scholarly journals Use of medicines for covid-19 treatment in patients with loss of kidney function: a narrative review

2020 ◽  
Author(s):  
Lucas Lobato Acatauassu Nunes ◽  
Tácio de Mendonça Lima
Keyword(s):  
Kidney Function ◽  
Specific Treatment ◽  
Kidney Injury ◽  
Alveolar Epithelial Cells ◽  
Renal Cells ◽  
Angiotensin Converting Enzyme 2 ◽  
Factors Associated ◽  
Alveolar Epithelial ◽  
Heart Blood ◽  
Dose Recommendations

ABSTRACT Covid-19 has been identified as the cause of acute respiratory disease with interstitial and alveolar pneumonia, but it can affect several organs, such as kidneys, heart, blood, nervous system and digestive tract. The disease-causing agent (Sars-CoV-2) has a binding structure to the angiotensin-converting enzyme 2 (ACE2) receptor, enabling entry into cells that express ACE2, such as the pulmonary alveolar epithelial cells. However, studies also indicate the possibility of damage to renal cells, since these cells express high levels of ACE2. Currently, there is no evidence to indicate a specific treatment for covid-19. Several drugs have been used, and some of them may have their excretion process altered in patients with abnormal kidney function. To date, there are no studies that assist health professionals in adjusting the dose of these drugs. Thus, this study aims to review and discuss the topic, taking into account factors associated with kidney injury in covid-19, as well as pharmacokinetic aspects and dose recommendations of the main drugs used for covid-19.

scholarly journals ACE2 polymorphisms and individual susceptibility to SARS-CoV-2 infection: insights from an in silico study

2020 ◽  
Author(s):  
Matteo Calcagnile ◽  
Patricia Forgez ◽  
Antonio Iannelli ◽  
Cecilia Bucci ◽  
Marco Alifano ◽  
...  
Keyword(s):  
In Silico ◽  
Alveolar Epithelial Cells ◽  
Nucleotide Polymorphisms ◽  
Related Factors ◽  
Single Nucleotide ◽  
Angiotensin Converting Enzyme 2 ◽  
Alveolar Epithelial ◽  
African People ◽  
In Silico Study ◽  
Ace2 Gene

AbstractThe current SARS covid-19 epidemic spread appears to be influenced by ethnical, geographical and sex-related factors that may involve genetic susceptibility to diseases. Similar to SARS-CoV, SARS-CoV-2 exploits angiotensin-converting enzyme 2 (ACE2) as a receptor to invade cells, notably type II alveolar epithelial cells. Importantly, ACE2 gene is highly polymorphic. Here we have used in silico tools to analyze the possible impact of ACE2 single-nucleotide polymorphisms (SNPs) on the interaction with SARS-CoV-2 spike glycoprotein. We found that S19P (common in African people) and K26R (common in European people) were, among the most diffused SNPs worldwide, the only two SNPs that were able to potentially affect the interaction of ACE2 with SARS-CoV-2 spike. FireDock simulations demonstrated that while S19P may decrease, K26R might increase the ACE2 affinity for SARS-CoV-2 Spike. This finding suggests that the S19P may genetically protect, and K26R may predispose to more severe SARS-CoV-2 disease.

scholarly journals Regulation of alveolar epithelial cell survival by the ACE-2/angiotensin 1–7/Mas axis

2011 ◽  
Vol 301 (3) ◽  
pp. L269-L274 ◽  
Author(s):  
Bruce D. Uhal ◽  
Xiaopeng Li ◽  
Anita Xue ◽  
Xu Gao ◽  
Amal Abdul-Hafez
Keyword(s):  
Culture Media ◽  
Alveolar Epithelial Cell ◽  
Primary Cultures ◽  
Competitive Inhibitor ◽  
Alveolar Epithelial Cells ◽  
Caspase Activation ◽  
Nuclear Fragmentation ◽  
Angiotensin Converting Enzyme 2 ◽  
Alveolar Epithelial ◽  
Interfering Rna

Earlier work from this laboratory demonstrated that apoptosis of alveolar epithelial cells (AECs) requires autocrine generation of angiotensin (ANG) II. More recent studies showed that angiotensin converting enzyme-2 (ACE-2), which degrades ANGII to form ANG1–7, is protective but severely downregulated in human and experimental lung fibrosis. Here it was theorized that ACE-2 and its product ANG1–7 might therefore regulate AEC apoptosis. To evaluate this hypothesis, the AEC cell line MLE-12 and primary cultures of rat AECs were exposed to the profibrotic apoptosis inducers ANGII or bleomycin (Bleo). Markers of apoptosis (caspase-9 or -3 activation and nuclear fragmentation), steady-state ANGII and ANG1–7, and JNK phosphorylation were measured thereafter. In the absence of Bleo, inhibition of ACE-2 by small interfering RNA or by a competitive inhibitor (DX600 peptide) caused a reciprocal increase in autocrine ANGII and corresponding decrease in ANG1–7 in cell culture media (both P < 0.05) and, moreover, induced AEC apoptosis. At baseline (without inhibitor), ANG1–7 in culture media was 10-fold higher than ANGII ( P < 0.01). Addition of purified ANGII or bleomycin-induced caspase activation, nuclear fragmentation, and JNK phosphorylation in cultured AECs. However, preincubation with ANG1–7 (0.1 μM) prevented JNK phosphorylation and apoptosis. Moreover, pretreatment with A779, a specific blocker of the ANG1–7 receptor mas, prevented ANG1–7 blockade of JNK phosphorylation, caspase activation, and nuclear fragmentation. These data demonstrate that ACE-2 regulates AEC survival by balancing the proapoptotic ANGII and its antiapoptotic degradation product ANG1–7. They also suggest that ANG1–7 inhibits AEC apoptosis through the ANG1–7 receptor mas.

