Search Results (6)

Chronic kidney disease (CKD) induces several systemic effects, including the accumulation and production of uremic toxins responsible for the activation of various harmful processes. Gut dysbiosis has been widely described in CKD patients, even in the early stages of the disease. The abundant discharge of urea and other waste substances into the gut favors the selection of an altered intestinal microbiota in CKD patients. The prevalence of bacteria with fermentative activity leads to the release and accumulation in the gut and in the blood of several substances, such as p-Cresol (p-C), Indoxyl Sulfate (IS) and p-Cresyl Sulfate (p-CS). Since these metabolites are normally eliminated in the urine, they tend to accumulate in the blood of CKD patients proportionally to renal impairment. P-CS, IS and p-C play a fundamental role in the activation of various pro-tumorigenic processes, such as chronic systemic inflammation, the increase in the production of free radicals and immune dysfunction. An up to two-fold increase in the incidence of colon cancer development in CKD has been reported in several studies, although the pathogenic mechanisms explaining this compelling association have not yet been described. Based on our literature review, it appears likely the hypothesis of a role of p-C, IS and p-CS in colon cancer development and progression in CKD patients. Full article

The gut microbiota consists of trillions of microorganisms, fulfilling important roles in metabolism, nutritional intake, physiology and maturation of the immune system, but also aiding and abetting the progression of chronic kidney disease (CKD). The human gut microbiome consists of bacterial species from five major bacterial phyla, namely Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, and Verrucomicrobia. Alterations in the members of these phyla alter the total gut microbiota, with a decline in the number of symbiotic flora and an increase in the pathogenic bacteria, causing or aggravating CKD. In addition, CKD-associated alteration of this intestinal microbiome results in metabolic changes and the accumulation of amines, indoles and phenols, among other uremic metabolites, which have a feedforward adverse effect on CKD patients, inhibiting renal functions and increasing comorbidities such as atherosclerosis and cardiovascular diseases (CVD). A classification of uremic toxins according to the degree of known toxicity based on the experimental evidence of their toxicity (number of systems affected) and overall experimental and clinical evidence was selected to identify the representative uremic toxins from small water-soluble compounds, protein-bound compounds and middle molecules and their relation to the gut microbiota was summarized. Gut-derived uremic metabolites accumulating in CKD patients further exhibit cell-damaging properties, damage the intestinal epithelial cell wall, increase gut permeability and lead to the translocation of bacteria and endotoxins from the gut into the circulatory system. Elevated levels of endotoxins lead to endotoxemia and inflammation, further accelerating CKD progression. In recent years, the role of the gut microbiome in CKD pathophysiology has emerged as an important aspect of corrective treatment; however, the mechanisms by which the gut microbiota contributes to CKD progression are still not completely understood. Therefore, this review summarizes the current state of research regarding CKD and the gut microbiota, alterations in the microbiome, uremic toxin production, and gut epithelial barrier degradation. Full article

Scientific evidence shows a positive association in the etiopathogenesis of periodontitis and chronic kidney disease (CKD). Various confounding factors, such as obesity, diabetes, and inflammation, also play a significant role in the progression of CKD, which remains unexplored. We hypothesise the role of red complex bacteria with various confounding factors associated with chronic kidney disease. The study comprised a total of 120 participants categorised into 4 groups: the control group (C), periodontitis subjects without CKD (P), periodontally healthy chronic kidney disease subjects (CKD), and subjects having both periodontitis and CKD (P + CKD), with 30 subjects in each group. Demographic variables, and periodontal, renal, and diabetic parameters were recorded. Tumour necrosis factor (TNF)-α levels and those of red complex bacteria such as Prophyromonas gingivalis (P.g), Treponema denticola (T.d), and Tonerella forsythia (T.f) were assessed, and the obtained results were statistically analysed. Among the various demographic variables, age showed a level of significance. Mean PI, GI, CAL, and PPD (the proportion of sites with PPD ≥ 5 mm and CAL ≥ 3 mm) were elevated in the P + CKD group. Diabetic parameters such as fasting blood sugar (FBS) and HbA1c levels were also greater in the P + CKD group. Renal parameters such as eGFR and serum creatinine levels were greater in CKD patients. The estimation of red complex periodontal pathogens such as Pg, Td and Tf levels were significantly greater in the P and P + CKD groups. Pearson correlation analysis revealed significant correlation of red complex bacteria with all variables. Greater levels of P.g, T.d and T.f were found in the P groups, thus indicating their important role in the initiation and progression of inflammation of periodontitis and CKD, with diabetes as one of the confounding factors. The study also confirmed a log-linear relationship between TNF-α levels and red complex bacteria, thereby demonstrating the role of inflammatory biomarkers in periodontal disease progression that could contribute to the development of systemic inflammation such as CKD. Full article

