Dietary Fibre Intake Is Associated with Serum Levels of Uraemic Toxins in Children with Chronic Kidney Disease.

Imbalanced colonic microbial metabolism plays a pivotal role in generating protein-bound uraemic toxins (PBUTs), which accumulate with deteriorating kidney function and contribute to the uraemic burden of children with chronic kidney disease (CKD). Dietary choices impact the gut microbiome and metabolism. The aim of this study was to investigate the relation between dietary fibre and gut-derived PBUTs in paediatric CKD. Sixty-one (44 male) CKD children (9 ± 5 years) were prospectively followed for two years. Dietary fibre intake was evaluated by either 24-h recalls (73%) or 3-day food records (27%) at the same time of blood sampling for assessment of total and free serum levels of different PBUTs using liquid chromatography. We used linear mixed models to assess associations between fibre intake and PBUT levels. We found an inverse association between increase in fibre consumption (g/day) and serum concentrations of free indoxyl sulfate (-3.1% (-5.9%; -0.3%) (p = 0.035)), free p-cresyl sulfate (-2.5% (-4.7%; -0.3%) (p = 0.034)), total indole acetic acid (IAA) (-1.6% (-3.0%; -0.3%) (p = 0.020)), free IAA (-6.6% (-9.3%; -3.7%) (p < 0.001)), total serum p-cresyl glucuronide (pCG) (-3.0% (-5.6%; -0.5%) (p = 0.021)) and free pCG levels (-3.3% (-5.8%; -0.8%) (p = 0.010)). The observed associations between dietary fibre intake and the investigated PBUTs highlight potential benefits of fibre intake for the paediatric CKD population. The present observational findings should inform and guide adaptations of dietary prescriptions in children with CKD.

Reducing the Risk of Stroke in Patients with Impaired Renal Function: Nutritional Issues.

Patients with renal failure have extremely high cardiovascular risk; in dialysis patients the risk of stroke is increased approximately 10-fold over that in the general population. Reasons include not only a high prevalence of traditional risk factors such as diabetes, hypertension and dyslipidemia, but also the accumulation of toxic substances that are eliminated by the kidneys, so have very high levels in patients with renal failure. These include plasma total homocysteine, asymmetric dimethylarginine, thiocyanate, and toxic products of the intestinal microbiome (Gut-Derived Uremic Toxins; GDUT), which include trimethylamine N- oxide (TMAO), produced from phosphatidylcholine (largely from egg yolk) and carnitine (largely from red meat). Other GDUT are produced from amino acids, largely from meat consumption. Deficiency of vitamin B12 is very common, raises plasma tHcy, and is easily treated. However, cyanocobalamin is toxic in patients with renal failure. To reduce the risk of stroke in renal failure it is important to limit the intake of meat, avoid egg yolk, and use methylcobalamin instead of cyanocobalamin, in addition to folic acid.

Uremic Sarcopenia: Clinical Evidence and Basic Experimental Approach.

Sustained physical activity extends healthy life years while a lower activity due to sarcopenia can reduce them. Sarcopenia is defined as a decrease in skeletal muscle mass and strength due not only to aging, but also from a variety of debilitating chronic illnesses such as cancer and heart failure. Patients with chronic kidney disease (CKD), who tend to be cachexic and in frail health, may develop uremic sarcopenia or uremic myopathy due to an imbalance between muscle protein synthesis and catabolism. Here, we review clinical evidence indicating reduced physical activity as renal function deteriorates and explore evidence-supported therapeutic options focusing on nutrition and physical training. In addition, although sarcopenia is a clinical concept and difficult to recapitulate in basic research, several in vivo approaches have been attempted, such as rodent subtotal nephrectomy representing both renal dysfunction and muscle weakness. This review highlights molecular mechanisms and promising interventions for uremic sarcopenia that were revealed through basic research. Extensive study is still needed to cast light on the many aspects of locomotive organ impairments in CKD and explore the ways that diet and exercise therapies can improve both outcomes and quality of life at every level.

Effect of caloric restriction on phosphate metabolism and uremic vascular calcification.

