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In this study, adults with progressive chronic kidney disease and an estimated glomerular filtration rate between 10 and 15 ml per minute per 1.73 m 2 (stage V chronic kidney disease) were randomly assigned to early or late initiation of dialysis. Early initiation of dialysis was not associated with an improvement in survival or clinical outcomes. The worldwide prevalence of long-term dialysis continues to rise, 1 , 2 driven in part by strong trends toward the initiation of dialysis earlier in the natural history of chronic kidney disease than was the practice previously. 3 – 5 Traditionally, the indicators for starting dialysis were the presence of signs and symptoms of uremia in combination with the results of biochemical measurements in serum and plasma. 6 However, a number of observational cohort and case–control studies have suggested that starting dialysis early may improve patients' survival, quality of life, and capacity for employment and decrease complications. 7 – 9 Although such studies were potentially limited by . . .

Purpose Uraemic pruritus (UP) is one of the most common complications in patients with end-stage renal disease (ESRD) undergoing dialysis and greatly undermines their quality of life. The present study was designed to compare the clinical effect of high-flux hemodialysis (HFHD) with hemodialysis filtration (HDF) in the treatment of UP in ESRD patients, and to explore the possible underlying mechanisms. Materials and methods In this 12-week randomized and controlled trial, the clinical efficacy of HFHD or HDF on UP patients undergoing dialysis was evaluated. A total of 51 uremia patients suffering from pruritus from January 2009 to May 2013 were recruited and randomly assigned to intervention ( n  = 27) and control ( n  = 24) groups. The control group was received only HDF therapy, and the intervention group underwent HFHD treatment three times a week for 12 weeks. Results The scores for Visual Analogue Scale in both two groups were obviously decreased, but the Visual Analogue Scale scores in the intervention group had a better improvement than the control group within 12 weeks. The PSQI and SF-12 values in the intervention group had a better improvement than the control group within 12 weeks. In comparison of the changes from baseline between the control groups, there was greater improvement in BUN, creatinine, calcium, phosphorus, PTH, β2-MG, histamine, CRP and IL-6 levels of intervention group. Conclusions Our results demonstrate that HFHD has a better efficacy in the treatment of UP than HDF. HFHD has an exactly therapeutical efficacy in the UP associated with the inhibition of microinflammation state in dialysis patients.

Background Uremic pruritus as a symptom that affects hemodialysis (HD) patients can decrease the quality of life and increase morbidity in these patients. The aim of this study was to evaluate the effects of turmeric on uremic pruritus in HD patients. Subjects and methods This was a double-blind placebo-controlled trial conducted on 100 HD patients suffering from pruritus. Patients (mean age 53.3 ± 15.8 years) were randomized into two groups: turmeric and placebo. The pruritus score and biochemical determinants including high-sensitivity C-reactive protein (hs-CRP) were compared before and at the end of the study between the two groups. Results The mean decrease in hs-CRP was significantly higher in the turmeric than the placebo group (−0.8 ± 2.6 vs. 0.4 ± 8.7 mg/l, p = 0.012). Also reduction of pruritus scores was greater in the turmeric than the placebo group (13.6 ± 2.6 vs. 7.2 ± 2.6, p = 0.001). No side effect was observed during the study due to the use of turmeric. Conclusions This study demonstrates the possible efficacy of turmeric in decreasing hs-CRP and uremic pruritus in end stage renal disease patients. Future studies are needed to further evaluate the efficacy and safety of turmeric.

Introduction. Uremic pruritus is one of the most common disabling symptoms in patients with end-stage renal disease. We aimed to study the effect of montelukast sodium for the treatment of uremic pruritus lasting more than 3 months in patients undergoing hemodialysis and compare it with placebo.Methods and Materials.Eighty patients undergoing hemodialysis at 3 centers in Shiraz, Iran, were recruited to a randomized double-blinded controlled trial to receive 10 mg of montelukast or placebo, daily for 30 days. To assess the severity of pruritus, a visual analogue scale and the Detailed Pruritus Score, based on a combined score of severity and distribution of pruritus and sleep disturbance, were used. Sleep disturbance, severity, and distribution scores were added up to calculate the patients' final score at the start and the end of the study.Results.The mean reduction of visual analogue scale score was significantly greater in the montelukast group (2.73 ± 2.03) compared to that in the placebo group (5.47 ± 2.37, P < .001). Mean reduction in Detailed Pruritus Score was also greater in the montelukast group (3.24 ± 2.2 versus 6.44 ± 3.25, respectively, P < .001). The mean high-sensitivity C-reactive protein in the montelukast group decreased from 5.48 ± 3.86 µg/mL to 3.86 ± 3.58 µg/mL, while it increased in the placebo group from 6.69 ± 4.49 µg/mL to 8.14 ± 5.20 µg/mL.Conclusions.Montelukast can be an add-on therapy in uremic pruritus, especially when pruritus is refractive to other treatments.

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.

Here we studied plasma metabolomic profiles as determinants of progression to end-stage renal disease (ESRD) in patients with type 2 diabetes (T2D). This nested case–control study evaluated 40 cases who progressed to ESRD during 8–12 years of follow-up and 40 controls who remained alive without ESRD from the Joslin Kidney Study cohort. Controls were matched with cases for baseline clinical characteristics, although controls had slightly higher eGFR and lower levels of urinary albumin excretion than cases. Plasma metabolites at baseline were measured by mass spectrometry–based global metabolomic profiling. Of the named metabolites in the library, 262 were detected in at least 80% of the study patients. The metabolomic platform recognized 78 metabolites previously reported to be elevated in ESRD (uremic solutes). Sixteen were already elevated in the baseline plasma of our cases years before ESRD developed. Other uremic solutes were either not different or not commonly detectable. Essential amino acids and their derivatives were significantly depleted in the cases, whereas certain amino acid–derived acylcarnitines were increased. All findings remained statistically significant after adjustment for differences between study groups in albumin excretion rate, eGFR, or HbA1c. Uremic solute differences were confirmed by quantitative measurements. Thus, abnormal plasma concentrations of putative uremic solutes and essential amino acids either contribute to progression to ESRD or are a manifestation of an early stage(s) of the disease process that leads to ESRD in T2D.

