Although there has been great interest in the effects of amino acids on immune function, little is known about the impact of changes in BCAA availability on the ability of the immune system to function. Human immune cells incorporate BCAA into proteins and are able to oxidize BCAA. The immune system exists to protect the host from pathogenic invaders and from other noxious insults. Upon infection, there is a marked increase in demand for substrates by the immune system; these substrates provide energy and are the precursors for the synthesis of new cells, effector molecules, and protective molecules. Cell culture studies show that BCAA are absolutely essential for lymphocytes to synthesize protein, RNA, and DNA and to divide in response to stimulation. In mice, dietary BCAA restriction impairs several aspects of the immune function and increases the susceptibility to pathogens. Postsurgical or septic patients given BCAA intravenously showed improved immunity and this may relate to improved outcome. BCAAs are therefore absolutely essential for lymphocyte responsiveness and are necessary to support other immune cell functions. However, many aspects of BCAA and its effects on immune function have been understudied or not studied at all. More research is needed to understand the extent of the immune system's requirement for BCAA. It is likely that the essentiality of BCAA for the function of immune cells relates to protein synthesis.

/pdf/branched-chain-amino-acids-and-immunity-4s1iquknxg.pdf

Branched-Chain Amino Acids and Immunity

Mechanisms of renal hemodynamic regulation in response to protein feeding

Deficiency of ornithine-δ-aminotransferase (OAT) in humans results in gyrate atrophy of the choroid and retina (GA), an autosomal recessive disorder characterized by ornithine accumulation and a progressive chorioretinal degeneration of unknown pathogenesis. To determine whether chronic, systemic reduction of ornithine can prevent this form of retinal degeneration, we used an arginine-restricted diet to maintain long term reduction of ornithine in a mouse model of OAT-deficiency (Oat−/−) produced by gene targeting. We evaluated the mice over a 12-month period by measurement of plasma amino acids, electroretinograms, and retinal histologic and ultrastructural studies. We found that an arginine-restricted diet substantially reduces plasma ornithine levels and completely prevents retinal degeneration in Oat−/−. This result indicates that ornithine accumulation is a necessary factor in the pathophysiology of the retinal degeneration in GA and that restoration of OAT activity in retina is not required for effective treatment of GA.

https://www.pnas.org/content/pnas/97/3/1224.full.pdf

Correction of ornithine accumulation prevents retinal degeneration in a mouse model of gyrate atrophy of the choroid and retina.

https://www.kidney-international.org/article/S0085-2538(15)33000-3/pdf

Oral essential aminoacid and ketoacid supplements in children with chronic renal failure

Renal transplantation using infant donors is associated with significantly less graft survival (GS) and increased morbidity, especially from very young and small donors. We report our results using specific strategies to determine which age and size donor require en bloc renal transplant reconstruction and associated immunologic protocols for optimization of subsequent GS. Forty cadaveric pediatric en bloc renal transplants were performed. Mean donor age was 23.6±18.4 months with subgroups: 2-12 months, n=14; 13-24 months, n=19; and 25-60 months, n=7. Mean donor weight was 14.4±4.5 kg. All kidneys were placed in primary, nonsensitized (peak PRA = 7.9±5.6%) adult (41.6±16 years) recipients. Low weight was preferred (62.4±12.8 kg). Mean cold ischemia time was 26.9±8.6 hr. Immunosuppression consisted of quadruple immunosuppression (QI) with OKT3 induction. All patients had ureteral stents placed intraoperatively. Mean follow-up was 16.9 months. Actuarial GS at 12, 24, and 33 months were 100% (n=13), 85% (n=20), and 71% (n=7), respectively. Total GS was 35/40=88%. All grafts functioned immediately and there were no technical losses. Biopsy proven rejections occurred in 12 (30%) patients, developing at 16-167 days postoperatively (mean = 50.3 days). Mean serum creatinine at one week and 1, 6, 12, and 18 months were 2.1±2.0, 1.5±0.8, 1.3±0.5, 1.1±0.4, and 0.9±0.4 mg/dl, respectively. Functional isotopic renography, as well as sonographic monitoring reflected rapid initial and continued growth in these kidneys. Mean BP at 12 and 24 months postoperatively were 145/83±18/13 and 122/ 76±20/10 mmHg, respectively, with no significant pro-teinuria noted. Excellent results with minimal complications utilizing very small and young infant donors can be achieved with QI immunosuppression, and selection of low immune reactive and noncomplicated adult recipients. Additionally, maximal renal dosing by minimizing recipient weight may prevent future hyperfiltration damage.

Immunologic and patient selection strategies for successful utilization of less than 15 kg pediatric donor kidneys--long term experiences with 40 transplants.

A metabolic study in a case of hyperornithinemia with gyrate atrophy of choroid and retina is presented. It is demonstrated that the lysine-ornithine antagonism is a physiological, safe, easy to handl

Lysine in Treatment of Hyperornithinemia

Amino acid and keto acid diet in uremic children and infants.

