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Background and Aims Little is known about the effects of probiotics on inflammation in the context of chronic kidney disease (CKD). We investigated the association between probiotic intake and inflammation in patients with moderate-to-advanced CKD. Methods We performed a cross-sectional study of 888 patients with stage 3–5 CKD and data on serum C-reactive protein (CRP) levels and a concomitant food frequency questionnaire. We estimated the odds ratios (ORs) [95% confidence interval (CI)] for various CRP thresholds (>3, >4, >5, >6, and >7 mg/L) associated with three intake categories (no yoghurt, ordinary yoghurt, and probiotics from yoghurts or dietary supplements) and two frequency categories (daily or less than daily). Results The 888 study participants (median age: 70; men: 65%) had a median estimated glomerular filtration rate of 28.6 mL/min/1.73 m 2 and a median [interquartile range] CRP level of 3.0 [1.6, 7.0] mg/L. Fifty-seven percent consumed ordinary yoghurt and 30% consumed probiotic yoghurt. The median intake frequency for yoghurt and probiotics was 7 per week. Relative to participants not consuming yoghurt, the ORs [95% CI] for CRP > 6 or >7 mg/L were significantly lower for participants consuming ordinary yoghurt (0.58 [0.37, 0.93] and 0.57 [0.35, 0.91], respectively) and for participants consuming probiotics (0.54 [0.33, 0.9] and 0.48 [0.28, 0.81], respectively), independently of age, sex, body mass index, CKD stage, cardiovascular disease, and fibre, protein and total energy intakes. The ORs were not significantly lower for CRP thresholds >3, >4, and >5 mg/L and were not significantly greater in daily consumers than in occasional consumers. Conclusion We observed independent associations between the consumption of yoghurt or probiotics and lower levels of inflammation in patients with CKD. There was no evidence of a dose-effect relationship. Clinical Trial Registration [ https://www.clinicaltrials.gov/ct2/show/NCT03381950 ], identifier [NCT03381950]., Contexte et objectifs : On sait peu de choses sur les effets des probiotiques surinflammation dansle contexte dechronique un rein maladie(MRC). Nous avons étudié l'association entreprobiotique admissionetinflammation dans les patientsavec un niveau modéré à avancéMRC. Méthodes : Nous avons réalisé une étude transversale de 888les patientsavec stade 3–5MRCet des données sur les taux sériques de protéine C-réactive (CRP) et un questionnaire sur la fréquence des aliments concomitants. Nous avons estimé les rapports de cotes (OR) [intervalle de confiance (IC) à 95 %] pour divers seuils de CRP (> 3, > 4, > 5, > 6 et > 7 mg/L) associés à troisadmissioncatégories (pas de yaourt, yaourt ordinaire et probiotiques issus de yaourts ou de compléments alimentaires) et deux catégories de fréquence (quotidiennement ou moins d'une fois par jour). Résultats : Les 888 participants à l'étude (âge médian : 70 ; hommes : 65 %) avaient un taux de filtration glomérulaire médian estimé de 28,6 mL/min/1,73 m 2 et un taux médian [écart interquartile] de CRP de 3,0 [1,6, 7,0] mg /L. Cinquante-sept pour cent consommaient du yaourt ordinaire et 30 % consommaientprobiotiqueYaourt. La médianeadmissionla fréquence pour le yaourt et les probiotiques était de 7 par semaine. Par rapport aux participants ne consommant pas de yaourt, les OR [IC à 95 %] pour la CRP > 6 ou > 7 mg/L étaient significativement plus faibles pour les participants consommant du yaourt ordinaire (0,58 [0,37, 0,93] et 0,57 [0,35, 0,91], respectivement) et pour les participants consommant des probiotiques (0,54 [0,33, 0,9] et 0,48 [0,28, 0,81], respectivement), indépendamment de l'âge, du sexe, de l'indice de masse corporelle,MRCstade, cardiovasculairemaladie, et les apports en fibres, en protéines et en énergie totale. Les OR n'étaient pas significativement inférieurs pour les seuils de CRP > 3, > 4 et > 5 mg/L et n'étaient pas significativement supérieursdansconsommateurs quotidiens quedansconsommateurs occasionnels. Conclusion : Nous avons observé des associations indépendantes entre la consommation de yaourt ou de probiotiques et des niveaux inférieurs deinflammation dans les patientsavecMRC. Il n'y avait aucune preuve d'une relation dose-effet. Enregistrement des essais cliniques : [https://www.clinicaltrials.gov/ct2/show/NCT03381950], identifiant [NCT03381950]. Copyright © 2022 Wagner, Merkling, Metzger, Koppe, Laville, Boutron-Ruault, Frimat, Combe, Massy, ​​Stengel et Fouque.

International audience; 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 some key uremic toxins production (such as PCS and IS), with a lower risk of malnutrition.