The observation that unhealthy diets (those that are low in whole grains, fruits and vegetables, and high in sugar, salt, saturated fat and ultra-processed foods) are a major risk factor for poor health outcomes has boosted interest in the concept of ‘food as medicine’. This concept is especially relevant to metabolic diseases, such as chronic kidney disease (CKD), in which dietary approaches are already used to ameliorate metabolic and nutritional complications. Increased awareness that toxic uraemic metabolites originate not only from intermediary metabolism but also from gut microbial metabolism, which is directly influenced by diet, has fuelled interest in the potential of ‘food as medicine’ approaches in CKD beyond the current strategies of protein, sodium and phosphate restriction. Bioactive nutrients can alter the composition and metabolism of the microbiota, act as modulators of transcription factors involved in inflammation and oxidative stress, mitigate mitochondrial dysfunction, act as senolytics and impact the epigenome by altering one-carbon metabolism. As gut dysbiosis, inflammation, oxidative stress, mitochondrial dysfunction, premature ageing and epigenetic changes are common features of CKD, these findings suggest that tailored, healthy diets that include bioactive nutrients as part of the foodome could potentially be used to prevent and treat CKD and its complications.Here, the authors discuss the mechanisms by which food and specific nutrients could affect the uraemic phenotype in chronic kidney disease (CKD). They suggest that a food-as-medicine approach could potentially be used to prevent and treat CKD and its complications.

Hemodialysis (HD) majorly represents the global treatment option for patients with chronic kidney disease stage 5, and, despite advances in dialysis technology, these patients face a high risk of morbidity and mortality from malnutrition. We aimed to provide a novel view that malnutrition susceptibility in the global HD community is either or both of iatrogenic and of non-iatrogenic origins. This categorization of malnutrition origin clearly describes the role of each factor in contributing to malnutrition. Low dialysis adequacy resulting in uremia and metabolic acidosis and dialysis membranes and techniques, which incur greater amino-acid losses, are identified modifiable iatrogenic factors of malnutrition. Dietary inadequacy as per suboptimal energy and protein intakes due to poor appetite status, low diet quality, high diet monotony index, and/or psychosocial and financial barriers are modifiable non-iatrogenic factors implicated in malnutrition in these patients. These factors should be included in a comprehensive nutritional assessment for malnutrition risk. Leveraging the point of origin of malnutrition in dialysis patients is crucial for healthcare practitioners to enable personalized patient care, as well as determine country-specific malnutrition treatment strategies.

Uraemic syndrome (also known as uremic syndrome) in patients with advanced chronic kidney disease involves the accumulation in plasma of small-molecule uraemic solutes and uraemic toxins (also known as uremic toxins), dysfunction of multiple organs and dysbiosis of the gut microbiota. As such, uraemic syndrome can be viewed as a disease of perturbed inter-organ and inter-organism (host–microbiota) communication. Multiple biological pathways are affected, including those controlled by solute carrier (SLC) and ATP-binding cassette (ABC) transporters and drug-metabolizing enzymes, many of which are also involved in drug absorption, distribution, metabolism and elimination (ADME). The remote sensing and signalling hypothesis identifies SLC and ABC transporter-mediated communication between organs and/or between the host and gut microbiota as key to the homeostasis of metabolites, antioxidants, signalling molecules, microbiota-derived products and dietary components in body tissues and fluid compartments. Thus, this hypothesis provides a useful perspective on the pathobiology of uraemic syndrome. Pathways considered central to drug ADME might be particularly important for the body’s attempts to restore homeostasis, including the correction of disturbances due to kidney injury and the accumulation of uraemic solutes and toxins. This Review discusses how the remote sensing and signalling hypothesis helps to provide a systems-level understanding of aspects of uraemia that could lead to novel approaches to its treatment.The plasma accumulation of uraemic solutes seen in chronic kidney disease is associated with dysregulated homeostasis. In this Review, Nigam and Bush discuss uraemic syndrome in the context of the remote sensing and signalling hypothesis, which describes small-molecule-mediated communication between tissues and organs.

The expression of the renoprotective antiaging gene Klotho is decreased in uremia. Recent studies suggest that Klotho may be a tumor suppressor, and its expression may be repressed by DNA hypermethylation in cancer cells. Here we investigated the effects and possible mechanisms by which Klotho expression is regulated during uremia in uninephrectomized B-6 mice given the uremic toxins indoxyl sulfate or p-cresyl sulfate. Cultured human renal tubular HK2 cells treated with these toxins were used as an in vitro model. Injections of indoxyl sulfate or p-cresyl sulfate increased their serum concentrations, kidney fibrosis, CpG hypermethylation of the Klotho gene, and decreased Klotho expression in renal tubules of these mice. The expression of DNA methyltransferases 1, 3a, and 3b isoforms in HK2 cells treated with indoxyl sulfate or p-cresyl sulfate was significantly increased. Specific inhibition of DNA methyltransferase isoform 1 by 5-aza-2′-deoxycytidine caused demethylation of the Klotho gene and increased Klotho expression in vitro. Thus, inhibition of Klotho gene expression by uremic toxins correlates with gene hypermethylation, suggesting that epigenetic modification of specific genes by uremic toxins may be an important pathological mechanism of disease.