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Nutrients
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Aminoacid Loss and Deregulation in Chronic Renal Disease and New...
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Aminoacid Loss and Deregulation in Chronic Renal Disease and New Protein Diet Strategies in Chronic Kidney Disease Patients

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: closed (1 November 2021) | Viewed by 5486

Special Issue Editor

Dr. Piergiorgio Bolasco

E-Mail Website
Guest Editor
Italian Society of Nephrology, Rome, Italy; Public Health Safeguard Institute of Sardinia, Cagliari, Italy.
Interests: chronic kidney disease; kidney stone pathologies; renal nutrition;
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In patients with advanced-stage Chronic Kidney Disease (stages 3b–5), the absorption and metabolism of amino acids is strongly influenced by the severe uremic dysbiosis in the intestinal microbiota. Moreover, in dialysis patients, there is further severe loss of nutrients that must be replaced using a mixture of amino acids and/or a diet rich in these fundamental substances. If a complete replacement therapy is not applied in conjunction with an adequate dietary caloric intake, these patients will suffer from progressive diminishing of lean mass, especially muscle volume, a condition known as Protein Energy Wasting and/or cachexia. Thus, it is necessary to develop new nutritional protocols for the reintegration of indispensable substances. In our opinion, the nutritional correction of the amino acid arrangement in chronic uremia is one of the most important factors in preventing nutritional decay.

For this Special Issue, we invite authors to submit relevant research and review articles on nutritional remedies for the severe nutritional disruption of amino acid metabolism in the uremic milieu of patients with Chronic Kidney Failure, particular those undergoing nutritional replacement dialytic treatment.

Dr. Piergiorgio Bolasco
Guest Editor

Keywords

  • amino acid metabolism
  • amino acid loss
  • Chronic Kidney Disease
  • dialysis

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Published Papers (2 papers)

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Research

19 pages, 696 KiB  
Article
Amino Acid Homeostasis and Fatigue in Chronic Hemodialysis Patients
by Adrian Post, Daan Kremer, Dion Groothof, Yvonne van der Veen, Pim de Blaauw, Jennifer van der Krogt, Ido P. Kema, Ralf Westerhuis, M. Rebecca Heiner-Fokkema, Stephan J. L. Bakker and Casper F. M. Franssen
Nutrients 2022, 14(14), 2810; https://doi.org/10.3390/nu14142810 - 8 Jul 2022
Cited by 5 | Viewed by 2490
Abstract
Patients dependent on chronic hemodialysis treatment are prone to malnutrition, at least in part due to insufficient nutrient intake, metabolic derangements, and chronic inflammation. Losses of amino acids during hemodialysis may be an important additional contributor. In this study, we assessed changes in [...] Read more.
Patients dependent on chronic hemodialysis treatment are prone to malnutrition, at least in part due to insufficient nutrient intake, metabolic derangements, and chronic inflammation. Losses of amino acids during hemodialysis may be an important additional contributor. In this study, we assessed changes in plasma amino acid concentrations during hemodialysis, quantified intradialytic amino acid losses, and investigated whether plasma amino acid concentrations and amino acid losses by hemodialysis and urinary excretion are associated with fatigue. The study included a total of 59 hemodialysis patients (65 ± 15 years, 63% male) and 33 healthy kidney donors as controls (54 ± 10 years, 45% male). Total plasma essential amino acid concentration before hemodialysis was lower in hemodialysis patients compared with controls (p = 0.006), while total non-essential amino acid concentration did not differ. Daily amino acid losses were 4.0 ± 1.3 g/24 h for hemodialysis patients and 0.6 ± 0.3 g/24 h for controls. Expressed as proportion of protein intake, daily amino acid losses of hemodialysis patients were 6.7 ± 2.4% of the total protein intake, compared to 0.7 ± 0.3% for controls (p < 0.001). Multivariable regression analyses demonstrated that hemodialysis efficacy (Kt/V) was the primary determinant of amino acid losses (Std. β = 0.51; p < 0.001). In logistic regression analyses, higher plasma proline concentrations were associated with higher odds of severe fatigue (OR (95% CI) per SD increment: 3.0 (1.3; 9.3); p = 0.03), while higher taurine concentrations were associated with lower odds of severe fatigue (OR (95% CI) per log2 increment: 0.3 (0.1; 0.7); p = 0.01). Similarly, higher daily taurine losses were also associated with lower odds of severe fatigue (OR (95% CI) per log2 increment: 0.64 (0.42; 0.93); p = 0.03). Lastly, a higher protein intake was associated with lower odds of severe fatigue (OR (95% CI) per SD increment: 0.2 (0.04; 0.5); p = 0.007). Future studies are warranted to investigate the mechanisms underlying these associations and investigate the potential of taurine supplementation. Full article
(This article belongs to the Special Issue Aminoacid Loss and Deregulation in Chronic Renal Disease and New Protein Diet Strategies in Chronic Kidney Disease Patients)
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18 pages, 300 KiB  
Article
Altered Amino Acid Metabolism in Patients with Cardiorenal Syndrome Type 2: Is It a Problem for Protein and Exercise Prescriptions?
by Roberto Aquilani, Roberto Maestri, Maurizia Dossena, Maria Teresa La Rovere, Daniela Buonocore, Federica Boschi and Manuela Verri
Nutrients 2021, 13(5), 1632; https://doi.org/10.3390/nu13051632 - 13 May 2021
Cited by 2 | Viewed by 2284
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Aminoacid Loss and Deregulation in Chronic Renal Disease and New Protein Diet Strategies in Chronic Kidney Disease Patients)
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