Abstract
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.
Highlights
We re-analyzed the data from chronic heart failure (CHF) patients who had participated in a previous study on Plasma Amino Acid Abnormalities [10]
In healthy C, in the current study, we considered the amino acids (AAs) ornithine, which had not been considered in the previous study [10], as this AA is a by-product of the urea cycle; we did not consider the AA taurine [10] because it was not available in cardiorenal syndrome type 2 (CRS 2) patients’ venous blood samples
The study found that patients with cardiorenal syndrome (CRS) 2 had low arterial and venous plasma amino acid (PAA) concentrations, even though these metabolic substrates were excessively released by skeletal muscle tissue
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The complication of chronic heart failure (CHF) with chronic kidney disease (CKD). Identifies the cardiorenal syndrome (CRS) which is classified as CRS type 2 (CRS 2) [1,2]. The development of CKD in the CHF setting amplifies the clinical difficulties in managing volume overload, using mechanical circulatory support in a cardiac transplantation [6]. Cachexia and physical deconditioning, which are three independent risk factors of survival and functional prognosis in CHF [7,8,9], might be aggravated. The development of renal failure reduces survival, even in patients with preserved left ventricular ejection fraction (LVEF) [3]
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