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Emerging Challenges in Oral Trials: Is Amino Acid Supplementation Beneficial in Replacing Amino Acid Losses Incurred During Haemodialysis?

Submitted:

08 September 2026

Posted:

09 September 2026

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Abstract
Introduction: Patients on a thrice-weekly haemodialysis (TWH) maintenance schedule require a protein intake of at least 1.0-1.2 g/kg, providing 30-35 Kcal/kg. The mean age of patients on TWH routinely exceeds the age of 70, with more than 25% of patients over the age of 80. It is widely acknowledged that comorbid conditions and anorexia frequently hamper protein and calorie intake in the elderly, thus resulting in the onset of sarcopenia and/or Protein Energy Wasting (PEW). These conditions are further complicated by the massive loss of amino acids (AAs) in dialysate caused by the diffusive-convective mechanisms routinely used in TWH. Materials and Methods: A review of the available literature was performed to identify trials focussed on the replacement of amino acids to replace AA losses incurred following the use of extracorporeal treatments such as haemodialysis (HD) and haemodiafiltration (HDF), and studies adopting oral amino acid replacement protocols subsequently extrapolated and examined. The authors moreover intended to highlight how procedures developed in recent years had evolved, with the aim of identifying novel and better-tailored mixtures of free amino acids (FAAs) capable of yielding additional benefits. Results: Literature reports relating to patients on TWH who receive amino acid supplementation to replace annual AA losses that, depending on the type of extracorporeal method used, potentially exceed 1.0-1.5 Kg/year, are currently considerably limited. More recent papers describe the main mechanisms of action of amino acid mixes capable of affording a series of significant results: improvement of anaemia and cardiac performance and a beneficial effect on the percentage of muscle mass and metabolic and nutritional status resulting from enhanced patient compliance. Conclusions: We hypothesize that supplementation using novel mixes of FAAs may slow down the inevitable progression of sarcopenia and/or PEW by replacing the severe haemodialysis-induced amino acid deficit and eliciting markedly positive metabolic and clinical effects.
Keywords: 
hemodialysis amino acid loss
;  
amino acids oral replacement
Subject: 
Biology and Life Sciences  -   Food Science and Technology

Introduction

Low-protein dietary protocols (0.4 – 0.6 g/kg/day) with a calorie intake of at least 25-30 kcal/kg/day have been used for decades in the conservative management of Chronic Kidney Disease (CKD) to slow down progressive deterioration of the disease from CKD3b to End Stage Failure, particularly in the elderly and frail, thus preventing the rapid progression of CKD and need for dialysis [1,2]. A completely different scenario is however encountered with patients undergoing TWH who, in order to prevent malnutrition, need to ensure a protein intake of at least 1.2 g/kg/day with a provision of at least 30-35 kcal/kg/day [3]. The availability and anabolic use of amino acids, already reduced due to the frequent onset of hypercatabolism elicited by the presence of a series of comorbidities, is further exacerbated by a major dialysis-induced loss of AAs [4]. All AAs are low molecular weight molecules (ranging from 89.1Da of alanine to 204.2 Da of tryptophan) which readily pass through the dialysis membrane, thus producing huge losses in spent dialysate caused by both diffusive concentration gradient and convection/ultrafiltration in the presence of high-flux haemodialysis membranes and high ultrafiltration gradients at varying levels of transmembrane pressure [5,6]. Whilst haemodialysis-associated AAs losses were first reported at the end of the 1970s [7], it was only towards the early 2000s that the scientific literature started to report how major AA losses during TWH exerted a negative effect on nutritional status and preservation of fat and muscle mass, and anaemia, thus adding to the growing awareness of the need to replace AAs losses in both patients with an adequate nutritional status and, in particular, frail patients at early or advanced stages of malnutrition. Cognisant of the quality and quantity of AAs lost and their metabolic fate [4,5], research studies focussed on developing targeted FAA mixes [8,9,10,11,12,13]. The studies undertaken confirmed remarkably high losses of both essential (EAAs) and non-essential amino acids (NEAAs), as well as a series of so-called conditionally essential AAs (arginine, cysteine, glutamine, glycine, proline and tyrosine) [5]. In more advanced cases of sarcopenia detected in the context of TWH, AAs supplementation may be administered parenterally during the haemodialysis session with calories largely comprised of intradialytic parenteral infusions of glucose. However, the influx of high amounts of AAs is largely invalidated by the high plasma levels reached following parenteral administration, with high AAs concentrations not only exceeding intra-cellular absorption capacity, but particularly producing a high plasma/dialysate concentration gradient with consequent increased elimination of AAs in spent dialysate (up to double the amount of AAs infused), thus hindering an adequate nutritional and clinical outcome [14]. This review is focussed on studies based on the oral administration of an amino acid supplement, potentially representing a long-term “buffer” therapeutic option aimed at preserving a metabolic and nutritional steady state for as long as possible, particularly in the elderly. A search of the available literature was performed to evaluate the results obtained in studies using a range of oral AAs formulations, taking into account study design, safety, effects on other organs and apparatus and patient adherence to the protocols adopted.