Caloric restriction (CR) is known to have multiple beneficial effects on health and longevity. To study the effect of CR on phosphorus metabolism and vascular calcification (VC), rats were fed normal or restricted calories (67% of normal). The phosphorus content of the diets was adjusted to provide equal phosphorus intake independent of the calories ingested. After 50 days of CR, rats had negative phosphorus balance, lower plasma phosphorus, glucose, triglycerides, and leptin, and higher adiponectin than rats fed normal calories. Uremia was induced by 5/6 nephrectomy (Nx). After Nx, rats were treated with calcitriol (80 ng/kg ip every other day) and high-phosphorus diets (1.2% and 1.8%). No differences in aortic calcium content were observed between rats that ate normal or restricted calories before Nx in either rats that received 1.2% phosphorus (11.5 ± 1.7 vs. 10.9 ± 2.1 mg/g tissue) or in rats that received 1.8% phosphorus (12.5 ± 2.3 vs. 12.0 ± 2.9 mg/g of tissue). However, mortality was significantly increased in rats subjected to CR before Nx in both the 1.2% phosphorus groups (75% vs. 25%, P = 0.019) and 1.8% phosphorus groups (100% vs. 45%, P < 0.001). After calcitriol administration was stopped and phosphorus intake was normalized, VC regressed rapidly, but no significant differences in aortic calcium were detected between rats that ate normal or restricted calories during the regression phase (5.7 ± 2.7 and 5.2 ± 1.5 mg/g tissue). In conclusion, CR did not prevent or ameliorate VC and increased mortality in uremic rats.

Microbiota issue in CKD: how promising are gut-targeted approaches?

In chronic kidney disease (CKD), the progressive decline in the renal excretory function leads to accumulation of urea and toxins in the blood. The CKD-associated dysbiosis of gut microbiota further contributes to uremia by increasing intestinal toxins production. Gut microbiota is involved in a complex network of human organs, mediated by microbial metabolites: in CKD, gut-heart and gut-brain axes may have a role in increased cardiovascular risk and neuropsychiatric disorders. While the cardiovascular toxicity of some microbial molecules is well known, their presumptive neurotoxicity needs to be confirmed by specific studies. In this review, we describe gut-heart and gut-brain axes in CKD, with an overview of the experimental and human studies characterizing CKD-associated gut microbiota, and we discuss the benefits coming from new approaches aimed at gut manipulation. Microbiota metabolism is emerging as a modifiable non-traditional risk factor in nephrology. In order to take advantage of this issue, it is necessary to consider the microbiota manipulation as part of the nutritional management of CKD. Integrating the low-protein nutritional approach with prebiotic, probiotic and synbiotic supplementation is a promising tool to control disease progression and comorbidities, though an extensive validation in large-scale clinical trials is still required.

Vegetarian diet may ameliorate uremic pruritus in hemodialysis patients.

OBJECTIVES: Systemic inflammation has been reported to be associated with uremic pruritus (UP). Although a vegetarian diet can reduce systemic inflammation in hemodialysis patients, the effect of vegetarian diet on UP is not clear. The purpose of the study was to know the possible effects of vegetarian diet on UP. METHODS: A cross-sectional study was done to compare the severity of UP and blood levels of systemic inflammatory markers between vegetarian and non-vegetarian hemodialysis patients. Six non-vegetarian patients with uremic pruritus changed their non-vegetarian diet to vegetarian diet for 2 months. Visual Analogue Scale (VAS) and pruritus score (PS) were used to measure the UP severity. The serum high-sensitivity C-reactive protein (hs-CRP), and interleukin-2 (IL-2) were used as markers of inflammation. RESULTS: Both the median VAS scores (p = .043) and the median PS scores (p < .001) were lower in the Vegetarian than in the non-vegetarian group. The median values of hs-CRP in Vegetarian were lower than that for the non-vegetarian (p = .020). The median value of IL-2 was also lower in Vegetarian than that of the non-vegetarian (p = .016). There were 6 non-vegetarian patients shift to vegetarian for 2 months. The pruritus score improved and IL-2 level decreased after change to vegetarian diet. CONCLUSION: We concluded that vegetarian diet might be associated with the amelioration of the uremic pruritus severity in hemodialysis patients.

Dietary magnesium supplementation prevents and reverses vascular and soft tissue calcifications in uremic rats.

