Intrarenal renin-angiotensin system activation in end-stage renal disease

Urushihara, Maki; Kobori, Hiroyuki

doi:10.1038/hr.2017.7

Cited by 10 publications

(7 citation statements)

References 11 publications

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“…It has been suggested that excessive activation of the RAS might contribute to the progression of COVID-19-related lung injury [26]. Chronic perturbations of the RAS and intra-renal RAS in ESRD-HD have been described [27,28]. Modifications in the activation of the RAS in response to the acute COVID-19 illness in patients with ESRD-HD might explain the "protective effect" seen in these patients.…”

Section: Discussionmentioning

confidence: 99%

End-Stage Renal Disease Patients on Chronic Hemodialysis Fare Better With COVID-19: A Retrospective Cohort Study From the New York Metropolitan Region

Naaraayan¹,

Nimkar²,

Hasan³

et al. 2020

Cureus

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Introduction Several comorbid conditions have been identified as risk factors in patients with coronavirus disease 2019 (COVID-19). However, there is a dearth of data describing the impact of COVID-19 infection in patients with end-stage renal disease on hemodialysis (ESRD-HD). Methods This retrospective case series analyzed 362 adult patients consecutively hospitalized with confirmed COVID-19 illness between March 12, 2020, and May 13, 2020, at a teaching hospital in the New York City metropolitan area. The primary outcome was severe pneumonia as defined by the World Health Organization. Secondary outcomes were the (1) the Combined Outcome of Acute respiratory distress syndrome or in-hospital Death (COAD), and (2) need for high levels of oxygen supplementation (HiO 2). Results Patients with ESRD-HD had lower odds for poor outcomes including severe pneumonia [odds ratio (OR) 0.4, confidence interval (CI) 0.2-0.9, p=.04], HiO 2 [OR 0.3, CI (0.1-0.8), p=.02] and COAD [OR 0.4, CI (0.2-1.05), p=.06], when compared to patients without ESRD. In contrast, higher odds for severe pneumonia, COAD and HiO 2 were seen with advancing age. African Americans were over-represented in the hospitalized patient cohort, when compared to their representation in the community (35% vs 18%). Hispanics had higher odds for severe illness and HiO 2 when compared to Caucasians. Conclusions Patients with ESRD-HD had a milder course of illness with a lower likelihood of severe pneumonia and a lesser need for aggressive oxygen supplementation when compared to patients not on chronic dialysis. The lower odds of severe illness in ESRD-HD patients might have a pathophysiologic basis and need to be further explored.

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Section: Discussionmentioning

confidence: 99%

End-Stage Renal Disease Patients on Chronic Hemodialysis Fare Better With COVID-19: A Retrospective Cohort Study From the New York Metropolitan Region

Naaraayan¹,

Nimkar²,

Hasan³

et al. 2020

Cureus

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“…60,75,76 Similar to systemic RAS, AngII is the major product of the IRAS and activation of the AngII type 1 receptor (AT1R) pathway results in the production of pro-inflammatory mediators, intracellular formation of reactive oxygen species (ROS), cell proliferation, and ECM synthesis, all of which facilitate renal injury. 77 Intrarenal AngII levels are regulated locally and distinct from circulating AngII concentration. 78 –80 All of the components necessary to generate intrarenal AngII are present within the interstitial and intratubular compartments of the kidney involving multiple independent mechanisms, including classic RAS pathways, (pro)-renin receptors (PRRs), and chymase (Figure 2).…”

Section: Renin–angiotensin System Is a Potential Factor In Cpn Pathogmentioning

confidence: 99%

Intrarenal Renin–Angiotensin System Involvement in the Pathogenesis of Chronic Progressive Nephropathy—Bridging the Informational Gap Between Disciplines

Obert

Frazier

2019

Toxicol Pathol

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Chronic progressive nephropathy (CPN) is the most commonly encountered spontaneous background finding in laboratory rodents. Various theories on its pathogenesis have been proposed, but there is a paucity of data regarding specific mechanisms or physiologic pathways involved in early CPN development. The current CPN mechanism of action for tumorigenesis is largely based on its associated increase in tubular cell proliferation without regard to preceding subcellular degenerative changes. Combing through the published literature from multiple biology disciplines provided insight into the preceding cellular events. Mechanistic pathways involved in the progressive age-related decline in rodent kidney function and several key inflexion points have been identified. These critical pathway factors were then connected using data from renal models from multiple rodent strains, other species, and mechanistic work in humans to form a cohesive picture of pathways and protein interactions. Abundant data linked similar renal pathologies to local events involving hypoxia (hypoxia-inducible factor 1α), altered intrarenal renin–angiotensin system (RAS), oxidative stress (nitric oxide), and pro-inflammatory pathways (transforming growth factor β), with positive feedback loops and downstream effectors amplifying the injury and promoting scarring. Intrarenal RAS alterations seem to be central to all these events and may be critical to CPN development and progression.

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“…Thus; we analyzed functionally similar genes with ACE2. We found that [43], [44] although, all constituents of the RAS have expressed in a lot of tumor tissues [45]. Thus; Cambell and coauthors have reported that ACE, AGT, AGTR1, and AGTR2 genes can promote renal function variation [45].…”

Section: Discussionmentioning

confidence: 85%

Role of ACE2 Gene Expression in Renin Angiotensin System and Its Importance in Covid-19: In Silico Approach

Taş

Kirkik

Işık

et al. 2020

Braz. arch. biol. technol.

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We aimed to analyze the expression profile of ACE2 and similar genes with ACE2, predict the number of variations in ACE2, detect the suspected SNPs on ACE2 gene, and perform the pathway analysis of renin-angiotensin system (RAS) and protein absorption-digestion. Moreover, we have predicted the generelated diseases with ACE2. STRING was used to analyze functionally similar genes with ACE2. Exome Variant Server, SIFT, Polyphen2 were used to predict the number of variations in ACE2 and detect the suspected SNPs on ACE2. KEGG database and STRING were used to draw pathway of ACE2. Then, DISEASES resource, FitSNPs, UniProt, BioXpress, IGV Browser, Ensembl Genome Browser, and HIGHLIGHTS  ACE2 is also expressed in testis, heart, thyroid, colon, esophagus, breast, pancreas, lung, liver.  Under expression of ACE2 can cause prostate cancer and head and neck cancer.  ACE2 is over-expressed in the small intestine.  Suggesting that over expression of ACE2 in small intesine can cause symptoms of in COVID-19. 2 Kalkanli Tas, S.; et al.

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Intrarenal renin-angiotensin system activation in end-stage renal disease

Cited by 10 publications

References 11 publications

End-Stage Renal Disease Patients on Chronic Hemodialysis Fare Better With COVID-19: A Retrospective Cohort Study From the New York Metropolitan Region

End-Stage Renal Disease Patients on Chronic Hemodialysis Fare Better With COVID-19: A Retrospective Cohort Study From the New York Metropolitan Region

Intrarenal Renin–Angiotensin System Involvement in the Pathogenesis of Chronic Progressive Nephropathy—Bridging the Informational Gap Between Disciplines

Role of ACE2 Gene Expression in Renin Angiotensin System and Its Importance in Covid-19: In Silico Approach

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