Dietary Amino Acid Patterns Are Associated With Incidence of Chronic Kidney Disease

Author(s):  
Golaleh Asghari ◽  
Farshad Teymoori ◽  
Hossein Farhadnejad ◽  
Parvin Mirmiran ◽  
Fereidoun Azizi
2005 ◽  
Vol 82 (2) ◽  
pp. 342-349 ◽  
Author(s):  
Mohammed E Suliman ◽  
A Rashid Qureshi ◽  
Peter Stenvinkel ◽  
Roberto Pecoits-Filho ◽  
Peter Bárány ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Christophe Barba ◽  
Bérengère Benoit ◽  
Emilie Bres ◽  
Stéphanie Chanon ◽  
Aurélie Vieille-Marchiset ◽  
...  

AbstractDespite decades of use of low protein diets (LPD) in the management of chronic kidney disease (CKD), their mechanisms of action are unclear. A reduced production of uremic toxins could contribute to the benefits of LPDs. Aromatic amino-acids (AA) are precursors of major uremic toxins such as p-cresyl sulfate (PCS) and indoxyl sulfate (IS). We hypothesize that a low aromatic amino acid diet (LA-AAD, namely a low intake of tyrosine, tryptophan and phenylalanine) while being normoproteic, could be as effective as a LPD, through the decreased production of uremic toxins. Kidney failure was chemically induced in mice with a diet containing 0.25% (w/w) of adenine. Mice received three different diets for six weeks: normoproteic diet (NPD: 14.7% proteins, aromatic AAs 0.019%), LPD (5% proteins, aromatic AAs 0.007%) and LA-AAD (14% proteins, aromatic AAs 0.007%). Both LPD and LA-AAD significantly reduced proteinuria, kidney fibrosis and inflammation. While LPD only slightly decreased plasma free PCS and free IS compared to NPD; free fractions of both compounds were significantly decreased by LA-AAD. These results suggest that a LA-AAD confers similar benefits of a LPD in delaying the progression of CKD through a reduction in some key uremic toxins production (such as PCS and IS), with a lower risk of malnutrition.


Author(s):  
Esthy Poespitaningtyas ◽  
Roedi Irawan ◽  
Ninik Asmaningsih Soemyarso ◽  
Jusak Nugraha

Chronic kidney disease (CKD) is not uncommon issue in children. CKD is the abnormality of structure or function of the kidney that occurs for more than 3 months. Progresivity of CKD characterized by the presence of longitudinal decline in Glomerulus Filtration Rate (GFR), proteinuria and hypertension. One of the recommendations of the prevention of nutritional supplementation in CKD by administering oral Branched Chain Amino Acid (BCAA). Recently, there has been no research to figure the effects of the of BCAA on children with CKD stage 2-4. Randomized pre-post test controlled trial study was conducted in Nephrology pediatric outpatient clinic Dr. Soetomo hospital with CKD stage 2-4, divided into 2 groups, the BCAA and placebo, followed for 8 weeks to be evaluated for GFR, albumin, proteinuria, blood pressure and nutritional status. Sixteen children with CKD stage 2-4 were enrolled in this study, 71.4% of patients were boys. The mean age was 12.5 (SD 2.90) years. CKD stage 2 about 50% (p=0,767). Nephrotic syndrome was the most common underlying cause of CKD (p=0,149). Moderate malnutrition was about 50% (p=1,000) and short stature was 64.28% (p=1.000). In BCAA group there was decrease of GFR -5.08±7,13 (p=0.055), increase of albumin serum 0.20±0.23 (p=0,062), decrease of delta systole -11,57±15.08 (p=0,565) and diastole -4,85±16.25 (p=0,708), weight loss -0.07±1.01 (p=0.828), an increase of height 0.14±0.24 (p=0,771), and a decrease in BMI -0.03±0.74 (p=0,389). The conclusion in this study is Branched chain amino acid (Leucine, Isoleucine and Valine) supplementation did not provide significant effect in inhibiting progresivity of CKD stage 2-4 in children and improvement of nutritional status.


2021 ◽  
Author(s):  
Yuan Gao ◽  
Shengnan Wang ◽  
Lijun Sun ◽  
Bing Li ◽  
Hong Liu ◽  
...  

Abstract Background: Recent evidence suggests alterations in the gut-kidney axis may drive chronic kidney disease (CKD). Results: In the present study, we observed that administration of adenine to rats induced CKD, gut microbial dysbiosis, kidney pathology, and amino acid metabolism. In this model of CKD hyperphosphatemia, lanthanum hydroxide improved kidney function in CKD rats by restoring gut microbial homeostasis, thereby increasing urine ammonium metabolism. These findings demonstrated that lanthanum hydroxide improves kidney function in a CKD model in mice by restoring homeostasis of the gut-metabolite-kidney axis, which alleviated an amino acid imbalance. Lanthanum hydroxide thus shows therapeutic potential for patients with CKD, through reshaping the composition of gut microbiota.Conclusions: Lanthanum hydroxide plays a kidney protective role through the gut-metabolite-kidney axis in a rat model of chronic kidney disease caused by adenine.


