Injury and regeneration in renal aging

2022 ◽  
pp. 281-301
Author(s):  
Janka Babickova ◽  
Hai-Chun Yang ◽  
Agnes B. Fogo
Keyword(s):  
Renal Aging

MO403ACUTE KIDNEY INJURY IN ELDERLY: EPIDEMIOLOGICAL, CLINICAL AND ETIOLOGICAL FEATURES

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Mouna Malki abidi ◽  
Rajaa Aoudia ◽  
Soumaya Chargui ◽  
Imen Gorsane ◽  
Mouna Jerbi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Injury ◽  
The Elderly ◽  
Major Interest ◽  
The Mean ◽  
Renal Aging ◽  
End Stage ◽  
Iatrogenic Origin

Abstract Background and Aims Acute kidney injury (AKI) is common in the elderly due to physiologic renal aging and underlying pathologies. Few studies focused on AKI in Tunisian elderly. The aim of our study was to highlight the epidemiological, clinical, etiological, therapeutic, and progressive characteristics of AKI in elderly. Method We conducted a descriptive retrospective study of AKI in patients admitted to our department over a period of 04 years from 01/01/2014 to 31/12/2017. Results We collected 40 patients including 25 women and 15 men with a sex ratio of 1.66. The mean age was 74 [65-87] years. We noted the presence of pre-existing chronic kidney disease in 58% of cases, diabetes in 50% of cases and hypertension in 73% of cases. Polypharmacy was found in 40% of cases. AKI was symptomatic in 80% of cases and found on a routine check-up in 20% of cases. Mean creatinine was 612+/-334 µmol/l. AKI was pre-renal in 37% and parenchymal in 63% of cases. Iatrogenic origin was found in 33% of cases. Renal biopsy was performed for diagnostic purposes in 6 cases. Haemodialysis was necessary in 50% of cases. Etiopathogenic treatment was initiated in 73% of cases. Intra-hospital mortality was 10%, recovery of renal function (RF) was partial in 40 % of cases and total in 20 % of cases. Follow-up time was 16 +/- 23.2 months. And at the last news, recovery of renal function (RF) was partial in 7 cases and total in 10 cases, 6 patients kept a chronic renal failure (CRF), among them 3 cases had and end-stage of CRF. Conclusion AKI is a frequent pathology in the elderly and its severity is linked to mortality and the transition to chronicity. Iatrogenic causes are frequent and preventable in this population, hence the major interest of prevention.

scholarly journals Vascular and renal telomere shortening in mice exposed to chronic intermittent hypoxia

2021 ◽  
Author(s):  
Mohammad Badran ◽  
Bisher Abuyassin ◽  
Najib Ayas ◽  
Don D. Sin ◽  
Ismail Laher
Keyword(s):  
Obstructive Sleep Apnea ◽  
Chronic Condition ◽  
Intermittent Hypoxia ◽  
Kidney Diseases ◽  
Chronic Intermittent Hypoxia ◽  
Telomere Shortening ◽  
Chronic Kidney Diseases ◽  
Biomarkers Of Aging ◽  
Obstructive Sleep ◽  
Renal Aging

AbstractObstructive sleep apnea (OSA) is a chronic condition characterized by chronic intermittent hypoxia (IH) and is associated with cardiovascular (CVD) and chronic kidney diseases (CKD). There is increased biomarkers of aging, such as telomere shortening, in patients with OSA. We assessed telomere lengths in aortic and renal tissues from mice exposed to 8 weeks of IH using a PCR protocol, and demonstrate significant telomere shortening in both tissues. This data indicates that IH, a hallmark of OSA, can accelerate vascular and renal aging that may contribute to OSA-induced CVD and CKD

scholarly journals Plasma and urinary p21: potential biomarkers of AKI and renal aging

2018 ◽  
Vol 315 (5) ◽  
pp. F1329-F1335 ◽  
Author(s):  
Ali C. Johnson ◽  
Richard A. Zager
Keyword(s):  
Aging Process ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Proximal Tubules ◽  
Renal Tubules ◽  
Protein Levels ◽  
Cycle Arrest ◽  
Early Injury ◽  
Renal Aging ◽  
Potential Biomarkers