Methods

When reading this review, it is important to consider that all patients recruited for the selected studies displayed good nutritional status, as defined by the KDIGO guidelines [3], taking into account protocols based on the sole oral administration of a range of different products and mixes of AAs indicated for use in patients on TWH, and excluding the concurrent use of other parenterally administered products. The studies selected were defined as focussing on either the treatment of a group of patients with amino acids (TG) or a control group receiving no treatment and/or placebo (CG). The main aim of the study was to assess the overall number of patients recruited to the various studies, and to determine, where available, the following parameters: age of the population studied, extracorporeal dialysis method adopted, study duration, prescribed calorie and protein intake, type of products or oral mixes in terms of quality and quantity of AAs, amino acid losses incurred at each dialysis session and per year, blood chemistry, clinical and nutritional findings, Above all, adherence to the prescribed AA supplementation is important, including strict compliance with the dosage and how long patients have adhered to the AAs protocol. Lastly, the lab techniques used to determine AAs are important. Research engines used: PubMed, Cochrane Library, Google Scholar. Research Criteria: Nutritional supplementation for replacing amino acids in patients undergoing thrice-weekly extra-corporeal treatment. The following were excluded: amino acids in paediatric trials; administration of proteins in which AAs content was not quantifiable; incremental haemodialysis protocols; patients with inadequate calorie-protein intake; administration of amino acids to patients with acute kidney injury (AKI) or in a critical situation, or those undergoing Continuous Renal Replacement Therapy (CRRT): see Figure 1.

Results

The literature search conducted yielded a total of 75 relevant publications, although only 9 of these met the established criteria for oral administration of amino acid replacement, Figure 1.
The only observational study performed with no control group (CG) on a total of 32 patients by Małgorzewicz S. [15] administered Oral Nutritional Supplementation (ONS) comprised of: Leucine, Isoleucine, Valine, Lysine, Threonine, Methionine and Phenylalanine. Three trials adopted a mix of AAs keto-analogues (KAAs) and FFAAs: In their prospective comparative observational studies, Neuhäuser M. [16] and Ulm A. [17] adopted a mix comprised of: Lysine, Threonine, Tryptophan, Histidine, Tyrosine and keto-analogues of Isoleucine, Leucine, Phenylalanine, Valin and Methionine, although no significant differences were observed between TG and CG. In a comparative randomised study performed by Li HL [19] between TG and CG, a mix comprising D,L-Alpha-keto isoleucine, Alpha-keto leucine, Alpha-keto phenylalanine, Alpha-keto valine, D,L-Alpha hydroxy-methionine, lysine, threonine, tryptophan, histidine and tyrosine was administered: the comparison highlighted the lack of any beneficial clinical effects and change in plasmatic levels of AAs. Moreover, the Authors deemed it opportune to administer up to 8-12 sachets of this KAAs mix daily in an attempt to replace at least 4-5 g/day (one sachet = 0.675g of AAs, with a prescription of one sachet per every 5 kg body weight). In the study by Hiroshige K. [8], protein intake was adjusted according to the mean body weight and BMI of the Chinese population [20], resulting in significant nutritional findings when using a mixture containing high doses of branched-chain amino acids. (BCAA): valine, leucine and isoleucine; in TG alone, the study observed: weight gain, increase in BMI and fat and lean mass, with increased appetite and protein and calorie intake during supplementation. In 2011, Bolasco P. [10] and in 2012, Sukkar SG. [18] adopted the first commercial mix of FFAAs comprised of: L-Leucine, L-Lysine, L-Isoleucine, L-Valine, L-Threonine, L-Cystine, L-Histidine, L-Phenylalanine, L-Methionine, L-Tyrosine, L-Tryptophan. The randomised parallel-group prospective study conducted by Bolasco P. obtained, in the TG group alone, an increase in: dry weight, protein catabolic rate, fat mass, albumin and haemoglobin, total IgG, and CRP decrease. In the double-blind, prospective, randomized, study undertaken by Sukkar SG using the same mix, no relevant differences were observed for TG versus CG, with the exception of a significant increase in transferrin in TG. In 2022, Murtas S. [12] conducted a randomised trial using a novel, and potentially more effective, amino acid mix with the addition of mitochondrial accelerators (Amino-Ther Pro® – Professional Dietetics – Milan – Italy) comprising: L-Threonine, L-Isoleucine, L-Valine, L-Cysteine, L-Histidine, L-Phenylalanine, L-Methionine, L-Tryptophan, citric acid, malic acid and succinic acid. A subsequent double-blind, randomised trial conducted by Murtas et al. in 2024 [13] studied a newly-developed novel amino acid mix comprised of identical amounts of each individual amino acid lost during haemodialysis, although containing a higher amount of glutamine (Amino-Dyal® – Professional Dietetics – Milan – Italy): L-Leucine, L-Isoleucine, L-Valine, L-Histidine, L-Phenylalanine, L-Lysine, L-Threonine, L-Tryptophan, L-Methionine, L-Proline, L-Cysteine, glutamic acid, L- Glutamine, L- Alanine, L-Glycine, L-Arginine, L-Tyrosine, L-Serine, Choline, aspartic acid. It should be highlighted how, in the studies undertaken by Bolasco et al. [10], Murtas S. 2022 [12], and Murtas 2024 [13], the AA mix was administered as far as possible from the haemodialysis session, following the end of post-dialysis rebound, cessation of hypercatabolism induced as a result of haemodialysis and cytokine release following blood/membrane contact during dialysis, and once a fluid compartment balance had been re-established [21,22,23]. In all 10 studies selected, dietary prescriptions for patients on TWH in terms of protein and calorie intake adhered to the official guidelines and are briefly summarised in Table 1.
In the studies listed in Table 1, patient adherence to treatment, based on percentage and duration of regular use, is rarely indicated. Lastly, studies describing the type of analytical assessment methods used highlight the progressive evolution and precision of technological and biochemical over time.