Several products consist of probiotics that are available in markets, and their potential uses are growing day by day, mainly because some strains of probiotics promote the health of gut microbiota, especially Furmicutes and Bacteroidetes, and may prevent certain gastrointestinal tract (GIT) problems. Some common diseases are inversely linked with the consumption of probiotics, i.e., obesity, type 2 diabetes, autism, osteoporosis, and some immunological disorders, for which the disease progression gets delayed. In addition to disease mitigating properties, these microbes also improve oral, nutritional, and intestinal health, followed by a robust defensive mechanism against particular gut pathogens, specifically by antimicrobial substances and peptides producing probiotics (AMPs). All these positive attributes of probiotics depend upon the type of microbial strains dispensed. Lactic acid bacteria (LAB) and Bifidobacteria are the most common microbes used, but many other microbes are available, and their use depends upon origin and health-promoting properties. This review article focuses on the most common probiotics, their health benefits, and the alleviating mechanisms against chronic kidney diseases (CKD), type 1 diabetes (T1D), type 2 diabetes (T2D), gestational diabetes mellitus (GDM), and obesity. Full article

In the intestines, probiotics can produce antagonistic effects such as antibiotic–like compounds, bactericidal proteins such as bacteriocins, and encourage the production of metabolic end products that may assist in preventing infections from various pathobionts (capable of pathogenic activity) microbes. Metabolites produced by intestinal bacteria and the adoptions of molecular methods to cross-examine and describe the human microbiome have refreshed interest in the discipline of nephology. As such, the adjunctive administration of probiotics for the treatment of chronic kidney disease (CKD) posits that certain probiotic bacteria can reduce the intestinal burden of uremic toxins. Uremic toxins eventuate from the over manifestation of glucotoxicity and lipotoxicity, increased activity of the hexosamine and polyol biochemical and synthetic pathways. The accumulation of advanced glycation end products that have been regularly associated with a dysbiotic colonic microbiome drives the overproduction of uremic toxins in the colon and the consequent local pro-inflammatory processes. Intestinal dysbiosis associated with significant shifts in abundance and diversity of intestinal bacteria with a resultant and maintained uremia promoting an uncontrolled mucosal pro-inflammatory state. In this narrative review we further address the efficacy of probiotics and highlighted in part the probiotic bacterium Streptococcus thermophilus as an important modulator of uremic toxins in the gut of patients diagnosed with chronic kidney disease. In conjunction with prudent nutritional practices it may be possible to prevent the progression of CKD and significantly downregulate mucosal pro-inflammatory activity with the administration of probiotics that contain S. thermophilus. Full article

Chronic kidney disease (CKD) is recognized as an irreversible reduction of functional nephrons and leads to an increased risk of various pathological conditions, including cardiovascular disease and neurological disorders, such as coronary artery calcification, hypertension, and stroke. In addition, CKD patients have impaired immunity against bacteria and viruses. Conversely, kidney transplantation (KT) is performed for patients with end-stage renal disease as a renal replacement therapy. Although kidney function is almost normalized by KT, immunosuppressive therapy is essential to maintain kidney allograft function and to prevent rejection. However, these patients are more susceptible to infection due to the immunosuppressive therapy required to maintain kidney allograft function. Thus, both CKD and KT present disadvantages in terms of suppression of immune function. Periodontal disease is defined as a chronic infection and inflammation of oral and periodontal tissues. Periodontal disease is characterized by the destruction of connective tissues of the periodontium and alveolar bone, which may lead to not only local symptoms but also systemic diseases, such as cardiovascular diseases, diabetes, liver disease, chronic obstructive pulmonary disease, and several types of cancer. In addition, the prevalence and severity of periodontal disease are significantly associated with mortality. Many researchers pay special attention to the pathological roles and clinical impact of periodontal disease in patients with CKD or KT. In this review, we provide information regarding important modulators of periodontal disease to better understand the relationship between periodontal disease and CKD and/or KT. Furthermore; we evaluate the impact of periodontal disease on various pathological conditions in patients with CKD and KT. Moreover, pathogens of periodontal disease common to CKD and KT are also discussed. Finally, we examine the importance of periodontal care in these patients. Thus, this review provides a comprehensive overview of the pathological roles and clinical significance of periodontal disease in patients with CKD and KT. Full article