Altered Amino Acid Metabolism in Patients with Cardiorenal Syndrome Type 2: Is It a Problem for Protein and Exercise Prescriptions?

• Published in: Nutrients Vol. 13; no. 5; p. 1632
• Main Authors: Aquilani, Roberto, Maestri, Roberto, Dossena, Maurizia, La Rovere, Maria Teresa, Buonocore, Daniela, Boschi, Federica, Verri, Manuela
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01.05.2021; MDPI
• Subjects: Amino acids; cardiorenal syndrome; Care and treatment; Chronic kidney failure; Creatinine; Epidermal growth factor receptors; Exercise; Exercise therapy; Glomerular filtration rate; Heart; Heart failure; Hemodynamics; Hypothesis testing; Kidney diseases; Kidneys; Low concentrations; Medical prognosis; Medical research; Medicine, Experimental; Metabolism; multiorgan impact; Muscles; Musculoskeletal system; Nitrogen; Physical fitness; Physiological aspects; Plasma; plasma amino acids; practical implications; Proteins; Transplantation
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu13051632

The goal of this retrospective study was to document any alterations in plasma amino acids (AAs) in subjects with cardiorenal syndrome type 2 (CRS 2). We analyzed data from sixteen patients with CRS 2 and eight healthy subjects (control group, C), whose plasma arterial (A) and venous (V) AA concentrations had been measured. Compared to C, the group of CRS 2 patients showed significant reductions by more than 90% in A (p < 0.01) and V (p < 0.01) individual AAs, whereas negative A-V differences that indicated a net muscle AA release (muscle hypercatabolism) were found in 59% of CRS 2 patients (p < 0.03). No significant differences in plasma A and V AA concentrations nor in A-V differences were found between patients with mild kidney damage (N = 5; estimated glomerular filtration rate, eGFR ≥ 60 mL/min/1.73 m2) and patients with moderate-severe kidney damage (N = 11; eGFR < 60 mL/min/1.73 m2). Several plasma arterial AAs correlated with hemodynamic variables, but not with GFR. The study showed that patients with CRS 2 had very low concentrations of circulating AAs, independent of the degree of GFR damage.