Selenium (Se) is a mineral with several biological functions, and studies have shown that its deficiency can be linked to many complications in patients with chronic kidney disease (CKD). This study aims to systematically review the effects of Se supplementation in patients with CKD undergoing haemodialysis (HD). This systematic review was carried out according to the PRISMA statement. Clinical trials were searched in PubMed, Lilacs, Embase, Scopus and Cochrane Library databases from inception to July 2021 and updated in July 2024. The protocol was registered on PROSPERO (CRD42021231444). Two independent reviewers performed the study screening and data extraction, and the risk of bias was evaluated using the Cochrane Collaboration tool. Thirteen studies were included in this review. Only nine studies showed results on Se levels; in all, reduced Se levels were observed before supplementation. A positive effect of supplementation on plasma Se level was demonstrated. Of the ten studies analysed, six demonstrated positive effects on antioxidant and inflammatory markers. Only one study analysed immunological parameters, showing a positive impact. From two studies that analysed thyroid hormones, only one showed positive results. All studies were classified as high risk of bias. The findings suggest that Se supplementation significantly increases plasma Se levels in these patients; however, there are still not enough studies to clarify the effects of Se supplementation on the antioxidant and inflammatory markers, immune system and thyroid hormones. Further studies are needed to elucidate the effects of Se supplementation and to provide a recommendation for patients with CKD undergoing HD.

The potential threshold for dietary energy intake (DEI) that might prevent protein-energy wasting (PEW) in chronic kidney disease (CKD) is uncertain. The subjects were non-dialysis CKD patients aged ≥ 14 years who were hospitalised from September 2019 to July 2022. PEW was measured by subjective global assessment. DEI and dietary protein intake (DPI) were obtained by 3-d diet recalls. Patients were divided into adequate DEI group and inadequate DEI group according to DEI ≥ 30 or < 30 kcal/kg/d. Logistic regression analysis and restricted cubic spline were used in this study. We enrolled 409 patients, with 53·8 % had hypertension and 18·6 % had diabetes. The DEI and DPI were 27·63 (sd 5·79) kcal/kg/d and 1·00 (0·90, 1·20) g/kg/d, respectively. 69·2 % of participants are in the inadequate DEI group. Malnutrition occurred in 18·6 % of patients. Comparing with patients in the adequate DEI group, those in the inadequate DEI group had significantly lower total lymphocyte count, serum cholesterol and LDL-cholesterol and a higher prevalence of PEW. For every 1 kcal/kg/d increase in DEI, the incidence of PEW was reduced by 12·0 % (OR: 0·880, 95 % CI: 0·830, 0·933, P < 0·001). There was a nonlinear curve relationship between DEI and PEW (overall P < 0·001), and DEI ≥ 27·6 kcal/kg/d may have a preventive effect on PEW in CKD. Low DPI was also significantly associated with malnutrition, but not when DEI was adequate. Decreased energy intake may be a more important factor of PEW in CKD than protein intake.

The association between sarcopenia and kidney function remains poorly investigated. We aimed to evaluate the associations between sarcopenia status and kidney function (rapid kidney function decline and chronic kidney disease (CKD)) in middle-aged and older Chinese population. A total of 9375 participants from the China Health and Retirement Longitudinal Study 2011 were included in the cross-sectional analyses. A total of 5864 participants with eGFRcr-cys ≥ 60 ml/min per 1·73 m2 at baseline were included in the longitudinal analyses and were followed up in 2015. Sarcopenia status was defined according to the Asian Working Group for Sarcopenia 2019 criteria. In the cross-sectional analyses, possible sarcopenia and sarcopenia were significantly associated with an increased risk of CKD. During the 4 years of follow-up, 359 (6·12 %) participants experienced rapid decline in kidney function and 126 (2·15 %) participants developed CKD. After multivariable adjustment of baseline eGFRcr-cys level and other risk factors, possible sarcopenia (OR, 1·33; 95 % CI 1·01, 2·12) and sarcopenia (OR, 1·49; 95 % CI 1·05, 2·12) were associated with an increased risk of primary outcome (composite of rapid decline in kidney function (annualised decline in eGFRcr-cys ≥ 5 ml/min per 1·73 m2) and progression to CKD (eGFRcr-cys < 60 ml/min per 1·73 m2). Individuals with low muscle mass or low muscle strength alone also had an increased risk of rapid decline in kidney function and progression to CKD.

