Background: Systematic reviews (SRs) are considered the highest level of evidence to answer research questions; however, they are time and resource intensive. Objective: When comparing SR tasks done manually, using standard methods, versus those same SR tasks done using automated tools, (1) what is the difference in time to complete the SR task and (2) what is the impact on the error rate of the SR task? Methods: A case study compared specific tasks done during the conduct of an SR on prebiotic, probiotic, and synbiotic supplementation in chronic kidney disease. Two participants (manual team) conducted the SR using current methods, comprising a total of 16 tasks. Another two participants (automation team) conducted the tasks where a systematic review automation (SRA) tool was available, comprising of a total of six tasks. The time taken and error rate of the six tasks that were completed by both teams were compared. Results: The approximate time for the manual team to produce a draft of the background, methods, and results sections of the SR was 126 hours. For the six tasks in which times were compared, the manual team spent 2493 minutes (42 hours) on the tasks, compared to 708 minutes (12 hours) spent by the automation team. The manual team had a higher error rate in two of the six tasks—regarding Task 5: Run the systematic search, the manual team made eight errors versus three errors made by the automation team; regarding Task 12: Assess the risk of bias, 25 assessments differed from a reference standard for the manual team compared to 20 differences for the automation team. The manual team had a lower error rate in one of the six tasks—regarding Task 6: Deduplicate search results, the manual team removed one unique study and missed zero duplicates versus the automation team who removed two unique studies and missed seven duplicates. Error rates were similar for the two remaining compared tasks—regarding Task 7: Screen the titles and abstracts and Task 9: Screen the full text, zero relevant studies were excluded by both teams. One task could not be compared between groups—Task 8: Find the full text. Conclusions: For the majority of SR tasks where an SRA tool was used, the time required to complete that task was reduced for novice researchers while methodological quality was maintained.

Microbiota-derived uremic toxins have been associated with inflammation that could corroborate with endothelial dysfunction (ED) and increase cardiovascular risk in patients with chronic kidney disease (CKD). This trial aimed to evaluate the effect of the prebiotic fructooligosaccharide (FOS) on endothelial function and arterial stiffness in nondialysis CKD patients. In a double-blind controlled trial, 46 nondiabetic CKD patients were randomized to receive 12 g/day of FOS or placebo (maltodextrin) for 3 months. Total p-cresyl sulfate (PCS) and indoxyl sulfate by high-performance liquid chromatography, urinary trimethylamine N-oxide by mass spectrometry, C-reactive protein, interleukin-6 (IL-6), serum nitric oxide and stroma-derived factor-1 alfa were measured at baseline and at the end of follow-up; endothelial function was assessed through flow-mediated dilatation (FMD) and arterial stiffness by pulse wave velocity (PWV). The mean (± standard deviation) age of the study participants was 57.6 ± 14.4 years, with an estimated glomerular filtration rate of 21.3 ± 7.3 mL/min/1.73 m². During the follow-up, regarding the inflammatory markers and uremic toxins, there was a significant decrease in IL-6 levels (3.4 ± 2.1 pg/mL versus 2.6 ± 1.4 pg/mL; P = 0.04) and a trend toward PCS reduction (55.4 ± 38.1 mg/L versus 43.1 ± 32.4 mg/L, P = 0.07) only in the prebiotic group. Comparing both groups, there was no difference in FMD and PWV. In an exploratory analysis, including a less severe ED group of patients (FMD ≥2.2% at baseline), FMD remained stable in the prebiotic group, while it decreased in the placebo group (group effect P = 0.135; time effect P = 0.012; interaction P = 0.002). The prebiotic FOS lowered circulating levels of IL-6 in CKD patients and preserved endothelial function only in those with less damaged endothelium. No effect of FOS in arterial stiffness was observed.

