scholarly journals Clinical and diagnostic significance of endothelial dysfunction and serotonin levels in children with hemolytic-uremic syndrome

Author(s):  
T. P. Makarova ◽  
R. R. Nigmatullina ◽  
L. A. Davlieva ◽  
Yu. S. Melnikova

Hemolytic-uremic syndrome is a serious problem in pediatrics and pediatric nephrology. Hemolytic-uremic syndrome is one of the leading causes of acute kidney injury with potential transformation into terminal chronic kidney disease. Currently, the endothelial dysfunction is strongly associated with changes in the serotonergic system in the pathogenesis of hemolytic-uremic syndrome. There are few studies that have revealed an increase in the blood plasma serotonin concentration in children with hemolytic-uremic syndrome, but its role in the pathogenesis of chronic kidney disease has been insufficiently studied. The progressive course of hemolytic-uremic syndrome, up to the terminal stage of renal failure, requires the search for markers of renal tissue damage as prognostically significant factors for the development of nephrosclerosis, which is of particular importance for optimizing the management of such children.

2017 ◽  
Vol 4 (3) ◽  
pp. 136-138
Author(s):  
M.O. Gonchar ◽  
T.B. Ishenko ◽  
N.V. Orlova ◽  
G.R. Muratov ◽  
T.F. Kolibaeva ◽  
...  

Gonchar M.O., Ishchenko T.B., Orlova N.V., Muratov G., Kolibaeva T., Khmara N., Podvalnaya N.Currently, hemolytic-uremic syndrome is one of the frequent causes of acute kidney failure in children, so the timeliness of diagnosis and treatment determines the outcome of the disease. In the given clinical case, a set of certain factors that lead to an unfavorable outcome of the disease and the progression of chronic renal failure are presented. Clinical case of a 14-year-old child K., who was admitted to the nephrology department of the Regional Children's Clinical Hospital with the diagnosis: 3rd stage CKD, subcompensated stage of chronic renal failure and condition after hemolytic-uremic syndrome.KeyWords: hemolytic-uremic syndrome in children, chronic kidney disease. СТАН ПЫСЛЯ ПЕРЕНЕСЕНОГО ГЕМОЛІТИКО-УРЕМІЧНОГО СИНДРОМУ У ДИТИНИ З III СТАДІЄЮ ХРОНІЧНОГО ЗАХВОРЮВАННЯ НИРОК (КЛІНІЧНЕ СПОСТЕРЕЖЕННЯ)Гончарь М.О., Іщенко Т.Б., Орлова Н.В., Муратов Г.Р., Колібаєва Т.Ф., Хмара Н.В., Підвальна Н.А. В даний час гемолітико-уремічний синдром є однією з найчастіших причин гострої ниркової недостатності у дітей, тому своєчасність постановки діагнозу і лікування визначає результат захворювання. На наведеному клінічному випадку, представлено сукупність певних факторів, які привели до несприятливого результату захворювання і прогресування хронічної ниркової недостатності. Клінічний випадок дитини К. 14 років, який знаходився в нефрологічному відділенні Обласної дитячої клінічної лікарні з діагноз: ХХН III ст. Хронічна ниркова недостатність субкомпенсированная стадія. Стан після перенесеного гемолітико-уремічного синдрому.Ключові слова: гемолітико-уремічний синдром, діти, клінічний випадок, хронічне захворювання нирок. СОСТОЯНИЕ ПОСЛЕ ПЕРЕНЕСЕННОГО ГЕМОЛИТИКО-УРЕМИЧЕСКОГО СИНДРОМА У РЕБЕНКА С III СТАДИЕЙ ХРОНИЧЕСКОГО ЗАБОЛЕВАНИЯ ПОЧЕК (КЛИНИЧЕСКОЕ НАБЛЮДЕНИЕ)Гончарь М.А., Ищенко Т.Б., Орлова Н.В., Муратов Г.Р., Колибаева Т.Ф., Хмара Н.В., Подвальная Н.А. В настоящее время гемолитико-уремический синдром является одной из частых причин острой почечной недостаточности у детей, поэтому своевременность постановки диагноза и лечения определяет исход заболевания. На приведенном клиническом случае, представлено совокупность определенных факторов, которые привели к неблагоприятному исходу заболевания и прогрессированию хронической почечной недостаточности. Клинический случай ребенка К. 14 лет, который находился в нефрологическом отделении Областной детской клинической больнице с диагноз: ХБП III ст. Хроническая почечная недостаточность субкомпенсированная стадия. Состояние после перенесенного гемолитико-уремического синдрома.Ключевые слова: гемолитико-уремический синдром, дети, клинический случай, хроническое заболевание почек.


2021 ◽  
Vol 25 (3) ◽  
pp. 43-51
Author(s):  
E. V. Gunkova ◽  
A. A. Vyalkova ◽  
I. V. Zorin

Typical hemolytic-uremic syndrome (tGUS) is an acute disease in which non-immune microangiopathic hemolytic anemia, thrombocytopenia and acute renal damage develop against the background of infection-related diarrhea in the prodromal period. Hemolytic-uremic syndrome is the main cause of acute kidney injury in children under 5 years of age. Hemolytic-uremic syndrome is one of the causes of the progression of renal dysfunction in children with the formation of chronic kidney disease. The clinical picture of hemolytic-uremic syndrome is characterized by multi-organ manifestations with symptoms of acute renal damage, damage to the gastrointestinal tract, nervous, cardiovascular, respiratory systems and hemostasis. The article presents the data of modern literature on the epidemiology, etiology, pathogenesis and clinical picture of HUS in children, own scientific results on the clinical and paraclinical characteristics of a typical hemolytic-uremic syndrome in children of the Orenburg region.


