within a cell in a process known as uncoating. The integrity of the viral capsid is critical for reverse transcription, yet the viral capsid must be breached to release the nascent viral DNA prior to integration. We employed atomic force microscopy to study the stiffness changes in HIV-1 cores during reverse transcription in vitro in reactions containing the capsid-stabilizing host metabolite IP6. Cores exhibited a series of stiffness spikes, with up to three spikes typically occurring between 10-30, 40-80, and 120-160 minutes after initiation of reverse transcription. Addition of the reverse transcriptase (RT) inhibitor efavirenz eliminated the appearance of these spikes and the subsequent disassembly of the capsid, thus establishing that both result from reverse transcription. Using timed addition of efavirenz, and analysis of an RNAseH-defective RT mutant, we established that the first stiffness spike requires minus-strand strong stop DNA synthesis, with subsequent spikes requiring later stages of reverse transcription. Additional rapid AFM imaging experiments revealed repeated morphological changes in cores that were temporally correlated with the observed stiffness spikes. Our study reveals discrete mechanical changes in the viral core that are likely related to specific stages of reverse transcription. Our results suggest that reverse-transcription-induced changes in the capsid progressively remodel the viral core to prime it for temporally accurate uncoating in target cells.

scholarly journals Closed Fractures of the Distal Part of the Shin Bones. Different Types and Methods of the Treatment in Adolescence. Short Period Results

2021 ◽  
Vol 3 (1) ◽  
pp. 11-23
Author(s):  
Alexander I. Dorokhin ◽  
Alexander I. Krupatkin ◽  
Anastasia A. Adrianova ◽  
Vladimir I. Khudik ◽  
Dmitriy S. Sorokin ◽  
...  
Keyword(s):  
Distal Part ◽  
Clinical Investigation ◽  
Morphological Changes ◽  
Treatment Algorithm ◽  
Age Groups ◽  
Growth Zone ◽  
Difficult Problem ◽  
Pathological Process ◽  
X Rays ◽  
Short Period

Background.Fractures of the distal leg bones in children, due to the peculiarities of localization, the presence of a growth zone, the proximity of the joint and the involvement of the ligamentous apparatus in the pathological process, present a difficult problem in the choice of treatment and rehabilitation.Aims:In order to our aims we create the diagnostic and treatment algorithm in the system of early rehabilitation after fractures in the distal part of the shin bone in adolescence.Methods.Our clinical investigation based on the treatment of 56 patients in the age 817 years. Cohort of patients consist from three age groups: 811 years (n=13), 1214 years (n=28) and 1517 years (n=15). Examination was done with X-rays, CT and Ultrasound, specialy in the cases where the damage of ligamentous apparatus was suspicious. The main method of treatment was surgical osteosynthesis by pins, plates and screws. In the rehabilitation period the legs were immobilized by Plaster of Paris for 46 weeks.Results.In majority of cases the outcomes in the period of 68 weeks after trauma were good and satisfactory. The method of laser Doppler fluometry was performed in 16 cases in follow up period after trauma for examination of the regional blood circulation as a argumentation of regeneration process.Conclusion.The different choice in treatment of compound fractures of the distal part of the shin bones according to morphological changes in adolescence permits to aid good results in majority of caces.

scholarly journals The association gene’s TNFα G(308) with quantity of TNFα and degree of liver’s fibrosis in patients with chronic hepatitis C

2018 ◽  
Vol 22 (4) ◽  
pp. 682-685
Author(s):  
E.N. Usychenko ◽  
Yu.I. Bazhora ◽  
E.M. Usychenko ◽  
V.A. Gudz
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Chronic Hepatitis C ◽  
Degrees Of Freedom ◽  
Morphological Changes ◽  
Polymorphic Marker ◽  
Pathological Process ◽  
Hepatic Tissue ◽  
The Individual

The data on the polymorphism of cytokine genes associated with individual reactivity on the effects of hepatitis C virus, predict the rate of progression of liver fibrosis. The purpose of this work is study the association of the polymorphic marker G308A of the TNFα gene with its quantitative content and degree of liver fibrosis in patients with chronic hepatitis C. A total of 100 patients with CSF were examined. The polymorphism of G308A gene’s TNFα was studied by amplification of the corresponding genome zones by PCR. The assessment of the degree of fibrosis was performed using the non-invasive Fibrotest method. The study of the quantity of TNFα cytokine in serum of patients was performed by ELISA. The distribution of genotypes on the investigated polymorphic loci was verified using Pearson's χ2 criterion. The frequencies of alleles and genotypes in the groups were compared using Pearson's χ2 criterion with Yates correction for continuity with the number of degrees of freedom 1. In order to detect the correlation dependencies between the individual parameters, the Spearman correlation coefficient was applied. It was found that a smaller degree of fibrosis was observed in carriers of the GG TNFα genotype, and a greater degree of fibrosis in the carriers of the genotype AA TNFα (moderate feedback between the degree of fibrosis and the genotypes of TNFα). The higher content of TNFα is noted in the carriers of the AA genotype TNFα, the lower content of TNFα - in the carriers of the GG TNFα genotype (moderate feedback between the TNFα genotypes and the TNFα content). It has been established that a higher TNFα content is observed in patients with F1-F0 fibrosis, a lower TNFα content in patients with F2-F3 fibrosis (a strong correlation between the degree of fibrosis and the amount of TNFα cytokine). It is assumed that the production of the cytokine is determined at the genetic level, and the severity of changes in the cytokine profile in chronic hepatitis C affects the course of the pathological process. An increase in the TNFα content in chronic hepatitis C may be a marker for significant morphological changes in the hepatic tissue and high activity of the inflammatory process.