Although the cardiovascular benefits of an increased urinary potassium excretion have been suggested, little is known about the potential cardiac association of urinary potassium excretion in patients with chronic kidney disease. In addition, whether the cardiac association of urinary potassium excretion was mediated by serum potassium levels has not been studied yet. We reviewed the data of 1633 patients from a large-scale multicentre prospective Korean study (2011–2016). Spot urinary potassium to creatinine ratio was used as a surrogate for urinary potassium excretion. Cardiac injury was defined as a high-sensitivity troponin T ≥ 14 ng/l. OR and 95 % (CI for cardiac injury were calculated using logistic regression analyses. Of 1633 patients, the mean spot urinary potassium to creatinine ratio was 49·5 (sd 22·6) mmol/g Cr and the overall prevalence of cardiac injury was 33·9 %. Although serum potassium levels were not associated with cardiac injury, per 10 mmol/g Cr increase in the spot urinary potassium to creatinine ratio was associated with decreased odds of cardiac injury: OR 0·917 (95 % CI 0·841, 0·998), P = 0·047) in multivariate logistic regression analysis. In mediation analysis, approximately 6·4 % of the relationship between spot urinary potassium to creatinine ratio and cardiac injury was mediated by serum potassium levels, which was not statistically significant (P = 0·368). Higher urinary potassium excretion was associated with lower odds of cardiac injury, which was not mediated by serum potassium levels.

Immune cells play a key role in maintaining renal dynamic balance and dealing with renal injury. The physiological and pathological functions of immune cells are intricately connected to their metabolic characteristics. However, immunometabolism in chronic kidney disease (CKD) is not fully understood. Pathophysiologically, disruption of kidney immune cells homeostasis causes inflammation and tissue damage via triggering metabolic reprogramming. The diverse metabolic characteristics of immune cells at different stages of CKD are strongly associated with their different pathological effect. In this work, we reviewed the metabolic characteristics of immune cells (macrophages, natural killer cells, T cells, natural killer T cells and B cells) and several non-immune cells, as well as potential treatments targeting immunometabolism in CKD. We attempt to elaborate on the metabolic signatures of immune cells and their intimate correlation with non-immune cells in CKD.

The current trial investigates the effect of renal diet therapy and nutritional education on the estimated glomerular filtration rate (eGFR), blood pressure (BP) and depression among patients with chronic kidney disease (CKD). A total of 120 CKD patients (stages 3–4) (15<eGFR < 60) were randomised into an intensive nutrition intervention group (individualised renal diet therapy plus nutrition counselling: 0·75 g protein/kg/d and 30–35 kcal/kg/d with Na restriction) and a control group (routine and standard care) for 24 weeks. The primary outcome was the change in the eGFR. Secondary outcomes included changes in anthropometric measures, biochemistry (serum creatinine (Cr), uric acid, albumin, electrolytes, Ca, vitamin D, ferritin, blood urea nitrogen (BUN), and Hb), BP, nutritional status, depression and quality of life. The eGFR increased significantly in the intervention group compared with the control group (P < 0·001). Moreover, serum levels of Cr and the systolic and diastolic BP decreased significantly in the intervention group relative to the control group (P < 0·001, P < 0·001 and P = 0·020, respectively). The nutrition intervention also hindered the increase in the BUN level and the depression score (P = 0·045 and P = 0·028, respectively). Furthermore, the reduction in protein and Na intake was greater in the intervention group (P = 0·003 and P < 0·001, respectively). Nutritional treatment along with supportive education and counselling contributed to improvements in renal function, BP control and adherence to protein intake recommendations. A significant difference in the mean eGFR between the groups was also confirmed at the end of the study using ANCOVA (β = -5·06; 95 % CI (−8·203, −2·999)).

The objective of this research communication was to produce low potassium milk in which other electrolyte changes and changes in taste were minimized. To reduce potassium concentrations, several studies have reported batch methods of directly mixing milk or formula with sodium polystyrene sulfonate, which can exchange cations such as potassium for sodium. However, they also reported increases in sodium content, decreases in calcium and magnesium content, and changes in taste, because sodium polystyrene sulfonate exchanged other substances such as calcium and magnesium for sodium. In the present study, a method of dialyzing whole cow's milk using both sodium polystyrene sulfonate and a small amount of water through cellophane membranes was developed. A batch method for comparison was also performed. Each milk sample was evaluated biochemically and analyzed for taste and aroma in a sensory analysis. We showed that the potassium concentration in the dialyzed milk was reduced to 38% of that in unreacted milk. It was also shown that changes in sodium (increased) as well as calcium and magnesium (decreased) in the dialyzed milk were less than half of those in the batch method milk. Sensory analysis showed that minimal changes occurred in the taste of the dialyzed milk.