Discussion

Over the last decade, sachets containing a mix of 4.0–4.6g FAAs, virtually all essential amino acids, have been commercially manufactured. Research in the specific field has thus received a significant impetus and promising findings from a series of trials using these new products have been published. Accordingly, extended trials investigating the administration of EAAs and NEAAs to both CKD and TWH patients should be undertaken in the future. Both palatability of these novel amino acid mixes together with the need to only take a single daily dose have boosted patient compliance in medium to long-term trials, thus facilitating replacement of the massive dialysis-induced amino acid losses experienced even in adequately nourished patients undergoing TWH. Indeed, one dialysis session after another, AAs leach largely from muscle mass, resulting in a gradual, but unstoppable, decline into sarcopenia, particularly in the elderly [24,25,26,27,28,29,30]. Unfortunately, trials such as that conducted in China by Li H-L (listed in Table 1) [19], together with others [16,17] which opted to use mixes of KAAs/AAs + FAAs, inextricably necessitating administration of a high number of tablets or sachets daily, have failed to achieve optimal patient adherence. Indeed, Table 1 highlights how several studies completely overlooked the importance of assessing patient adherence. Conversely, when a mix of FAAs was orally administered and patients closely monitored, an adherence rate ranging between 93.3% and 100% was observed throughout the duration of the trial [10,12,13]. This led to the development of novel mixtures which were better tailored to uremic status and dialysis techniques used in TWH. In 2022, [12] the Amino-Ther PRO® mix (Professional Dietetics -Milan), in addition to effectively replacing dialysis-induced AA losses from both a qualitative and quantitative point of view, also comprised additional compounds known as mitochondrial accelerators [31]. These are represented by citric acid which combines with oxaloacetic acid to kick start the Krebs cycle, regulating and controlling the activity of key enzymes (such as phosphofructokinase), thus instantly providing the driving force needed to facilitate ribosome binding and incorporation of AAs into cell structures [32,33]. In the latter process, succinate produces ATP and is further oxidised by the succinate dehydrogenase enzyme, thus allowing the inner mitochondrial membrane to produce additional energy (ATP) and prevent premature cell senescence by maintaining the flow of electrons through mitochondrial II complex and optimising the production of further cellular energy (ATP) [34]. Lastly, malic acid [35] is involved in the malate-aspartate shuttle [36] which, as an intermediate in the Krebs cycle, acts mainly within the mitochondrial matrix to produce large amounts of clean energy (ATP) by crossing the mitochondrial membranes. Consequently, an improved recovery and tolerance to hypoxia are observed, thus contributing to the production of key molecules implicated in protecting cells against oxidative stress via NADPH synthesis. No side effects have been reported in the TG population. In 2024, the benefits of the Amino-Dyal ® (Professional Dietetics -Milan) novel mix of AAs [13] were reported, with the mix, devoid of mitochondrial accelerators, comprising the exact amount of each individual amino acid lost during haemodialysis. This amino acid mix was developed taking into account the need to reintroduce glutamine, the amino acid most widely present in biological fluids which, although not an essential amino acid, assumes a crucial role in haemodialysis patients due to the high levels of glutamine lost during haemodialysis. Thus, glutamine is supplemented to boost its metabolic role with the aim of protecting the mitochondrial metabolism in muscle and brain by exerting a major antioxidant and anti-inflammatory action, particularly in the context of chronic diseases such as CKD, and in haemodialysis patients affected by negative changes to the tricarboxylic acid cycle (TCA) [37,38]. The addition of glutamine to AAs mixes in TWH patients has proven beneficial for the following reasons: a) it readily crosses the blood-brain barrier, thus representing an important energy substrate and precursor of key neurotransmitters [39]. Glutamine protects the central nervous system primarily through the action of glutamine synthetase, which converts it into glutamate the main excitatory neurotransmitter in the central nervous system. This “glutamate-glutamine” cycle is repeated to reduce NH3 and convey it to the liver, where it is converted into urea and is rapidly eliminated through dialysis. Moreover, Glutamate is a precursor of gamma-amino-butyric acid (GABA), a fundamental inhibitory brain neurotransmitter [40]; b) glutamine contrasts sarcopenia by stimulating the production and muscle uptake of BCAAs [41]; c) glutamine exerts a crucial anti-inflammatory action on the permeability of intestinal mucosa by preserving the multi-protein complex of the intestinal tight junction [42]; d) moreover, lymphocytes, macrophages and natural killer cells use glutamine (glutaminolysis) as a primary source of energy [43]. The amino acid tryptophan, whilst necessitating supplementation, must be carefully regulated in the amino acid mix to ensure that dialysis-induced losses are not exceeded. Tryptophan exerts a protective action on intestinal cells and peristalsis, thus ensuring a regular production of serotonin which acts on the gut-brain axis, promoting use by BCAAs [44,45,46]. However, during the later stages of CKD, and particularly in haemodialysis patients, the gut microbiome undergoes a series of detrimental changes due to the uremic environment [47]. Tryptophan is readily converted in the liver, where it may go on to produce toxic molecules such as Indoxyl Sulfate and indole-3-Acetic Acid which bind to proteins, thus forming Protein Bound Uremic Toxins (PBUTs) [48], particularly toxic for organ systems and apparatus in TWH patients; moreover, only scarce quantities of PBUTs are eliminated during haemodialysis, even when using High-Flux HDF techniques [48]. Accordingly, the amino acid mix should only supplement tryptophan with amounts corresponding to those lost via dialysis [13]. Likewise, stable tyrosine levels should be ensured to adequately preserve adrenergic neurotransmitters and prevent the onset of cognitive and motor impairment. Methionine supplementation should also correspond to the precise amounts lost during dialysis, long being considered a “double-edged sword” as, despite the beneficial action on cellular oxidative stress [50], elevated plasma concentrations may undergo conversion into homocysteine via a continual biochemical cycle of hepatic transmethylation [51]

Conclusions

The long-term efficacy of amino acid supplementation is dependent on the use of an optimal (from both a qualitative and quantitative point of view) blend of EAAs, together with a series of NEAAs aimed at boosting intracellular protein anabolism and optimising the Krebs cycle and energy production. It is undeniable that haemodialysis patients tend to prefer products involving the lowest possible number of tablets or sachets to be taken on a daily basis. The Authors wish to underline how the present review did not include studies to which haemodialysis patients featuring initial or evident signs of malnutrition, sarcopenia and/or PEW had been recruited, but only those in which patients on TWH had been adequately nourished in line with the KDIGO guidelines. Indeed, studies performed over the last 15 years using a mix of free amino acids FFAAs have contributed towards slowing down the onset of malnutrition and have yielded a series of key nutritional, blood chemistry and anthropometric findings. We look forward to additional studies being conducted by other Authors on a larger patient population using updated innovative amino acid mixes, and trust that optimal levels of patient compliance may be associated with a single daily or intermittent administration, or indeed even short monthly or bi-monthly cycles of amino acids.