2020 ◽  
Vol 39 (12) ◽  
pp. 1628-1638 ◽  
Author(s):  
J-Y Zhao ◽  
X-L Wang ◽  
Y-C Yang ◽  
B Zhang ◽  
Y-B Wu

Acute kidney injury (AKI) is an independent risk factor for chronic kidney disease (CKD). However, the role and mechanism of microRNA (miRNA, miR) in AKI-CKD transition are elusive. In this study, a murine model of renal ischemia/reperfusion was established to investigate the repairing effect and mechanism of miR-101a-3p on renal injury. The pathological damage of renal tissue was observed by hematoxylin and eosin and Masson staining. The levels of miR-101, profibrotic cytokines, and epithelial–mesenchymal transition (EMT) markers were analyzed using Western blotting, real-time polymerase chain reaction, and/or immunofluorescence. MiR-101 overexpression caused the downregulation of α-smooth muscle actin, collagen-1, and vimentin, as well as upregulation of E-cadherin, thereby alleviating the degree of renal tissue damage. MiR-101 overexpression mitigated hypoxic HK-2 cell damage. Collagen, type X, alpha 1 and transforming growth factor β receptor 1 levels were downregulated in hypoxic cells transfected with miR-101 mimic. Our study indicates that miR-101 is an anti-EMT miRNA, which provides a novel therapeutic strategy for AKI-CKD transition.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Fatemeh Masjedi ◽  
Jamshid Roozbeh ◽  
Zeinab Karimi

Abstract Background and Aims Coronavirus disease 2019 (COVID 19) was identified in December 2020 and is still growing in most parts of the world. The wide range of affected organs is likely based on the shared expression of the main severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry-receptor angiotensin-converting enzyme 2 (ACE2). Therefore, broad distribution of ACE2 receptors in various tissues play a key role in the multi-organ dysfunction and death due to COVID-19. Method International databases including PubMed, Embase, Web of Science, Scopus, and Cochrane Library Databases were used for search of articles by 30 December 2020. Keywords were nephropathy, COVID-19, coronavirus, renal injury, acute kidney injury, chronic kidney injury, and SARS-CoV-2 or a combination of them in the titles/abstracts. After the collection of related studies, Mendeley software was used to categorize and eliminate the duplicate titles. Then, studies with inappropriate purposes were removed. The selected studies were done on humans and published in English. Results Due to high prevalence of acute kidney injury (AKI) in patients with COVID-19, we summarize the molecular insights into viral infection mechanisms and implications for AKI. Moreover, mechanisms of the AKI to chronic kidney disease (CKD) transition such as relative contribution of immune cell response, fibroblasts activation, endothelial dysfunction and subsequent hypoxia may contribute to association of AKI with worse outcomes during this virus pandemic. Conclusion We highlight the state of the knowledge on SARS-CoV-2-dependent mechanisms for AKI and list the potential management options for prevention of AKI worsening and the imminent possibility of CKD. Finally, we aim to provide a better understanding of why Coronavirus induce AKI and, subsequently, progression to CKD in the coming years and further discuss the acute as well as long-term renal consequences. MO469   Figure: Potential interrelationship between endothelial dysfunction, tubular epithelial injury, interstitial inflammation, and fibrosis are likely to create a vicious cycle that can lead to the progression of acute kidney injury to chronic kidney disease (AKI to CKD) during COVID-19.


2018 ◽  
Vol 20 (6) ◽  
pp. 454-460 ◽  
Author(s):  
Tatiana N. Markova ◽  
Viktoriia V. Sadovskaya ◽  
Marina Y. Bespyatova

Chronic kidney disease (CKD) is a general concept that involves renal tissue regardless of the aetiology of the leading disease. CKD occurs in one out of every two patients with diabetes mellitus (DM) and appreciably limits the duration and quality of life. CKD can be diagnosed by glomerular filtration rate (GFR), which is recognised as the most representative indicator of the quantity and total workload of nephrons. However, the decrease in GFR occurs at an advanced stage of nephropathy and causes irreversible renal damage, which ultimately requires substitutive renal therapy and, thereby, increases the expense. In this regard, clinical trials have been conducted to identify the biomarkers of CKD reflecting renal damage at earlier stages of the disease. This article presents an overview of modern methods for the diagnosis of CKD and preclinical markers of kidney injury in patients with DM.


2018 ◽  
Vol 315 (1) ◽  
pp. F161-F172 ◽  
Author(s):  
Cierra N. Sharp ◽  
Mark A. Doll ◽  
Judit Megyesi ◽  
Gabrielle B. Oropilla ◽  
Levi J. Beverly ◽  
...  

Cisplatin is used to treat many solid cancers, but its dose-limiting side effect is nephrotoxicity, causing acute kidney injury in 30% of patients. Previously, we have developed a mouse model that better recapitulates the cisplatin dosing regimen humans receive and found that repeated dosing of cisplatin induces interstitial renal fibrosis. Chronic kidney disease is progressive and is characterized by chronic inflammation, worsening interstitial fibrosis, development of glomerulosclerosis, and endothelial dysfunction. To determine if damage caused by repeated cisplatin dosing results in bona fide chronic kidney disease, mice were treated with our repeated dosing regimen and then aged for 6 mo. These mice had progressive, chronic inflammation and worsened interstitial fibrosis compared with mice euthanized after day 24. Mice aged for 6 mo developed glomerular pathologies, and endothelial dysfunction was persistent. Mice treated with only two doses of cisplatin had little inflammation or kidney damage. Thus repeated dosing of cisplatin causes long-term effects that are characteristic of chronic kidney disease. This translational mouse model of cisplatin injury may better represent the 70% of patients that do not develop clinical acute kidney injury and can be used to identify both biomarkers for early injury, as well as novel therapeutic targets for the prevention of cisplatin-induced chronic kidney disease.


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