Although magnesium has been shown to prevent vascular calcification in vitro, controlled in vivo studies in uremic animal models are limited. To determine whether dietary magnesium supplementation protects against the development of vascular calcification, 5/6 nephrectomized Wistar rats were fed diets with different magnesium content increasing from 0.1 to 1.1%. In one study we analyzed bone specimens from rats fed 0.1%, 0.3%, and 0.6% magnesium diets, and in another study we evaluated the effect of intraperitoneal magnesium on vascular calcification in 5/6 nephrectomized rats. The effects of magnesium on established vascular calcification were also evaluated in uremic rats fed on diets with either normal (0.1%) or moderately increased magnesium (0.6%) content. The increase in dietary magnesium resulted in a marked reduction in vascular calcification, together with improved mineral metabolism and renal function. Moderately elevated dietary magnesium (0.3%), but not high dietary magnesium (0.6%), improved bone homeostasis as compared to basal dietary magnesium (0.1%). Results of our study also suggested that the protective effect of magnesium on vascular calcification was not limited to its action as an intestinal phosphate binder since magnesium administered intraperitoneally also decreased vascular calcification. Oral magnesium supplementation also reduced blood pressure in uremic rats, and in vitro medium magnesium decreased BMP-2 and p65-NF-κB in TNF-α-treated human umbilical vein endothelial cells. Finally, in uremic rats with established vascular calcification, increasing dietary magnesium from 0.1% magnesium to 0.6% reduced the mortality rate from 52% to 28%, which was associated with reduced vascular calcification. Thus, increasing dietary magnesium reduced both vascular calcification and mortality in uremic rats.

Low-protein diet supplemented with ketoacids ameliorates proteinuria in 3/4 nephrectomised rats by directly inhibiting the intrarenal renin-angiotensin system.

Low-protein diet plus ketoacids (LPD+KA) has been reported to decrease proteinuria in patients with chronic kidney diseases (CKD). However, the mechanisms have not been clarified. As over-activation of intrarenal renin-angiotensin system (RAS) has been shown to play a key role in the progression of CKD, the current study was performed to investigate the direct effects of LPD+KA on intrarenal RAS, independently of renal haemodynamics. In this study, 3/4 subtotal renal ablated rats were fed 18 % normal-protein diet (Nx-NPD), 6 % low-protein diet (Nx-LPD) or 5 % low-protein diet plus 1 % ketoacids (Nx-LPD+KA) for 12 weeks. Sham-operated rats fed NPD served as controls. The level of proteinuria and expression of renin, angiotensin II (AngII) and its type 1 receptors (AT1R) in the renal cortex were markedly higher in Nx-NPD group than in the sham group. LPD+KA significantly decreased the proteinuria and inhibited intrarenal RAS activation. To exclude renal haemodynamic impact on intrarenal RAS, the serum samples derived from the different groups were added to the culture medium of mesangial cells. It showed that the serum from Nx-NPD directly induced higher expression of AngII, AT1R, fibronectin and transforming growth factor-ß1 in the mesangial cells than in the control group. Nx-LPD+KA serum significantly inhibited these abnormalities. Then, proteomics and biochemical detection suggested that the mechanisms underlying these beneficial effects of LPD+KA might be amelioration of the nutritional metabolic disorders and oxidative stress. In conclusion, LPD+KA could directly inhibit the intrarenal RAS activation, independently of renal haemodynamics, thus attenuating the proteinuria in CKD rats.

Back to the future: restricted protein intake for conservative management of CKD, triple goals of renoprotection, uremia mitigation, and nutritional health.

Lowering dietary protein intake (DPI) to approximately 0.6-0.8 g/kgBW/day may be renoprotective through various mechanisms, and it has been recommended in patients with non-dialysis-dependent chronic kidney disease (NDD-CKD) as a means to also control various metabolic consequences of advanced CKD, such as uremic symptoms, hyperparathyroidism, hypertension, hyperkalemia, and hyperphosphatemia. A meta-analysis in this issue of the Journal suggests that low-protein diet is effective and safe when used to retard progression of CKD and alleviate uremic complications. A potential deleterious consequence of lowering DPI in this population is the development or worsening of protein-energy wasting (PEW), which can contribute to poor clinical outcomes such as higher mortality and morbidity. There is currently insufficient high-level evidence to determine the ideal level of DPI in patients with NDD-CKD with high risk of PEW. For the time being we recommend a DPI of 0.6-0.8 g/kgBW/day, and increasing this as needed on an individual basis in patients with PEW. Further examination of this dilemma in randomized controlled clinical trials will be necessary.

Nonextracorporeal methods for decreasing uremic solute concentration: a future way to go?

The uremic milieu is consequential to a disrupted balance between availability of retention solutes and the excretory capacity of the kidneys. Although metabolism is the prime contributor to the internal milieu, a significant fraction of uremic retention solutes originates from other sources. The main route of entrance is via the intestinal tract, directly from the diet and indirectly from commensal microbial metabolism. This latter dynamic interplay between the intestines and kidney has been coined the gut-kidney axis. This review summarizes current understanding of the gut-kidney axis and explores the impact of dietary and other nonextracorporeal therapeutic interventions in patients with chronic kidney disease.