Using a sample of US adults aged 65 years and older, we examined the role of dietary quality in cystatin C change over 4 years and whether this association varied by race/ethnicity. The Health and Retirement Study provided observations with biomarkers collected in 2012 and 2016, participant attributes measured in 2012, and dietary intake assessed in 2013. The sample was restricted to respondents who were non-Hispanic/Latino White (n 789), non-Hispanic/Latino Black (n 108) or Hispanic/Latino (n 61). Serum cystatin C was constructed to be equivalent to the 1999–2002 National Health and Nutrition Examination Survey (NHANES) scale. Dietary intake was assessed by a semi-quantitative FFQ with diet quality measured using an energy-adjusted form of the Alternative Healthy Eating Index-2010 (AHEI-2010). Statistical analyses were conducted using autoregressive linear modelling adjusting for covariates and complex sampling design. Cystatin C slightly increased from 1·2 mg/l to 1·3 mg/l over the observational period. Greater energy-adjusted AHEI-2010 scores were associated with slower increase in cystatin C from 2012 to 2016. Among respondents reporting moderately low to low dietary quality, Hispanic/Latinos had significantly slower increases in cystatin C than their non-Hispanic/Latino White counterparts. Our results speak to the importance of considering racial/ethnic determinants of dietary intake and subsequent changes in health in ageing populations. Further work is needed to address measurement issues including further validation of dietary intake questionnaires in diverse samples of older adults.

The aim of the present study was to develop and validate a test to evaluate dietitian's clinical competence (CC) about nutritional care in patients with early chronic kidney disease (CKD). The study was conducted through five steps: (1) CC and its dimensions were defined; (2) test items were elaborated, and choice of response format and scoring system was selected; (3) content and face validity were established; (4) test was subjected to a pilot test and those items with inadequate performance were removed; (5) criterion validity and internal consistency for final validation were established. A 120-items test was developed and applied to 207 dietitians for validation. Dietitians with previous CKD training obtained higher scores than those with no training, confirming the test validity criterion. According to item analysis, Cronbach's α was 0⋅85, difficulty index 0⋅61 ± 0⋅22, discrimination index 0⋅26 ± 0⋅15 and inter-item correlation 0⋅19 ± 0⋅11, displaying adequate internal consistency.

We aimed to investigate the relationship between the neutrophil to lymphocyte ratio (NLR) and nutritional parameters in chronic kidney disease (CKD) patients. In this cross-sectional study, 187 non-dialysis CKD patients were enrolled. Daily dietary energy intake (DEI) and daily dietary protein intake (DPI) were assessed by 3-d dietary records. Protein-energy wasting (PEW) was defined as Subjective Global Assessment (SGA) class B and C. Spearman correlation analysis, logistic regression analysis and receiver operating characteristic (ROC) curve analysis were performed. The median NLR was 2·51 (1·83, 3·83). Patients with CKD stage 5 had the highest NLR level. A total of 19·3 % (n 36) of patients suffered from PEW. The NLR was positively correlated with SGA and serum P, and the NLR was negatively correlated with BMI, waist and hip circumference, triceps skinfold thickness, mid-arm muscle circumference, DPI and Hb. Multivariate logistic regression analysis adjusted for DPI, DEI, serum creatinine, blood urea nitrogen, uric acid and Hb showed that a high NLR was an independent risk factor for PEW (OR = 1·393, 95 % CI 1·078, 1·800, P = 0·011). ROC analysis showed that an NLR ≥ 2·62 had the ability to identify PEW among CKD patients, with a sensitivity of 77·8 %, a specificity of 62·3 % and an AUC of 0·71 (95 % CI 0·63, 0·81, P < 0·001). The NLR was closely associated with nutritional status. NLR may be an indicator of PEW in CKD patients.

In recent years, a wealth of factors are associated with increased risk of developing non-alcoholic fatty liver disease (NAFLD) and NAFLD is now thought to increase the risk of multiple extra-hepatic diseases. The aim of this review is first to focus on the role of ageing and sex as key, poorly understood risk factors in the development and progression of NAFLD. Secondly, we aim to discuss the roles of white adipose tissue (WAT) and intestinal dysfunction, as producers of extra-hepatic factors known to further contribute to the pathogenesis of NAFLD. Finally, we aim to summarise the role of NAFLD as a multi-system disease affecting other organ systems beyond the liver. Both increased age and male sex increase the risk of NAFLD and this may be partly driven by alterations in the distribution and function of WAT. Similarly, changes in gut microbiota composition and intestinal function with ageing and chronic overnutrition are likely to contribute to the development of NAFLD both directly (i.e. by affecting hepatic function) and indirectly via exacerbating WAT dysfunction. Consequently, the presence of NAFLD significantly increases the risk of various extra-hepatic diseases including CVD, type 2 diabetes mellitus, chronic kidney disease and certain extra-hepatic cancers. Thus changes in WAT and intestinal function with ageing and chronic overnutrition contribute to the development of NAFLD – a multi-system disease that subsequently contributes to the development of other chronic cardiometabolic diseases.