International audience; La maladie rénale chronique a été associée à des changements dans la fonction et la composition du microbiote intestinal. L'écosystème de l'intestin humain se compose de milliards de micro-organismes formant un authentique organe métaboliquement actif qui est alimenté par des nutriments pour produire des composés bioactifs. Ces métabolites dérivés du microbiote peuvent être protecteurs pour la fonction rénale (par exemple, les acides gras à chaîne courte issus de la fermentation des fibres alimentaires) ou délétères (par exemple, les toxines urémiques dérivées de l'intestin telles que le N-oxyde de triméthylamine, le sulfate de p-crésyle et le sulfate d'indoxyle de la fermentation des acides aminés). Bien que l'alimentation soit la pierre angulaire de la prise en charge du patient atteint d'insuffisance rénale chronique, elle reste une composante relativement sous-utilisée de l'arsenal thérapeutique du clinicien. Dans cette revue, nous décrivons les dernières avancées dans la compréhension de la diaphonie alimentation-microbiote dans le contexte urémique et comment cette communication pourrait contribuer à la progression et aux complications de la maladie rénale chronique. Nous discutons ensuite de la manière dont ces connaissances pourraient être exploitées pour des stratégies nutritionnelles personnalisées afin d'empêcher les patients atteints d'insuffisance rénale chronique de progresser vers l'insuffisance rénale et ses conséquences néfastes.

International audience; Protein energy wasting is a common feature of patients with chronic kidney disease (CKD) and is associated with poor outcomes. Protein energy wasting and cachexia, a severe form of protein energy wasting, are characterized by increased resting energy expenditure but the underlying mechanisms are unclear. Browning corresponds to the activation of inducible brown adipocytes in white adipose tissue and occurs in states of cachexia associated with hypermetabolic disease such as cancer. Here we tested the hypothesis that CKD-associated protein energy wasting could result from browning activation as a direct effect of the uremic environment on adipocytes. In a murine model of CKD (5/6 nephrectomy), there was increased resting energy expenditure, expression of uncoupling protein 1 (a thermogenic protein uncoupling oxidative phosphorylation in mitochondria) and citrate synthase activity (a proxy of mitochondria) density in white adipose tissue). Mice with CKD also exhibited increased levels of atrial natriuretic peptide, a well known activator of browning. The incubation of primary adipose cells with plasma from patients receiving dialysis treatment and having signs of protein energy wasting led to an increased synthesis of uncoupling protein 1. Similarly, primary adipose cells exposed to atrial natriuretic peptide at concentrations relevant of CKD led to a significant increase of uncoupling protein 1 content. Thus, accumulation of cardiac natriuretic peptides during CKD could contribute the browning of white adipose tissue and protein energy wasting.

The COVID-19 pandemic is characterized by a disease with mainly respiratory tropism and varying severity. Viral excretion of COVID-19 has been described in both urine and stool with the risk of contamination by stool. No viral replication in the peritoneal dialysis fluid has been reported to date. We report an observation demonstrating the presence of the virus in the peritoneal dialysis drainage fluid of a COVID-19 patient. This underlines the importance in COVID-19 patients of considering dialysis fluid as a possible source of contamination., Bulletin de la Dialyse à Domicile, Vol 3 No 1 (2020): Bulletin de la Dialyse à Domicile

International audience

Author(s): Koppe, Laetitia; Fouque, Denis; Kalantar-Zadeh, Kamyar | Abstract: BackgroundWeight loss and homeostatic disturbances of both energy and protein balances are characteristics of several illnesses including cancer, heart failure, and chronic kidney disease (CKD). Different definitions have been used to describe this deleterious process. The term protein-energy wasting (PEW) has been proposed for CKD patients by the International Society of Renal Nutrition and Metabolism.MethodsWe searched the publication in Medline from February 2008 to September 2018 using PEW or cachexia in their title.ResultsSince its inception, the term PEW has been exceptionally successful, highlighted by 327 original publications referenced in PubMed over 10 years. Using this classification, several studies have confirmed that PEW is among the strongest predictors of mortality in CKD patients [hazard ratio of 3.03; confidence interval of 1.69-5.26 in 1068 haemodialysis patients and 1.40 (1.04-1.89) in 1487 non-dialysed patients across PEW stages 0 to 4]. Based on this classification, prevalence of PEW is 28% to 54% among 16 434 adults undergoing maintenance dialysis. PEW prevalence increases when renal function declines, that is, from l2% in CKD stages 1-2 to 11-54% in CKD stages 3-5. A more general definition of cachexia for all chronic diseases proposed by the Society on Sarcopenia, Cachexia and Wasting Disorders was also published concurrently. In the CKD area, we found 180 publications using 'cachexia' underlining that some confusion or overlap may exist. The definitions of PEW and cachexia are somewhat similar, and the main difference is that a loss of body weight g5% is a mandatory criterion for cachexia but supportive for PEW.ConclusionsThe recent understanding of cachexia physiopathology during CKD progression suggests that PEW and cachexia are closely related and that PEW corresponds the initial state of a continuous process that leads to cachexia, implicating the same metabolic pathways as in other chronic diseases. Despite the success of the definition of PEW, using a more uniform term such as 'kidney disease cachexia' could be more helpful to design future research through collaborative groups of researchers with focus on cachexia.