Dietary L-lysine prevents arterial calcification in adenine-induced uremic rats.

Vascular calcification (VC) is a life-threatening complication of CKD. Severe protein restriction causes a shortage of essential amino acids, and exacerbates VC in rats. Therefore, we investigated the effects of dietary l-lysine, the first-limiting amino acid of cereal grains, on VC. Male Sprague-Dawley rats at age 13 weeks were divided randomly into four groups: low-protein (LP) diet (group LP), LP diet+adenine (group Ade), LP diet+adenine+glycine (group Gly) as a control amino acid group, and LP diet+adenine+l-lysine·HCl (group Lys). At age 18 weeks, group LP had no VC, whereas groups Ade and Gly had comparable levels of severe VC. l-Lysine supplementation almost completely ameliorated VC. Physical parameters and serum creatinine, urea nitrogen, and phosphate did not differ among groups Ade, Gly, and Lys. Notably, serum calcium in group Lys was slightly but significantly higher than in groups Ade and Gly. Dietary l-lysine strongly suppressed plasma intact parathyroid hormone in adenine rats and supported a proper bone-vascular axis. The conserved orientation of the femoral apatite in group Lys also evidenced the bone-protective effects of l-lysine. Dietary l-lysine elevated plasma alanine, proline, arginine, and homoarginine but not lysine. Analyses in vitro demonstrated that alanine and proline inhibit apoptosis of cultured vascular smooth muscle cells, and that arginine and homoarginine attenuate mineral precipitations in a supersaturated calcium/phosphate solution. In conclusion, dietary supplementation of l-lysine ameliorated VC by modifying key pathways that exacerbate VC.

p-Cresyl sulfate promotes insulin resistance associated with CKD.

The mechanisms underlying the insulin resistance that frequently accompanies CKD are poorly understood, but the retention of renally excreted compounds may play a role. One such compound is p-cresyl sulfate (PCS), a protein-bound uremic toxin that originates from tyrosine metabolism by intestinal microbes. Here, we sought to determine whether PCS contributes to CKD-associated insulin resistance. Administering PCS to mice with normal kidney function for 4 weeks triggered insulin resistance, loss of fat mass, and ectopic redistribution of lipid in muscle and liver, mimicking features associated with CKD. Mice treated with PCS exhibited altered insulin signaling in skeletal muscle through ERK1/2 activation. In addition, exposing C2C12 myotubes to concentrations of PCS observed in CKD caused insulin resistance through direct activation of ERK1/2. Subtotal nephrectomy led to insulin resistance and dyslipidemia in mice, and treatment with the prebiotic arabino-xylo-oligosaccharide, which reduced serum PCS by decreasing intestinal production of p-cresol, prevented these metabolic derangements. Taken together, these data suggest that PCS contributes to insulin resistance and that targeting PCS may be a therapeutic strategy in CKD.

To eat or not to eat: dietary fat in uremia is the question.

Although a diet low in protein is well known to reduce the risk of progression in patients with chronic kidney disease (CKD), the impact of dietary fat content and fat quality has largely been ignored. As a reduced protein intake results in an obligatory reduction in energy intake, and as CKD patients often suffer from energy malnutrition, this issue deserves greater attention. The present review aims to summarize what is currently known about dietary fat intake in CKD and suggests areas for further study. We conclude that although overweight per se is an important risk factor for the development of CKD, the role of obesity as a risk factor for complications in manifest CKD remains unclear. Current data support a balanced increase in dietary fat intake in patients with CKD to compensate for reduced energy intake in protein-restricted diets and anorexic patients. However, patients who are obese should be encouraged to lose weight while maintaining or, preferably, increasing muscle mass.

Nutritional intervention in uremia--myth or reality?

Nutritional intervention in uremia, specifically the restricted protein diet, has been under debate for decades. The results of various clinical trials have not been concordant, as some studies have reported positive effects of the low-protein diets, whereas others have shown no benefit. Recently published data show that the restricted protein diets seem to be effective and safe in ameliorating nitrogen waste products retention and the disturbances in acid-base and calcium-phosphorus metabolism, and in delaying the initiation of renal replacement therapy (RRT), without any deleterious effect on the nutritional status of patients with chronic kidney disease. The nutritional support and particularly the supplemented very low protein diet could be a new link to the RRT-integrated care model. A possible delay in RRT initiation through nutrition could have a major economic effect, particularly in developing countries, where the dialysis facilities still do not meet the requirements. However, a careful selection of motivated patients who could benefit from such a diet, closer nutritional monitoring, and dietary counseling are required.