Author Contributions

PB: Conceptualization, Methodology, Validation, Formal Analysis, Data Curation, Writing – Original Draft Preparation. SM: Validation, data curation. GB: Data curation.

Funding

This research received no external funding.

Conflicts of Interest

the Authors declare no conflict of interest.

Abbreviations

The following abbreviations are used in this manuscript:
AAs Amino Acids
AKI Acute Kidney Injury
ATP Adenosine Triphosphate
BCAAs Branched-Chain Amino Acids
CG Control Groups
CKD Chronic Kidney Disease
CRP C-Reactive Protein
CRRT Continuous Renal Replacement Therapy
EAAs Essential Amino Acids
FAAs Free Amino Acids
GABA gamma-amino-butyric acid
HD Hemodialysis
HDF hemodiafiltration
KAAs Keto-Analogues of Amino Acids
NADPH Nicotinamide Adenine Dinucleotide Phosphate
NEAAs Non-Essential Amino Acids
PBUTs Protein Bound Uremic Toxins
PEW Protein Energy Wasting
TCA tricarboxylic acid cycle
TG Treatment Groups Patients
TWH Thrice-Weekly-Hemodialysis

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Preprints 232308 g001
Figure 1. Flow-Chart.
Figure 1. Flow-Chart.
Preprints 232308 g001
Table 1. Replacement of Amino Acid losses in patients on thrice-weekly maintenance haemodialysis. 
Table 1. Replacement of Amino Acid losses in patients on thrice-weekly maintenance haemodialysis. 
Author, Journal, year Number of Patients, Statistical comparison methods Mean Age of Treatment and Control groups in years Extracorporeal Treatment Strategy Study Duration Dietary Prescription Amino Acid Replacement Protocol Assessment of Amino Acid Losses Amino Acid
Mixes		 Adherence and duration to AAs trial
(%, months)		 Blood chemistry and Clinical findings Analytical Technique used
Neuhäuser M.
et Al. [16] Proc Eur Dial Transplant Assoc 1977		 TG: 9 patients CG: 11 patients no supplement Prospective observational unreported Unreported 3 months protein 1.0 g/kg/d calorie intake
31 Kcal/d		 Lysine, Threonine, Tryptophan, Histidine Tyrosine and
keto-analogues of Isoleucine, Leucine, Phenylalanine, Valine, Methionine		 not evaluated unreported unreported ineffective unreported
Ulm A. et Al. [17] Am J Clin Nutr 1978 TG: 9 patients
CG: 11 patients no supplement Prospective observational		 56±13.2 Haemodialysis 3 months protein 1.0 g/kg/d calorie intake
31 Kcal/d		 Lysine, Threonine, Tryptophan, Histidine, Tyrosine and
keto-analogues of Isoleucine, Leucine, Phenylalanine, Valine, Methionine		 not evaluated unreported unreported ineffective unreported
Hiroshige K.et Al. [8] NDT 2001 6 cross-over evaluation months of TG versus 6 months of CG (14 vs 14) prospective randomly assigned TG: 75±7 CG: 74±8 Polysulphone 12 months protein 1.0-1.2 g/kg/d; calorie intake 30-35 Kcal/d TG: 12gr/daily BCAA granules orally with dextrose;
CG: placebo. 		not evaluated 12 g/day of BCAA granules containing: valine 1.1 gr, leucine 1.9 g; isoleucine 1.0 gr
+ dextrose 2 gr		 unreported Weight gain; increased: BMI, lean body mass, appetite, protein and calorie intake Beckman 121M amino acid analyser using a lithium buffer system
Bolasco P. et Al. [10] Renal Failure 2011 15 TG versus 15 CG prospective randomised TG: 72.7±10.2. CG 75.2±11.2 10 patients HDF low- and high-flux with polysulphone and 5 patients with AN69 3 months protein 1.2 g/kg/d; calorie intake
30-35 Kcal/d		 2 sachets of EAAs a day not evaluated 4g sachets containing: Leucine, Lysine, Iso-leucine, Valine, Threonine, Cystine, Histidine, Methionine, Phenylalanine, Tyrosine and Tryptophan 100%, 3 months TG group: increase in dry weight, protein catabolic rate, fat mass, albumin, Hb and total IgG, decreased CRP Amino acid analyser HPLC X-LC-Jasco linked to an HP ProDesk elaborator
