Steamed Panax notoginseng attenuates renal anemia in an adenine-induced mouse model of chronic kidney disease

2022 ◽  
pp. 114941
Author(s):  
Min Gao ◽  
Zejun Zhang ◽  
Yiming Zhang ◽  
Minghui Li ◽  
Xiaoyan Che ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mouse Model ◽  
Panax Notoginseng ◽  
Renal Anemia

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.

SP344THE EFFICACY AND SAFETY OF BCD-131 IN TREATMENT OF RENAL ANEMIA IN CHRONIC KIDNEY DISEASE

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Maria Morozova ◽  
Daria Bolsun ◽  
Arina Zinkina-Orihan ◽  
Yulia Linkova ◽  
Roman Ivanov
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Anemia ◽  
Efficacy And Safety

scholarly journals FO001INSULIN SECRETORY DEFECT IN A MOUSE MODEL OF CHRONIC KIDNEY DISEASE

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii1-iii1
Author(s):  
Laetitia Koppe ◽  
Elsa Nyam ◽  
Valentine Moulle ◽  
Vincent Poitout
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mouse Model

scholarly journals Serum hepcidin-25 levels predict the progression of renal anemia in patients with non-dialysis chronic kidney disease

2012 ◽  
Vol 27 (12) ◽  
pp. 4378-4385 ◽  
Author(s):  
K. Niihata ◽  
N. Tomosugi ◽  
T. Uehata ◽  
T. Shoji ◽  
K. Mitsumoto ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Anemia ◽  
Serum Hepcidin

scholarly journals Superoxide and hydrogen peroxide counterregulate myogenic contractions in renal afferent arterioles from a mouse model of chronic kidney disease

2017 ◽  
Vol 92 (3) ◽  
pp. 625-633 ◽  
Author(s):  
Lingli Li ◽  
En Yin Lai ◽  
Zaiming Luo ◽  
Glenn Solis ◽  
Kathy K. Griendling ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Hydrogen Peroxide ◽  
Kidney Disease ◽  
Mouse Model ◽  
Afferent Arterioles

P1751THE GUANYLATE CYCLASE C AGONIST LINACLOTIDE LIMITS PROGRESSION TO RENAL FIBROSIS AND IMPROVE RENAL FUNCTION IN MOUSE MODEL OF CHRONIC KIDNEY DISEASE AFTER ISCHEMIA-REPERFUSION INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yuki Nakayama ◽  
Naohito Isoyama ◽  
Kimihiko Nakamura ◽  
Toshiya Hiroyoshi ◽  
Kouki Fujikawa ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Renal Transplantation ◽  
Kidney Disease ◽  
Mouse Model ◽  
Guanylate Cyclase ◽  
Renal Fibrosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Guanylate Cyclase C

Abstract Background and Aims Renal ischemia-reperfusion injury (IRI) is a clinically significant condition that leads to acute kidney injury (AKI). AKI is followed by tissue repair characterized by collagen deposition and fibrosis which ultimately results in progression to chronic kidney disease (CKD). Especially in renal transplantation, the degree of IRI has directly led to poor long-term graft survival. Trimethylamine-N-oxide (TMAO), a hepatic metabolic product of trimethylamine generated from dietary phosphatidylcholine, has been linked with progression of CKD. Linaclotide, a guanylate cyclase C agonist, has been reported decrease the plasma levels of TMAO. We investigated whether the reduction of TMAO by linaclotide protect renal function after IRI using an experimental mouse model. Method Linaclotide (100μg/kg) was administered for 2weeks before IRI and continued for 2weeks after IRI. After 2weeks since IRI, the renal function was evaluated by serum creatinine level and removed kidneys sections were performed Azan stain to evaluate the level of fibrosis. Results The administration of linaclotide before IRI significantly improved renal function. (Fig.1) Histological examination of kidneys showed linaclotide limits to expand fibrosis area after I/R injury. (Fig.2) Conclusion The reduction of TMAO by linaclotide before renal IRI could prevent renal fibrosis and improve renal function. Linaclotide may be useful for the patient expected to suffer renal IRI for example renal transplantation and partial nephrectomy. Fig2

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