How to manage elderly patients with chronic renal failure: conservative management versus dialysis.

Over the past decade the number of elderly patients reaching end-stage renal disease has more than doubled. A fundamental medical decision that nephrologists commonly have to make is when to start dialytic treatment in elderly patients. Evidence is needed to inform about decision-making for or against dialysis, in particular in those patients frequently affected by multiple comorbidities for which dialysis may not increase survival. In fact, this decision affects quality of life, incurs significant financial costs, and finally mandates use of precious dialysis resources. The negative consequence of initiating dialysis in this group of patients can be deleterious as elderly people are sensitive to lifestyle changes. Furthermore, among dialysis patients, the elderly suffer the highest overall hospitalization and complication rates and most truncated life expectancy on dialysis of any age group. Studies of the factors that affect outcomes in elderly patients on dialysis, or the possibility in postponing in a safe way the start of a dialytic treatment, were lacking until recent years. Recently in the literature, papers have been published that address these questions: the effects of dialysis on morbidity and mortality in elderly patients and the use of a supplemented very low protein diet (sVLPD) in postponing the start of dialysis in elderly. The first study demonstrated that, although dialysis is generally associated with longer survival in patients aged >75 years, those with multiple comorbidities, ischemic heart disease in particular, do not survive longer than those treated conservatively. The second one is a randomized controlled study that compared a sVLPD with dialysis in 112 non-diabetic patients aged >70 years. Survival was not different between the two groups and the number of hospitalizations and days spent in hospital were significantly lower in those on a sVLPD. These studies add to the limited evidence that is currently available to inform elderly patients, their carers and their physicians about the risk and the benefit of dialysis.

Efeito da suplementação crônica com leucina na composição corporal e no estado protéico de ratos submetidos à restrição alimentar e a período de recuperação nutricional / Effect of the chronic supplementation with leucine on the body composition and on protein status of rats submitted to dietary restriction followed by a period of dietary recovery

Diversos estudos demonstraram que a administração aguda de leucina é capaz de estimular a síntese protéica. Contudo, poucos estudos verificaram os efeitos crônicos dessa suplementação em parâmetros que refletem o estado nutricional protéico (ENP). O presente estudo avaliou o efeito da suplementação crônica com leucina na composição corporal e no estado protéico de ratos submetidos à restrição alimentar (RA) e a período de recuperação nutricional (RN). Foram realizados dois experimentos com 88 ratos Wistar machos e adultos que foram mantidos em gaiolas individuais, em ambiente climatizado e com cicio biológico de 12 h claro/12 h escuro. No experimento I, 28 animais foram distribuídos em dois grupos: CON (ração AIN93-M) (n =15) e LEU (ração suplementada com 0,59% de L-Ieucina) (n=13) e submetidos à RA de 50% por seis semanas. No experimento II, 60 animais foram distribuídos em dois grupos: CON (ração AIN93-M) (n=30) e LEU (ração suplementada com 0,59% de L-Ieucina) (n=30) e submetidos à RA de 50% durante uma semana. Findo o período, 15 animais de cada grupo foram sacrificados; o restante dos animais (n=15 por grupo) foi submetido a duas semanas de RN com suas respectivas rações. No período de RN, as rações foram consumidas ad libitum. Avaliou-se: a composição química da carcaça; a massa de órgãos e do músculo gastrocnêmio; os conteúdos e as concentrações de proteína, RNA e DNA no fígado e no músculo gastrocnêmio; as concentrações séricas de IGF-1, corticosterona, leptina, proteínas totais, albumina e globulina; e as concentrações plasmáticas de uréia e glicose. No experimento I, a suplementação reduziu a gordura corporal e aumentou as concentrações de proteína hepática e de RNA muscular. No experimento II, não houve alterações na massa do intestino e nos conteúdos de proteína e de RNA no fígado dos animais suplementados durante os períodos de RA e RN. A suplementação com leucina aumentou a uremia dos animais do grupo LEU; em relação ao grupo CON, após RN...

Protein intake of more than 0.5 g/kg BW/day is not effective in suppressing the progression of chronic renal failure.

