Details

Autor(en) / Beteiligte

• Reyes, Loretta Z
• Winterberg, Pamela D
• George, Roshan Punnoose
• Kelleman, Michael
• Harris, Frank
• Jo, Hanjoong
• Brown, Lou Ann S
• Morris, Claudia R

Titel

Arginine Dysregulation and Myocardial Dysfunction in a Mouse Model and Children with Chronic Kidney Disease

Ist Teil von

• Nutrients, 2023-04, Vol.15 (9), p.2162

Ort / Verlag

Switzerland: MDPI AG

Erscheinungsjahr

2023

Link zum Volltext

Quelle

EZB Electronic Journals Library

Beschreibungen/Notizen

• Cardiovascular disease is the leading cause of death in chronic kidney disease (CKD). Arginine, the endogenous precursor for nitric oxide synthesis, is produced in the kidneys. Arginine bioavailability contributes to endothelial and myocardial dysfunction in CKD. Plasma from 129X1/SvJ mice with and without CKD (5/6th nephrectomy), and banked plasma from children with and without CKD were analyzed for amino acids involved in arginine metabolism, ADMA, and arginase activity. Echocardiographic measures of myocardial function were compared with plasma analytes. In a separate experiment, a non-specific arginase inhibitor was administered to mice with and without CKD. Plasma citrulline and glutamine concentrations correlated with multiple measures of myocardial dysfunction. Plasma arginase activity was significantly increased in CKD mice at 16 weeks vs. 8 weeks ( = 0.002) and ventricular strain improved after arginase inhibition in mice with CKD ( = 0.03). In children on dialysis, arginase activity was significantly increased vs. healthy controls ( = 0.04). Increasing ADMA correlated with increasing RWT in children with CKD (r = 0.54; = 0.003). In a mouse model, and children, with CKD, arginine dysregulation correlates with myocardial dysfunction.