Uremic Toxicity: Urinary Indoxyl Sulfate is a Clinical Factor that Affects the Progression of Renal Failure

1999 ◽  
Vol 25 (1-2) ◽  
pp. 118-122 ◽  
Author(s):  
Toshimitsu Niwa ◽  
Isao Aoyama ◽  
Fumio Takayama ◽  
Saori Tsukushi ◽  
Takashi Miyazaki ◽  
...  
Keyword(s):  
Renal Failure ◽  
Indoxyl Sulfate ◽  
Clinical Factor ◽  
Progression Of Renal Failure

Progression of Renal Failure in Chronic Primary Glomerular Diseases

Nephron ◽  
1994 ◽  
Vol 68 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Ana Gonzalo ◽  
Araceli Gallego ◽  
Maite Rivera ◽  
Nieves Gallego ◽  
Joaquín Ortuño
Keyword(s):  
Renal Failure ◽  
Glomerular Diseases ◽  
Progression Of Renal Failure ◽  
Primary Glomerular Diseases

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.

Effects of Dietary Protein on the Progression of Renal Failure in the Fawn-Hooded Rat

Nephron ◽  
1990 ◽  
Vol 55 (2) ◽  
pp. 203-209 ◽  
Author(s):  
M.H. De Keijzer ◽  
A.P. Provoost
Keyword(s):  
Renal Failure ◽  
Dietary Protein ◽  
Progression Of Renal Failure

Epidemiology and chronic kidney disease as a cardiovascular risk factor

ESC CardioMed ◽  
2018 ◽  
pp. 979-981
Author(s):  
Stephan Segerer ◽  
Harald Seeger
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Fold Increase ◽  
Progression Of Renal Failure ◽  
Major Factors

Chronic kidney disease defined by an estimated glomerular filtration rate of less than 60 mL/min or the presence of albuminuria is present in about 10% of the European populations. The risk increases with age, arterial hypertension, and diabetes. Both aspects—reduced estimated glomerular filtration rate, and albuminuria—are major factors associated with the progression of renal failure, cardiovascular events, and all-cause mortality. Patients on dialysis have a 10- to 20-fold increase in the cardiovascular event rate. Furthermore, heart failure and sudden cardiac death are associated with the severity of renal failure.

Dietary Protein Loading and the Oral Adsorbent AST-120 in the Progression of Chronic Renal Failure in the Rat

1992 ◽  
Vol 15 (12) ◽  
pp. 708-714 ◽  
Author(s):  
K. Kumano ◽  
T. Sakai ◽  
S. Kuwao ◽  
M. Ise
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Dietary Protein ◽  
Diet Group ◽  
Normal Diet ◽  
High Protein ◽  
Renal Infarction ◽  
Protein Loading ◽  
Progression Of Renal Failure ◽  
Oral Adsorbent

Excess protein intake enhances the progression of renal failure. The oral carbonaceous adsorbent, AST-120, was found experimentally and clinically to retard the progression of renal failure. This study was designed to determine whether deterioration of renal function by dietary protein loading can be prevented or mitigated by this oral adsorbent. Rats with uremia induced by partial renal infarction were fed a normal or high-protein diet for 70 days with or without AST-120, in which the inorganic phosphate content was adjusted to the same level. The survival rate deteriorated with the high dietary protein, but was improved from 30% to 100% with AST-120. Dietary protein loading reduced renal function, based on creatinine clearance. AST-120 improved renal function and renal histopathology not only in the normal diet group but in the high-protein group as well. The progression of renal failure induced by protein loading is thus shown to be prevented by oral AST-120. The mechanism for its action remains to be clarified.

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