BACKGROUND: Although it is well-known that the restriction of protein intake in chronic renal failure (CRF) is effective in slowing the progressive loss of renal function, recent randomized controlled trials have not consistently shown a beneficial effect on CRF. There is controversy regarding the amount of protein intake that results in this effect. In this study, various amounts of protein intake were compared in CRF patients due to chronic glomerulonephritis (CGN) in order to explore effective restriction of dietary protein. METHODS: CGN patients (121 in total) with a serum creatinine level of 6 mg/dl were studied. They were subdivided into six groups depending on their protein intake: 0.3 g/kg BW/day (0.3 g), 0.4, 0.5, 0.6, 0.7, and > or =0.8 g (control group C). Deterioration of renal function was evaluated by the mean rate of decline in creatinine clearance, and the amount of protein intake was estimated on the basis of the urea nitrogen appearance rate in a 24-hour urine sample. RESULTS: There was no significant difference in the suppression of the progression of renal dysfunction in the 0.6- and 0.7-g groups. However, significant suppression was observed in the 0.5-, 0.4-, and 0.3-g groups in comparison with those that received more than 0.6 g (p < 0.05). The renal survival rate in the groups that received less than 0.5 g was higher than that in the groups that received more than 0.6 g (p < 0.05). Malnutrition was not observed in all patients studied. CONCLUSION: We found that a protein intake of more than 0.5 g/kg BW/day is not effective in suppressing further deterioration of renal function in CRF resulting from CGN.

Effects of nutritional status on the L-arginine-nitric oxide pathway in platelets from hemodialysis patients.

BACKGROUND: Malnutrition is a common feature in chronic renal failure and adversely affects patient morbidity and mortality. We here investigate the effects of nutritional status on the L-arginine-nitric oxide signaling pathway and platelet function in chronic renal failure patients on regular hemodialysis. METHODS: Platelet aggregation was correlated with plasma amino acid profiles, L-arginine transport, and nitric oxide synthase (NOS) activity determined by conversion of L-[(3)H]-arginine to L-[(3)H]-citrulline and accumulation of intracellular cyclic guanosine monophospate (cGMP) in platelets from malnourished and well-nourished chronic renal failure patients on regular hemodialysis (N = 78). RESULTS: Transport of L-arginine (pmol/10(9)cells/min) via y(+) L system was increased in well-nourished (104 +/- 15) compared to controls (57 +/- 11) or malnourished chronic renal failure patients (55 +/- 13). Basal NOS activity (pmol/10(8)cells) was enhanced in well-nourished chronic renal failure patients (0.51 +/- 0.01) compared to controls (0.18 +/- 0.01) or malnourished chronic renal failure patients (0.08 +/- 0.03). In addition, basal cGMP levels are elevated in platelets from well-nourished chronic renal failure compared to malnourished uremic patients. Platelet aggregation induced by collagen is impaired in well-nourished chronic renal failure patients compared to malnourished patients and controls. Plasma L-arginine levels are reduced in chronic renal failure patients and even lower in malnourished patients. CONCLUSION: Our findings provide the first evidence that L-arginine transport via the high affinity system y(+) L and nitric oxide synthesis are only stimulated in platelets from well-nourished chronic renal failure patients, leading to impaired platelet aggregation. The absence of this adaptive response in the l-arginine-nitric oxide pathway in platelets from malnourished chronic renal failure patients may account for the enhanced occurrence of thrombotic events in these patients.

[Role of dietary fibers in the nutritional management of chronic renal failure]. / Place des fibres alimentaires dans la prise en charge nutritionnelle de l'insuffisance rénale chronique.

During the past few decades, considerable attention has been given to the impact of nutrition on kidney disease. Although most dietary attempts to treat chronic renal failure (CRF) and to decrease uremia recommend a protein restriction, another dietetic approach, based on dietary fibers (DF), can lead to the same urea-lowering effect by increasing urea-nitrogen (N) excretion in stool with a concomitant decrease of the total N quantity excreted in urine. In fact, feeding DF results in a greater rate of urea N transfer from blood to large bowel, where it will be hydrolyzed by bacterial ureases before subsequent microflora metabolism and proliferation. Because elevated concentration of serum urea N have been associated with adverse clinical symptoms of CRF, these results suggested a possible usefulness of combining DF with a low protein diet to increase N excretion via the fecal route. These results have been shown in animal models of experimental renal failure and in CRF patients. Further investigations in this population of patients are currently in progress to study whether DF may be beneficial on CRF progression and on CRF terminal stage tolerance. A part of this work is financed by the French Society of Nephrology.