Microcirculation in Acute and Chronic Kidney Diseases

Zafrani, Lara; İnce, Can

doi:10.1053/j.ajkd.2015.06.019

Cited by 75 publications

(45 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Eventually, the excess deposition of ECM in interstitium extends distance between the capillaries and nearby nephrons, and then leads to endothelial dysfunction and peritubular microvascular rarefaction, this, in turn, aggravating hypoxia and forming a vicious circle. Together, these fibrogenic events conjunctly result in tissue destruction [13][14][15][16][17][18][19][20][21][22]. Renal fibrogenesis is a complex and dynamic process involved in almost all types of renal cells, during which myofibroblasts are considered as the determining cells.…”

Section: Hypoxia Promotes Tubulointerstitial Fibrosismentioning

confidence: 99%

Signalling pathways involved in hypoxia‐induced renal fibrosis

Liu

Ning

et al. 2017

J Cellular Molecular Medi

186

126

View full text Add to dashboard Cite

Renal fibrosis is the common pathological hallmark of progressive chronic kidney disease (CKD) with diverse aetiologies. Recent researches have highlighted the critical role of hypoxia during the development of renal fibrosis as a final common pathway in end‐stage kidney disease (ESKD), which joints the scientist's attention recently to exploit the molecular mechanism underlying hypoxia‐induced renal fibrogenesis. The scaring formation is a multilayered cellular response and involves the regulation of multiple hypoxia‐inducible signalling pathways and complex interactive networks. Therefore, this review will focus on the signalling pathways involved in hypoxia‐induced pathogenesis of interstitial fibrosis, including pathways mediated by HIF, TGF‐β, Notch, PKC/ERK, PI3K/Akt, NF‐κB, Ang II/ROS and microRNAs. Roles of molecules such as IL‐6, IL‐18, KIM‐1 and ADO are also reviewed. A comprehensive understanding of the roles that these hypoxia‐responsive signalling pathways and molecules play in the context of renal fibrosis will provide a foundation towards revealing the underlying mechanisms of progression of CKD and identifying novel therapeutic targets. In the future, promising new effective therapy against hypoxic effects may be successfully translated into the clinic to alleviate renal fibrosis and inhibit the progression of CKD.

show abstract

Section: Hypoxia Promotes Tubulointerstitial Fibrosismentioning

confidence: 99%

Signalling pathways involved in hypoxia‐induced renal fibrosis

Liu

Ning

et al. 2017

J Cellular Molecular Medi

186

126

View full text Add to dashboard Cite

show abstract

“…Several features are seen in the kidney regardless of the initiating insult and are known to be important for prognosis and progression to end stage renal disease. Microvascular loss occurs along with increased fibrosis, leading to increased relative hypoxia within the kidney and in particular within the outer medulla (21). This change is associated with and potentially related to a change in pericyte location and behavior, with a loss of pericyte-endothelial contact and pericyte migration to adopt a pro-fibrotic myofibroblast phenotype (22, 23), which then deposit interstitial collagen.…”

Section: Functional and Structural Changes Of Chronic Kidney Diseasementioning

confidence: 99%

Acute kidney injury and chronic kidney disease: From the laboratory to the clinic

Ferenbach

Bonventre

2016

Néphrologie & Thérapeutique

117

View full text Add to dashboard Cite

Chronic Kidney Disease and Acute Kidney Injury have traditionally been considered as separate entities with different etiologies. This view has changed in recent years, with chronic kidney disease recognized as a major risk factor for the development of new acute kidney injury, and acute kidney injury now accepted to lead to de novo or accelerated chronic and end stage kidney diseases. Patients with existing chronic kidney disease appear to be less able to mount a complete ‘adaptive’ repair after acute insults, and instead repair maladaptively, with accelerated fibrosis and rates of renal functional decline. This article reviews the epidemiological studies in man that have demonstrated the links between these two processes. We also examine clinical and experimental research in areas of importance to both acute and chronic disease: acute and chronic renal injury to the vasculature, the pericyte and leukocyte populations, the signaling pathways implicated in injury and repair, and the impact of cellular stress and increased levels of growth arrested and senescent cells. The importance and therapeutic potential raised by these processes for acute and chronic injury are discussed.

show abstract

“…Recent studies have identified persistent renal hypoxia as a key player in the pathogenesis of the AKI to CKD transition. 81,82 AKI has been shown to result in decreased expression of critical angiogenesis factors such as vascular endothelial growth factor (VEGF), as well as the detachment of supportive pericyte cells, leading to failure of endothelial cells to regenerate and to profound peritubular capillary rarefaction. This further exacerbates tissue hypoxia, and has three major downstream effects that promote tubulointerstitial fibrosis: (a) failure of tubule epithelial cells to regenerate and repair, (b) recruitment of inflammatory cells that secrete profibrotic cytokines, and (c) activation of fibroblasts.…”

Section: Aki To Ckd – Experimental Evidencementioning

confidence: 99%

Progression of chronic kidney disease after acute kidney injury

Devarajan

Jefferies

2016

Progress in Pediatric Cardiology

View full text Add to dashboard Cite

The incidence of chronic kidney disease (CKD) in children and adults is increasing. Cardiologists have become indispensable members of the care provider team for children with CKD. This is partly due to the high incidence of CKD in children and adults with congenital heart disease, with current estimates of 30–50%. In addition, the high incidence of acute kidney injury (AKI) due to cardiac dysfunction or following pediatric cardiac surgery that may progress to CKD is also well documented. It is now apparent that AKI and CKD are uniquely intertwined as interconnected syndromes. Furthermore, the well-known long-term cardiovascular morbidity and mortality associated with CKD require the joint attention of both nephrologists and cardiologists. Children with both congenital heart disease and CKD are increasingly surviving to adulthood, with synergistically negative medical, financial, and quality of life impact. An improved understanding of the epidemiology, mechanisms, early diagnosis, and preventive measures is of importance to cardiologists, nephrologists, scientists, economists, and policy makers alike. Herein, we report the current definitions, epidemiology, and complications of CKD in children, with an emphasis on children with congenital heart disease. We then focus on the clinical and experimental evidence for the progression of CKD after episodes of AKI commonly encountered in children with heart disease, and explore the role of novel biomarkers for the prediction of CKD progression.

show abstract

Microcirculation in Acute and Chronic Kidney Diseases

Cited by 75 publications

References 98 publications

Signalling pathways involved in hypoxia‐induced renal fibrosis

Signalling pathways involved in hypoxia‐induced renal fibrosis

Acute kidney injury and chronic kidney disease: From the laboratory to the clinic

Progression of chronic kidney disease after acute kidney injury

Contact Info

Product

Resources

About