p21 is upregulated in renal tubules in response to acute kidney injury ( AKI). and localizes in the nucleus, where it induces cell cycle arrest (CCA). These events can mitigate early injury but can also facilitate the onset of the degenerative cell senescence/“aging” process. Hence, we asked the following: 1) can AKI-induced p21 upregulation be gauged by plasma and/or urinary p21 assay; 2) might p21 serve as an AKI/CCA biomarker; and 3) does p21 accumulate during normal renal aging, and might plasma p21 reflect this process? Mice were subjected to either ischemia-reperfusion (I/R) or nephotoxic (maleate) AKI. Renal cortical p21 expression (protein, mRNA) was assessed 2–18 h later and contrasted with plasma/urine p21 concentrations (ELISA). p21 mRNA/protein levels were also measured in aging mice (2, 12, 24 mo). AKI induced marked, progressive, increases in renal cortical p21 mRNA and protein levels. These changes were marked by acute (within 2–4 h) and profound increases (up to 200×) in both plasma and urine p21 concentrations. Renal I/R also activated p21 gene expression in extrarenal organs (heart, brain), consistent with so-called “organ cross talk”. p21 efflux from damaged cells was confirmed with studies of hypoxia-injured, isolated proximal tubules. Aging was associated with progressive renal cortical p21 expression, which correlated ( r, 0.83) with rising plasma p21 concentrations. We concluded that 1) during AKI, renal p21 increases can be gauged by either plasma or urine p21 assay, serving as potentially useful AKI/CCA biomarkers; 2) AKI can activate p21 in extrarenal organs; and 3) plasma p21 levels may provide an index of the renal/systemic aging process.

Genome-wide expression profile associated with renal aging

2010 ◽  
Vol 27 ◽  
pp. S35
Author(s):  
S.J. Noppert ◽  
M. Rudnicki ◽  
J. Enrich ◽  
P. Perco ◽  
I. Muehlberger ◽  
...  
Keyword(s):  
Expression Profile ◽  
Genome Wide ◽  
Renal Aging ◽  
Genome Wide Expression

scholarly journals Fibrosis and renal aging

2014 ◽  
Vol 4 (1) ◽  
pp. 75-78 ◽  
Author(s):  
Hai-Chun Yang ◽  
Agnes B. Fogo
Keyword(s):  
Renal Aging

Renal aging in WKY rats: Changes in Na+,K+-ATPase function and oxidative stress

2010 ◽  
Vol 45 (12) ◽  
pp. 977-983 ◽  
Author(s):  
E. Silva ◽  
V. Pinto ◽  
S. Simão ◽  
M.P. Serrão ◽  
J. Afonso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wky Rats ◽  
Renal Aging ◽  
And Oxidative Stress

scholarly journals Quantitative analysis of the renal aging in rats. Stereological study

2016 ◽  
Vol 31 (5) ◽  
pp. 346-352 ◽  
Author(s):  
Eduardo Felippe Melchioretto ◽  
Marcelo Zeni ◽  
Djanira Aparecida da Luz Veronez ◽  
Eduardo Lopes Martins Filho ◽  
Rogério de Fraga
Keyword(s):  
Quantitative Analysis ◽  
Renal Aging

scholarly journals Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage

2020 ◽  
Vol 11 ◽  
Author(s):  
Rossana Franzin ◽  
Alessandra Stasi ◽  
Marco Fiorentino ◽  
Giovanni Stallone ◽  
Vincenzo Cantaluppi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Complement System ◽  
Kidney Diseases ◽  
Critical Role ◽  
Graft Function ◽  
Kidney Injury ◽  
Increased Risk ◽  
Wide Range ◽  
Renal Aging

The aberrant activation of complement system in several kidney diseases suggests that this pillar of innate immunity has a critical role in the pathophysiology of renal damage of different etiologies. A growing body of experimental evidence indicates that complement activation contributes to the pathogenesis of acute kidney injury (AKI) such as delayed graft function (DGF) in transplant patients. AKI is characterized by the rapid loss of the kidney’s excretory function and is a complex syndrome currently lacking a specific medical treatment to arrest or attenuate progression in chronic kidney disease (CKD). Recent evidence suggests that independently from the initial trigger (i.e., sepsis or ischemia/reperfusions injury), an episode of AKI is strongly associated with an increased risk of subsequent CKD. The AKI-to-CKD transition may involve a wide range of mechanisms including scar-forming myofibroblasts generated from different sources, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of epigenetic, gene, and protein alterations leading to common final signaling pathways [i.e., transforming growth factor beta (TGF-β), p16ink4a, Wnt/β-catenin pathway] involved in renal aging. Research in recent years has revealed that several stressors or complications such as rejection after renal transplantation can lead to accelerated renal aging with detrimental effects with the establishment of chronic proinflammatory cellular phenotypes within the kidney. Despite a greater understanding of these mechanisms, the role of complement system in the context of the AKI-to-CKD transition and renal inflammaging is still poorly explored. The purpose of this review is to summarize recent findings describing the role of complement in AKI-to-CKD transition. We will also address how and when complement inhibitors might be used to prevent AKI and CKD progression, therefore improving graft function.

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