International audience

International audience; Although gastrointestinal complications are a common feature of patients with chronic kidney disease (CKD), the impact of uremia on bowel motility remains poorly understood. The present study was, therefore, designed to investigate the impact of uremia on gut motility. Kidney failure was induced in mice by chemical nephrectomy using an adenine diet (0.25% w/w). Gastrointestinal transit time and colon motility were explored in vivo and ex vivo. Colons from control mice were incubated with uremic plasma or uremic toxins (urea, indoxyl-sulfate or p-cresyl-sulfate) at concentrations encountered in patients with end-stage renal disease. Mice fed an adenine diet for 3 weeks exhibited a 3-fold increase in plasma urea (p \textless 0.001) evidencing kidney failure. The median gastrointestinal transit time was doubled (1.8-fold, p \textless 0.001) while a reduction in colonic propulsive motility was observed in CKD mice (3-fold, p \textless 0.001). Colon from CKD mice exhibited an abnormal pattern of contraction associated with a blunted maximal force of contraction. Control colons incubated with plasma from hemodialysis patients exhibited a blunted level of maximal contraction (p \textless 0.01). Incubation with urea did not elicit any difference but incubation with indoxyl-sulfate or p-cresyl-sulfate decreased the maximal force of contraction (-66% and -55%, respectively. p \textless 0.01). Taken together, these data suggest that uremia impairs colon motility probably through the retention of uremic toxins. Colon dysmotility might contribute to the gastrointestinal symptoms often reported in patients with CKD.

International audience; Uremic retention solutes (URS) are associated with cardiovascular complications and poor survival in chronic kidney disease. The better understanding of the origin of a certain number of these toxins enabled the development of new strategies to reduce their production. URS can be classified according to their origins (i.e., host, microbial, or exogenous). The discovery of the fundamental role that the intestinal microbiota plays in the production of many URS has reinstated nutrition at the heart of therapeutics to prevent the accumulation of URS and their deleterious effects. The intestinal microbiota is personalized and is strongly influenced by dietary habits, such as the quantity and the quality of dietary protein and fibers. Herein, this review out lines the role of intestinal microbiota on URS production and the recent discoveries on the effect of diet composition on the microbial balance in the host with a focus on the effect on URS production.

article in Press; Recent data have shown that the host-intestinal microbiota interaction is intrinsically linked with overall health. Chronic kidney disease (CKD) could influence intestinal microbiota and gut dysbiosis is also considered as a cause of progression of kidney disease. An increasing body of evidence indicates that dysbiosis is a key contributor of uremic retention solutes (URS) accumulating in patients with CKD. The discovery of the kidney-gut axis has created new therapeutic opportunities for nutritional intervention in order to prevent adverse outcomes. One of these strategies is prebiotics, which refers to nondigestible food ingredients or substances that beneficial affect growth and/or activity of limited health-promoting bacteria in the gastrointestinal tract. The influence of prebiotics on the production and concentration of URS have been investigated in various animal and human CKD studies. However, to date, there is still paucity of high-quality intervention trials. Randomized controlled trials and adequately powered intervention studies are needed before recommending prebiotics in clinical practice. This review will outline the interconnection between CKD progression, dysbiosis and URS production and will discuss mechanisms of action and efficacy of prebiotics as a new CKD management tool, with a particular emphasis on URS generation.

The factors that precipitate the transition from insulin resistance to type 2 diabetes mellitus (T2DM) remain elusive. A recent study showed that circulating levels of the furan fatty acid (FA) metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanopropanoic Acid (CMPF) increase in individuals who progress from prediabetes to T2DM. CMPF increases oxidative stress and impairs insulin granule maturation and secretion.

International audience; Probiotics are the focus of a thorough investigation as a natural biotreatment due to their various health-promoting effects and inherent ability to fight specific diseases including chronic kidney disease (CKD). Indeed, intestinal microbiota has recently emerged as an important player in the progression and complications of CKD. Because many of the multifactorial physiological functions of probiotics are highly strain specific, preselection of appropriate probiotic strains based on their expression of functional biomarkers is critical. The interest in developing new research initiatives on probiotics in CKD have increased over the last decade with the goal of fully exploring their therapeutic potentials. The efficacy of probiotics to decrease uremic toxin production and to improve renal function has been investigated in in vitro models and in various animal and human CKD studies. However to date, the quality of intervention trials investigating this novel CKD therapy is still lacking. This review outlines potential mechanisms of action and efficacy of probiotics as a new CKD management tool, with a particular emphasis on uremic toxin production and inflammation.

Protein-energy wasting occurs frequently during maintenance dialysis. Known aetiologies include a loss of nutrients during the haemodialysis procedure and anorexia. Providing energy and protein during dialysis improves metabolism; however, the benefits of long-term support are debated. Weiner and colleagues report convincing data with an intradialytic oral nutritional intervention using protein supplements.