scholarly journals Single cell census of human kidney organoids shows reproducibility and diminished off-target cells after transplantation

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ayshwarya Subramanian ◽  
Eriene-Heidi Sidhom ◽  
Maheswarareddy Emani ◽  
Katherine Vernon ◽  
Nareh Sahakian ◽  
...  
Keyword(s):  
Single Cell ◽  
Single Cells ◽  
Human Kidney ◽  
Mouse Kidney ◽  
Target Cells ◽  
Rna Seq ◽  
Kidney Capsule ◽  
Time Points ◽  
Human Ipsc ◽  
Kidney Organoids

AbstractHuman iPSC-derived kidney organoids have the potential to revolutionize discovery, but assessing their consistency and reproducibility across iPSC lines, and reducing the generation of off-target cells remain an open challenge. Here, we profile four human iPSC lines for a total of 450,118 single cells to show how organoid composition and development are comparable to human fetal and adult kidneys. Although cell classes are largely reproducible across time points, protocols, and replicates, we detect variability in cell proportions between different iPSC lines, largely due to off-target cells. To address this, we analyze organoids transplanted under the mouse kidney capsule and find diminished off-target cells. Our work shows how single cell RNA-seq (scRNA-seq) can score organoids for reproducibility, faithfulness and quality, that kidney organoids derived from different iPSC lines are comparable surrogates for human kidney, and that transplantation enhances their formation by diminishing off-target cells.

scholarly journals Biochemistry and metabolism of vitamin D / Biohemija i metabolizam vitamina D

2012 ◽  
Vol 31 (4) ◽  
pp. 309-315 ◽  
Author(s):  
Snežana Jovičić ◽  
Svetlana Ignjatović ◽  
Nada Majkić-Singh
Keyword(s):  
Vitamin D ◽  
Cytochrome P450 ◽  
Vitamin D3 ◽  
Mammalian Cells ◽  
Parent Compound ◽  
Endocrine System ◽  
Target Cells ◽  
Plasma Vitamin ◽  
Endocrine Gland ◽  
Target Organs

Summary Vitamin D is not technically a vitamin, since it is not an essential dietary factor. It is rather a prohormone produced photochemically in the skin from 7-dehydrocholesterol. Vitamin D and its metabolites may be categorized as either cholecalciferols or ergocalciferols. Cholecalciferol (vi - tamin D3) is the parent compound of the naturally occurring family and is produced in the skin from 7-dehydrocholesterol on exposure to the ultraviolet B portion of sunlight. Vitamin D2 (ergocalciferol), the parent compound of the other family, is manufactured by irradiation of ergosterol produced by yeasts and its potency is less than one-third of vitamin D3’s potency. The steps in the vitamin D endocrine system include the following: 1) the photoconversion of 7- dehydrocholesterol to vitamin D3 in the skin or dietary intake of vitamin D3; 2) metabolism of vitamin D3 by the liver to 25-hydroxyvitamin-D3 [25(OH)D3 ], the major form of vitamin D circulating in the blood compartment; 3) conversion of 25(OH)D3 by the kidney (functioning as an endocrine gland) to the hormone 1,25-dihydroxyvitamin D3 [1,25(OH)2D3 ]; 4) systemic transport of the dihydroxylated metabolite 1,25(OH)2D3 to distal target organs; and 5) binding of 1,25(OH)2D3 to a nuclear receptor (VDR) at target organs, followed by generation of appropriate biological responses. The activation of vitamin D to its hormonal form is mediated by cytochrome P450 enzymes. Six cytochrome P450 (CYP) isoforms have been shown to hydroxylate vitamin D. Four of these, CYP27A1, CYP2R1, CYP3A4 and CYP2J3, are candidates for the enzyme vitamin D 25-hy - droxylase that is involved in the first step of activation. The highly regulated, renal enzyme 25-hydroxyvitamin D-1a-hy - dro xylase contains the component CYP27B1, which completes the activation pathway to the hormonal form 1,25(OH)2D3. A five-step inactivation pathway from 1,25(OH)2D3 to calcitroic acid is attributed to a single multifunctional CYP, CYP24A1, which is transcriptionally in du - ced in vitamin D target cells by the action of 1,25(OH)2D3. An additional key component in the operation of the vitamin D endocrine system is the plasma vitamin D binding protein (DBP), which carries vitamin D3 and its metabolites to their metabolism and target organs. DBP is a specific, high-affinity transport protein. It is synthesized by the liver and circulates in great excess, with fewer than 5% of the binding sites normally occupied. 1,25(OH)2D3, acts as a ligand for a nuclear transcription factor, vitamin D receptor - VDR, which like all other nuclear receptors, regulates gene transcription and cell function. The widespread presence of VDR, and the key activating (1a-hydroxylase, CYP27B1) and inactivating (24-hydroxylase, CYP24A1) en - zy mes in most mammalian cells means that the cells in these tissues have the potential to produce biological res pon ses, depending on the availability of appropriate amounts of vi - tamin D3. Thanks to this widespread presence of elements of vitamin D endocrine system, its biological features are being recognized outside bone tissue, i.e. calcium and pho - sphate metabolism.

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