Sukkar SG. et Al. [18] Mediterr J Nutr Metab 2012 12 TG versus 12 CG. prospective, randomized, double blind unreported Unreported 4 months protein 1.2 g/kg/d; calorie intake
25 Kcal/d		 2 sachets of EAAs a day not evaluated 4g sachets containing: Leucine, Lysine, Isoleucine, Valine, Threonine, Cystine, Histidine, Methionine, Phenylalanine, Tyrosine and Tryptophan unreported TG: increase of transferrin unreported
Małgorzewicz S. et Al [15] Nutrition 2019 32 TG observational 59.1 ± 9.5 HD with polysulphone membrane 3 months unreported ONS: 125 ml twice a day not evaluated ONS containing: Leucine, Isoleucine, Valine, Lysine, Threonine, Methionine, Phenyl- alanine, Tryptophan, Histidine unreported Increase of prealbumin, albumin, and AAs plasma concentration Precolumn orthophtaldehyde derivatization and HPLC
Hai-Long Li et Al. [19] Chinese Medical Journal 2020 TG 15 versus 14 CG. randomized, controlled TG:55.3±10.1 CG:52±12.3 unreported 6 months protein 0.9 g/kg/d; calorie intake
30 Kcal/d		 TG group of KA mix
0.1 g/Kg/day		 not evaluated 0.1 g/kg/day containing:
Alpha-keto-isoleucine,
Alpha-keto leucine, Alpha-keto Phenylalanine, Alpha-keto valine, Alpha-hydroxy- methionine, Lysine, Threonine, Tryptophan, Histidine, Tyrosine		 unreported Administration of KA in TG did not modify AA levels compared with CG High performance liquid chromatography
Murtas S. et Al [12] Nutrients 2022 22 (11TG vs 11CG) Prospective double-blind centralized randomization TG:67.2±9.5 CG: 68.2±10.5 HDFpost 3 months protein 1.2 g/kg/d; calorie intake
30-35 Kcal/d		 1 sachet per day, taken orally at a distance from the haemodialysis session per session: TAAs: 5.2 g; EAAs: 2.0 g of which BCAAs 1.5g and NEAAs: 3.3 g AMINO-THER PRO mix: Threonine, Isoleucine, Valine, Cysteine, Histidine, Phenylalanine, Methionine, Tryptophan in addition to the AAs mix, mitochondrial accelerators 100%,
6 months		 CG: decrease in phase angle and muscle mass.
TG: unchanged Hb levels with decreased EPO requirement with better ERI, and raised LVEF.		 Amino acid analyser HPLC X-LC-Jasco linked to an HP ProDesk elaborator
Murtas S. et Al. [13] Clin Nutr ESPEN 2024 30 (TG 14 vs CG 15) prospective double-blind randomization TG:73.1±11.1. CG:74.2±10.1 HHD, HDFpost, HDFpre 3 months pre-treatment; 3 months treatment;
3 months post-treatment 		Protein 1.2 g/kg/d; calorie intake
30-35 Kcal/d		 1 sachet per day, taken orally at a distance from the haemodialysis session per session: TAAs: 5.3 g; EAAs:2.0 g of which BCAA: 1.1g and NEAAs: 3.2 g AMINO-DYAL: Leucine, Isoleucine, Valine, Histidine, Phenylalanine, Lysine, Threonine, Tryptophan, Methionine, Proline, Cysteine, glutamic acid, Glutamine, Alanine, Glycine, Arginine, Tyrosine, Serine, Choline, Aspartic acid 93.3%,
3 months		 TG: decreased PCR, increased IgG, C3, and Hb at lower EPO requirement dosage, with decreased ferritin depots. CG: increased PCR, loss of fat mass Amino acid analyser HPLC X-LC-Jasco linked to an HP ProDesk elaborator
TG: Treatment Group; CG: Control no supplement or Placebo Group; HD: Haemodialysis; HHD: High Efficiency HD; HDFpost: post-dilution Haemodiafiltration, HDFpre: pre-dilution Hemodiafiltration; AAs: Amino Acids; TAAS: total Amino Acids; EAAS: Essential Amino Acids; NEAAs: Non-Essential Amino Acids; BCAA: Branched Chain Amino Acids; EPO: Erythropoietin; ERI: Erythropoietin Resistance Index.
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