In recent decades, special attention has been given to the potential association between the gut ecosystem and chronic diseases. Several features and complications of chronic kidney disease (CKD) may induce an unbalanced gut environment, leading to unfavorable consequences for a patient’s health. The first section of this review is dedicated to a description of some aspects of gut microbiota and intestinal barrier physiology. The following section explores the impact of CKD on the gut ecosystem and intestinal barrier, particularly the association with uremic toxins, inflammation, and immunodeficiency. Finally, the review describes the state of the art of potential therapies with prebiotics, probiotics, and synbiotics employed to modulate the gut environment and to reduce the generation of colon-derived uremic toxins in CKD.

SUMMARY A healthy diet is an essential requirement to promote and preserve health, even in the presence of diseases, such as chronic kidney disease (CKD). In this review, nutritional therapy for CKD will be addressed considering not only the main nutrients such as protein, phosphorus, potassium, and sodium, which require adjustments as a result of changes that accompany the reduction of renal functions, but also the benefits of adopting dietary patterns associated with better outcomes for both preventing and treating CKD. We will also emphasize that these aspects should also be combined with a process of giving new meaning to a healthy diet so that it can be promoted. Finally, we will present the perspective of an integrated approach to the individual with CKD, exploring the importance of considering biological, psychological, social, cultural, and economic aspects. This approach has the potential to contribute to better adherence to treatment, thus improving the patient's quality of life.

Background Gut-derived uremic toxins have been associated with adverse outcomes in chronic kidney disease (CKD). Alterations in bowel habits, including constipation, seem to play an additional role in uremic toxicity. The aim of this study is to investigate the association of bowel habits with gut-derived uremic toxins and intestinal permeability in patients on automated peritoneal dialysis (APD). Methods This cross-sectional study enrolled 58 APD patients (age 52.5 ± 15.1 years; dialysis vintage 14.1 (6.0–36.5) months). Constipation was defined according to the Rome IV criteria. Bowel habits were assessed by the Bristol Stool Scale (BSS < 3 characterized by hard consistency of stools and/or low frequency of evacuation, a surrogate of slow intestinal transit time, and BSS ≥ 3, defining regular bowel habit). The total and free serum concentration of p-cresyl sulfate (PCS), indoxyl sulfate (IS) and indole-3-acetic acid (IAA) were dosed by high-performance liquid chromatography. Lipopolysaccharide (LPS) and zonulin were assessed by ELISA and d(–)-lactate by colorimetric method. Dietary intake was assessed by the 3-day food records. Results No differences were observed in clinical, demographic, and dietary characteristics between constipated (n = 30) and non-constipated (n = 28) groups. A trend for higher total PCS (p = 0.07) and free PCS (p = 0.06) was found in constipated patients. Patients with BSS < 3 (n = 11) exhibited significantly higher levels of total and free PCS (p < 0.01) and total IAA (p = 0.04). Conversely, No difference was found in IS levels. Except for a lower serum level of d(–)-lactate in patients with BSS < 3 (p = 0.01), zonulin and LPS levels were not different. Conclusions Disturbed bowel habits, mainly characterized by slow transit time, may play a role in the accumulation of uremic toxins, particularly PCS, in patients on automatized peritoneal dialysis.

In this narrative review, we briefly describe the general features of constipation, our understanding of its physiopathology, and its diagnosis and treatment, focusing on chronic kidney disease (CKD). Considering that constipation is poorly characterized in CKD, we referred to studies that used the Rome criteria to diagnose constipation in patients to describe a more realistic prevalence based on a standardized tool. A highly variable prevalence of the condition was reported, ranging from 4.5% to 71.7%. The main risk factors associated with constipation reported in these studies were advanced age, low fruit intake, presence of diabetes, and medication use, and the main consequence of constipation in CKD was a worse quality of life. We found a paucity of interventional studies for constipation treatment in CKD; however, in the general population, meta-analyses published in the last decade have reported the beneficial effects of non-pharmacological strategies, which may guide the management of constipated patients with CKD. These strategies include the consumption of fiber, prebiotics, and probiotics, as well as physical exercise and acupuncture. In conclusion, although constipation is a frequent complaint among patients with CKD, there remains a considerable knowledge gap regarding its epidemiology, prognosis, and treatment.