2010 ◽  
Vol 29 (4) ◽  
pp. 424-433 ◽  
Author(s):  
Giacomo Garibotto ◽  
Antonella Sofia ◽  
Stefano Saffioti ◽  
Alice Bonanni ◽  
Irene Mannucci ◽  
...  

2005 ◽  
Vol 82 (2) ◽  
pp. 342-349 ◽  
Author(s):  
Mohammed E Suliman ◽  
A Rashid Qureshi ◽  
Peter Stenvinkel ◽  
Roberto Pecoits-Filho ◽  
Peter Bárány ◽  
...  

2018 ◽  
Vol 4 (2) ◽  
pp. 205511691878675
Author(s):  
Cécile Dor ◽  
Jessica L Adamany ◽  
Caroline Kisielewicz ◽  
Simone de Brot ◽  
Kerstin Erles ◽  
...  

Case summary A 5-year-old male neutered Persian cat was referred for investigation of a 4 week history of weight loss, inappetence and intermittent vomiting. Chronic kidney disease (CKD) and inflammatory bowel disease were diagnosed, and despite immunosuppressive therapy and assisted enteral nutrition, the cat experienced persistent anorexia, vomiting and severe weight loss. After 2 additional weeks of treatment, the cat developed acute-onset neurological signs associated with severe hyperammonaemia and was euthanased. Plasma amino acid assessment revealed deficiency of several amino acids involved in the urea cycle, including arginine. Relevance and novel information To our knowledge, this is the first reported case of an acquired urea cycle amino acid deficiency without nutritional deprivation in a cat. Several contributing factors were suspected, including intestinal malabsorption and CKD. This case demonstrates the importance of urea cycle amino acids in feline metabolism and possible necessity for parenteral supplementation, particularly in the context of persistent weight loss despite adequate enteral nutrition.


2021 ◽  
Author(s):  
Christophe Barba ◽  
Bérengère Benoit ◽  
Bres Emilie ◽  
Stéphanie Chanon ◽  
Aurélie Vieille-Marchiset ◽  
...  

Abstract Despite decades of use of low protein diets (LPD) in the management of chronic kidney disease (CKD), their mechanisms of action are unclear. A reduced production of uremic toxins could contribute to the benefits of LPDs. Aromatic amino-acids (AA) are precursors of major uremic toxins such as p-cresyl sulfate (PCS) and indoxyl sulfate (IS). We hypothesize that a low aromatic amino acid diet (LA-AAD, namely a low intake of tyrosine, tryptophan and phenylalanine) while being normoproteic, could be as effective as a LPD, through the decreased production of uremic toxins. Kidney failure was chemically induced in mice with a diet containing 0.25% (w/w) of adenine. Mice received three different diets for six weeks: normoproteic diet (NPD: 14.7% proteins, aromatic AAs 0.019%), LPD (5% proteins, aromatic AAs 0.007%) and LA-AAD (14% proteins, aromatic AAs 0.007%). Both LPD and LA-AAD significantly reduced proteinuria, kidney fibrosis and inflammation. While LPD only slightly decreased plasma free PCS and free IS compared to NPD; free fractions of both compounds were significantly decreased by LA-AAD. These results suggest that a LA-AAD confers similar benefits of a LPD in delaying the progression of CKD through a reduction in uremic toxins production, with a lower risk of malnutrition.


2020 ◽  
Vol 106 (1) ◽  
pp. 143-152
Author(s):  
Lilian Fernandes Silva ◽  
Jagadish Vangipurapu ◽  
Ulf Smith ◽  
Markku Laakso

Abstract Objective To investigate the metabolite signature of albuminuria in individuals without diabetes or chronic kidney disease to identify possible mechanisms that result in increased albuminuria and elevated risk of type 2 diabetes (T2D). Research Design and Methods The study cohort was a population-based Metabolic Syndrome In Men (METSIM) study including 8861 middle-aged and elderly Finnish men without diabetes or chronic kidney disease at baseline. A total of 5504 men participated in a 7.5-year follow-up study, and 5181 of them had metabolomics data measured by Metabolon’s ultrahigh performance liquid chromatography-tandem mass spectroscopy. Results We found 32 metabolites significantly (P < 5.8 × 10-5) and positively associated with the urinary albumin excretion (UAE) rate. These metabolites were especially downstream metabolites in the amino acid metabolism pathways (threonine, phenylalanine, leucine, arginine). In our 7.5-year follow-up study, UAE was significantly associated with a 19% increase (hazard ratio 1.19; 95% confidence interval, 1.13–1.25) in the risk of T2D after the adjustment for confounding factors. Conversion to diabetes was more strongly associated with a decrease in insulin secretion than a decrease in insulin sensitivity. Conclusions Metabolic signature of UAE included multiple metabolites, especially from the amino acid metabolism pathways known to be associated with low-grade inflammation, and accumulation of reactive oxygen species that play an important role in the pathogenesis of UAE. These metabolites were primarily associated with an increase in UAE and were secondarily associated with a decrease in insulin secretion and insulin sensitivity, resulting in an increased risk of incident T2D.


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