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
Toxins ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 50
Author(s):  
Satoshi Kumakura ◽  
Emiko Sato ◽  
Akiyo Sekimoto ◽  
Yamato Hashizume ◽  
Shu Yamakage ◽  
...  

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.


Nephron ◽  
1990 ◽  
Vol 55 (2) ◽  
pp. 203-209 ◽  
Author(s):  
M.H. De Keijzer ◽  
A.P. Provoost

ESC CardioMed ◽  
2018 ◽  
pp. 979-981
Author(s):  
Stephan Segerer ◽  
Harald Seeger

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.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Roxana Bury ◽  
Irene Agraz ◽  
Maria Jose Soler Romeo ◽  
Clara Garcia Carro ◽  
Eugenia Espinel ◽  
...  

Abstract Background and Aims Biosimilar drugs need to prove similar effectiveness to the brand name drug, in order to have their authorization from regulatory agencies. Rituximab initially developed as a treatment for non-Hodgkin lymphoma, is used as a therapeutic alternative to several autoimmune diseases, including primary glomerular diseases. The objective of this study is to observe if there were differences in terms of effects measured in proteinuria and relapse episodes between rituximab brand versus biosimilar in primary glomerular diseases Method This is a retrospective descriptive study that included patients receiving rituximab brand or biosimilar for the first time between March 2018 to March 2019, collecting information from the reported medical records with primary glomerulopathy were included. The collected laboratory data included creatinine, proteinuria, leukocyte and lymphocyte count before (0-60 days before) and after (0-60 days after) administration of rituximab. Results A total of 19 patients with primary glomerulopathy were included. Six patients (59-years-old (26-74); 50% female) with baseline 6.52±2.00x10^9/L leucocyte count, 2.28±1.10x10^9/L lymphocyte count, 1.63±1.04 mg/dL creatinine and 6.84±3.36g/24h proteinuria, were treated with biosimilar-rituximab. Thirteen patients (58-years-old (25-81); 30% female) with baseline 9.80±4.62x10^9/L leucocyte count, 1.92±1.13 x10^9/L lymphocyte count, 1.61±0.85 mg/dL creatinine and 5.81±4.55 g/24h proteinuria, were treated with brand-rituximab. After the rituximab administration, these values were 6.13±1.94x10^9/L leucocyte count, 1.30±0.59x10^9/L lymphocyte count, 1.16±1.19 mg/dL creatinine, 3.29±0.58g/24h and proteinuria for the biosimilar group; and 8.77±3.78x10^9/L leucocyte count, 1.67±1.13x10^9/L lymphocyte count, 1.56±1.19 mg/dL creatinine and 3.36±2.20g/24h proteinuria for the brand group. After rituximab administration CD19+ lymphocytes become negative in both groups (5/5 for the biosimilar group; 6/6 for the brand group). There were 2 total remissions, 1 partial remission and 3 without response with the biosimilar and 1 total remission, 5 partial remissions and 7 without response with the rituximab brand. Biosimilar was well tolerated in 6/6 patients and Rituximab brand infection did not develop was well tolerated in 11/13 patients and 4/13 patients showed an episode of infection. No statistically significant results were observed for the response to treatment between both groups. Conclusion The biosimilar shows a similar profile in terms of proteinuria and remissions against rituximab mark in the reported follow-up period, however our study is limited since it has a small sample, so a larger study is necessary to demonstrate these results with statistical significance


1992 ◽  
Vol 15 (12) ◽  
pp. 708-714 ◽  
Author(s):  
K. Kumano ◽  
T. Sakai ◽  
S. Kuwao ◽  
M. Ise

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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