scholarly journals Role of uromodulin and complement activation in the progression of kidney disease

2021 ◽  
Vol 22 (6) ◽  
Author(s):  
Fei Shen ◽  
Maojing Liu ◽  
Fei Pei ◽  
Li Yu ◽  
Xiangdong Yang
Keyword(s):  
Kidney Disease ◽  
Complement Activation ◽  
Progression Of Kidney Disease

scholarly journals Nicotinamide Attenuates the Progression of Renal Failure in a Mouse Model of Adenine-Induced Chronic Kidney Disease

Toxins ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 50
Author(s):  
Satoshi Kumakura ◽  
Emiko Sato ◽  
Akiyo Sekimoto ◽  
Yamato Hashizume ◽  
Shu Yamakage ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Kidney Disease ◽  
Mouse Model ◽  
Metabolic Pathways ◽  
Krebs Cycle ◽  
Inflammatory Reactions ◽  
Progression Of Kidney Disease ◽  
Progression Of Renal Failure

Nicotinamide adenine dinucleotide (NAD+) supplies energy for deoxidation and anti-inflammatory reactions fostering the production of adenosine triphosphate (ATP). The kidney is an essential regulator of body fluids through the excretion of numerous metabolites. Chronic kidney disease (CKD) leads to the accumulation of uremic toxins, which induces chronic inflammation. In this study, the role of NAD+ in kidney disease was investigated through the supplementation of nicotinamide (Nam), a precursor of NAD+, to an adenine-induced CKD mouse model. Nam supplementation reduced kidney inflammation and fibrosis and, therefore, prevented the progression of kidney disease. Notably, Nam supplementation also attenuated the accumulation of glycolysis and Krebs cycle metabolites that occurs in renal failure. These effects were due to increased NAD+ supply, which accelerated NAD+-consuming metabolic pathways. Our study suggests that Nam administration may be a novel therapeutic approach for CKD prevention.

scholarly journals Role of renal urothelium in the development and progression of kidney disease

2016 ◽  
Vol 32 (4) ◽  
pp. 557-564 ◽  
Author(s):  
Ashley R. Carpenter ◽  
Kirk M. McHugh
Keyword(s):  
Kidney Disease ◽  
Progression Of Kidney Disease

scholarly journals Role of IL-10 in the progression of kidney disease

2013 ◽  
Vol 3 (4) ◽  
pp. 91 ◽  
Author(s):  
Inna Sinuani ◽  
Ilia Beberashvili ◽  
Zhan Averbukh ◽  
Judith Sandbank
Keyword(s):  
Kidney Disease ◽  
Progression Of Kidney Disease

scholarly journals Targeting STAT3 signaling in kidney disease

2019 ◽  
Vol 316 (6) ◽  
pp. F1151-F1161 ◽  
Author(s):  
Jesse Pace ◽  
Praharshasai Paladugu ◽  
Bhaskar Das ◽  
John C. He ◽  
Sandeep K. Mallipattu
Keyword(s):  
Kidney Disease ◽  
Kidney Diseases ◽  
Janus Kinase ◽  
Disease Models ◽  
Pharmacological Inhibition ◽  
Stat3 Signaling ◽  
Stat Signaling ◽  
Progression Of Kidney Disease ◽  
Central Member

The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway is a multifaceted transduction system that regulates cellular responses to incoming signaling ligands. STAT3 is a central member of the JAK/STAT signaling cascade and has long been recognized for its increased transcriptional activity in cancers and autoimmune disorders but has only recently been in the spotlight for its role in the progression of kidney disease. Although genetic knockout and manipulation studies have demonstrated the salutary benefits of inhibiting STAT3 activity in several kidney disease models, pharmacological inhibition has yet to make it to the clinical forefront. In recent years, significant effort has been aimed at suppressing STAT3 activation for treatment of cancers, which has led to the development of a wide variety of STAT3 inhibitors, but only a handful have been tested in kidney disease models. Here, we review the detrimental role of dysregulated STAT3 activation in a variety of kidney diseases and the current progress in the treatment of kidney diseases with pharmacological inhibition of STAT3 activity.

Potential effect of pharmaceutical care to improve outcomes in patients with chronic kidney disease-mineral bone disorder in Sulaimani dialysis centers

2020 ◽  
pp. 82-94
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Pharmaceutical Care ◽  
Biochemical Parameters ◽  
Positive Impact ◽  
Potential Effect ◽  
Care Group ◽  
Mineral Bone Disorder ◽  
Bone Disorder

Objective: the present study was aimed to evaluate the role of pharmaceutical services in improving the outcome of mineral bone disorder in patients with advanced chronic kidney disease. Methodology: One hundred and twenty patients with chronic kidney disease-mineral bone disorder (CKD-MBD) screened for eligibility, seventy-six patients enrolled in the study and randomly allocated into two groups: pharmaceutical care and usual care, both groups interviewed by the pharmacist using specific questionnaire for assessing the quality of life (QoL). All the drug related problems (DRPs) including drug-drug interactions (DDIs) were recorded by the pharmacist. Blood samples were collected and utilized for analyzing the levels of vitamin D, phosphorous, calcium, albumin and parathyroid hormone at baseline and three months after. The pharmaceutical care group received all the educations about their medications and how to minimize DRPs; improve the QoL. Additionally, the pharmaceutical intervention included correcting the biochemical parameters. Results: Pharmaceutical care significantly improved patients QoL and minimized DRPs and DDIs. It was also effective in improving the biochemical parameters. Conclusion: Pharmaceutical care has a positive impact on improving the outcome of patients with CKD-MBD through attenuating DRPs, improving the biochemical parameters and the QoL.

MOLECULAR ASPECTS OF SARCOPENIA PATHOGENESIS IN CHRONOC KIDNEY DISEASE: INTEGRATED ROLE OF mTOR

2018 ◽  
Vol 22 (5) ◽  
pp. 9-16 ◽  
Author(s):  
M. Z. Gasanov
Keyword(s):  
Kidney Disease ◽  
Muscle Mass ◽  
Protein Metabolism ◽  
Mammalian Target Of Rapamycin ◽  
Healthy Person ◽  
Scientific Review ◽  
Cytoskeleton Organization ◽  
Molecular Aspects ◽  
End Stage

In recent decades, the main pathogenetic mechanisms for maintaining muscle mass and strength have been discovered. Most of the scientific papers on the molecular aspects of the  pathogenesis of sarcopenia were focused on the Akt-signaling  pathway. The subject of the study were people of elderly and senile  age, immobilized patients, patients with CKD 1-4 stages, animals. However, recently more attention has been paid to the role  of protein – the mammalian target of rapamycin mTOR. It seems to be a key link in the control of muscle mass and is a promising  marker in understanding the mechanisms of the pathogenesis of  sarcopenia. Its importance in protein metabolism in patients with  end stage kidney disease is not studied and requires further research. The presented scientific review contains  information on the role of mTOR and its components – mTORC1 and mTORC2 in maintaining muscle mass and strength in a healthy  person and in the formation of sarcopenia in patients with CKD. The  general aid of mTORC1 complex is regulation of protein production  which is necessary for cell growth and differentiation. mTORC2  complex functions are not enough studied. It is established that it  plays important role in such biological processes as cytoskeleton  organization, intracellular homeostasis maintaining, so it provides  cell resistance and cell survivability in negative external and internal  impulses. mTOR protein can be considered as promising molecular  marker in diagnostics of protein metabolism early disturbances in  patients with CKD and also as additory factor of sarcopenia severity assessment.

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