scholarly journals Microbiota and Its Impact on the Immune System in COVID-19—A Narrative Review

2021 ◽  
Vol 10 (19) ◽  
pp. 4537
Author(s):  
Marzena Jabczyk ◽  
Justyna Nowak ◽  
Bartosz Hudzik ◽  
Barbara Zubelewicz-Szkodzińska
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Alveolar Epithelial Cells ◽  
Host Immune System ◽  
Angiotensin Converting Enzyme 2 ◽  
Neural Connections ◽  
Alveolar Epithelial ◽  
The Face ◽  
Almost All ◽  
Intestinal Enterocytes

The microbiota is of interest for the development of a therapeutic strategy against SARS-CoV-2 coronavirus disease 2019 (COVID-19) due to its impact on the host immune system. Proven communications of the gut microbiota with the pulmonary microbiota (gut–lung axis) and the pathway of neural connections between the gut and brain (gut–brain axis) may be important in the face of the pandemic. SARS-CoV-2 was shown to affect almost all organs because of the presence of a host receptor known as angiotensin converting enzyme 2 (ACE2). The ACE2 receptor is mainly present in the brush border of intestinal enterocytes, ciliary cells, and type II alveolar epithelial cells in the lungs. The transport function of ACE2 has been linked to the ecology of gut microbes in the digestive tract, suggesting that COVID-19 may be related to the gut microbiota. The severity of COVID-19 may be associated with a number of comorbidities, such as hypertension, diabetes, obesity, and/or old age; therefore, attention is also paid to multiple morbidities and the modulation of microbiota through comorbidities and medications. This paper reviews the research in the context of the state of the intestinal microbiota and its impact on the cells of the immune system during the SARS-CoV-2 pandemic.

scholarly journals Effects of Pulmonary Hypertension and Right Ventricular Function in Short and Long-Term Kidney Function

2018 ◽  
Vol 15 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Mario Naranjo ◽  
Kevin Bryan Lo ◽  
Kenechukwu Mezue ◽  
Janani Rangaswami
Keyword(s):  
Pulmonary Hypertension ◽  
Kidney Disease ◽  
Renal Disease ◽  
Kidney Transplant ◽  
Kidney Function ◽  
Large Body ◽  
Specific Treatment ◽  
Kidney Injury ◽  
Transplant Outcomes ◽  
Pulmonary Hemodynamic

Background: Pulmonary hypertension is not uncommon in patients with renal disease and vice versa; therefore, it influences treatments and outcomes. There is a large body of literature on pulmonary hypertension in patients with kidney disease, its prognostic implications, economic burden, and management strategies. However, the converse, namely the hemodynamic effects of pulmonary hypertension on kidney function (acute and chronic kidney injury) is less studied and described. There is also increasing interest in the effects of pulmonary hypertension on kidney transplant outcomes. The relationship is a complex phenomenon and multiple body systems and mechanisms are involved in its pathophysiology. Although the definition of pulmonary hypertension has evolved over time with the understanding of multiple interplays between the heart, lungs, kidneys, etc; there is limited evidence to provide a specific treatment strategy when kidneys and lungs are affected at the same time. Nevertheless, available evidence appears to support new therapeutics and highlights the importance of individualized approach. There is sufficient research showing that the morbidity and mortality from PH are driven by the influence of the pulmonary hemodynamic dysfunction on the kidneys. Conclusion: This concise review focuses on the effects of pulmonary hypertension on the kidneys, including, the patho-physiological effects of pulmonary hypertension on acute kidney injury, progression of CKD, effects on kidney transplant outcomes, progression of kidney disease in situations such as post LVAD implantation and novel diagnostic indices. We believe a review of this nature will fill in an important gap in understanding the prognostic implication of pulmonary hypertension on renal disease, and help highlight this important component of the cardio-reno-pulmonary axis.

Alveolar epithelial cells type II show a high sensitivity to cigarette smoke extract

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
S Seehase ◽  
B Baron-Luehr ◽  
C Kugler ◽  
E Vollmer ◽  
T Goldmann
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
High Sensitivity ◽  
Cigarette Smoke Extract ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial
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