Nitrogen balance in uremic patients on different amino acid and keto acid formulations--a proposed reference pattern.

It has been hypothesized that both the cyclosporine (CsA) treatment and the reduction of renal mass may affect the renal hemodynamic regulation in kidney transplant recipients. To address this question, we evaluated the renal hemodynamic response to hyperaminoacidemia (i.v. mixed amino acid infusion 3.3 mg/kg/minute for 150 minutes) in four study groups: (1) 16 renal transplant recipients (Tx), (2) 6 uninephrectomized (Nx) subjects, (3) 7 subjects treated with CsA for chronic uveitis (CsA), and (4) 9 normal controls (NC). In response to amino acid administration (AA), glomerular filtration rate (GFR) rose significantly in NC subjects (80 +/- 6 vs. 91 +/- 6 ml/minute; P<0.01) and Nx patients (57 +/- 3 vs. 68 +/- 7 ml/minute; P<0.01) and failed to increase in Tx recipients (39 +/- 3 vs. 37 +/- 3 ml/minute) and CsA-treated patients (58 +/- 3 vs. 53 +/- 4 ml/minute). Renal plasma flow (RPF) did not change in Tx recipients (243 +/- 27 vs. 235 +/- 25 ml/minute) but rose significantly in all other groups (257 +/- 17 vs. 344 +/- 33 in NX, 364 +/- 6l vs. 441 +/- 55 in CsA, 412 +/- 49 vs. 472 +/- 72 ml/min in NC subjects; P<0.05 vs. basal). Basal renal vascular resistances were significantly higher in Tx (0.29 +/- 0.04 mmHg/mlxmin; P<0.01 vs. all other groups) than in Nx (0.21 +/- 0.01 mmHg/mlxmin), CsA (0.23 +/- 0.04 mmHg/mlxmin) (both P<0.01 vs. NC subjects), and NC subjects (0.13 +/- 0.02 mmHg/mlxmin). Renal vascular resistance failed to decline in Tx (0.31 +/- 0.04 mmHg/mlxmin) during AA infusion but declined significantly in all other groups. In Tx, basal GFR was positively correlated to renal allograft volume (r=0.547, P<0.03); however, no relationship was found between the latter and basal RPF or the AA induced changes in GFR. In summary, the present study demonstrates that in kidney transplant recipients and in CsA-treated subjects, the renal functional reserve to hyperaminoacidemia is impaired. This is at variance to what is observed in normal controls and uninephrectomized subjects. In renal transplant recipients, basal but not amino acid stimulated GFR correlates with renal allograft volume. We conclude that basal GFR is related to renal volume in Tx and that the response to hyperaminoacidemia seems to be affected by chronic CsA administration.

Renal hemodynamics in renal transplant recipients. The role of reduced kidney mass and cyclosporine administration

Rationale. To establish relationship, if any, between renal morphology and renal haemodynamic response to amino acids. Design and methods. We investigated the correlation between renal haemodynamic regulation and morphology in a group of 15 patients with primary IgA nephropathy (IgAN) (age 26±2 years, BMI 24.4±1, GFR 64±5 ml/min, RPF 377±34 ml/min, FF 0.17±0.02). Twelve normal subjects (age 30±3 years, BMI 24±1, GFR 82±6 ml/min, RPF 421±42 ml/min, FF 0.19±0.02) were studied as controls. IgA patients were divided into two groups according to the histological staging of glomerular lesions : group I (n=7) stage II, and group II (n=8) stage III-IV. Results. In the basal state GFR was similar in the two groups and averaged 64 ± 9 and 64 ± 6 ml/min respectively. In contrast, FF was significantly lower in group II (0.14±0.01) (P<0.05) in comparison to group I (0.21±0.03) and controls (0.19±0.02). In order to evaluate the renal functional reserve, all study groups underwent to an intravenous amino-acid infusion designed to increase plasma amino acid levels twofold (total from 2096±145 to 4301±221 μmol/l in IgA nephropathy patients and from 2272±83 to 3844±238 μmol/l in controls). In response to amino-acid infusion, GFR rose significantly in group I (GFR 20±2% and RPF 37±4% versus basal) and controls (GFR 20±2% and RPF 20±3% versus basal) (both P<0.01 vs basal). In contrast, in patients with more severe glomerular lesions (group II) neither GFR nor RPF rose significantly (GFR -1±4% and RPF -8±6% versus basal) (P NS versus basal, P<0.01 versus group I and controls). Conclusions. The data show that in IgA nephropathy : severe forms of glomerular lesions are associated with a complex alteration of glomerular haemodynamic regulation, characterized by lower basal FF and loss of haemodynamic response to hyperaminoacidaemia.

Correlation between glomerular morphology and renal haemodynamic response to amino-acid administration in patients with IgA nephropathy

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