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Special Issue "Dietary Habits, Vitamin and Mineral Supplementations in Patients with Chronic Kidney Disease (CKD)"

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (31 January 2019)

Special Issue Editor

Guest Editor
Prof. Piergiorgio Messa

Full professor of Nephrology – Università degli Studi di Milano; Director of The nephrology, Dialysis and Renal Transplant Unit – Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico di Milano, Via Commenda 15, 20122
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Special Issue Information

Dear Colleagues,

Patients with chronic kidney diseases (CKD) are particularly exposed to malnutrition not only due to the frequent involvement of the gastrointestinal tract in the course of CKD, but also to the spontaneous or doctor-recommended modifications of their dietary habits and to the adverse effects of the large series of drugs usually prescribed.

This nutritional derangement can involve  particularly  vitamins and other micronutrients, whose altered availability has been put in relationship not only with the consequences strictly related to the well known classical effects of these compounds, but also with  some relevant clinical complications commonly observed in CKD patients. Furthermore, such nutritional modifications might be directly or indirectly related with some change in the quantitative and/or qualitative composition of the intestinal microbiota.

In this special issue of Nutrients, some experts in these fields will deal with some of the most critical conditions related to the altered dietary habits and availability of some of the most relevant vitamins and micronutrients in CKD patients.

Prof. Piergiorgio Messa
Guest Editor

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Published Papers (12 papers)

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Research

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Open AccessFeature PaperArticle
Moderate Protein Restriction in Advanced CKD: A Feasible Option in An Elderly, High-Comorbidity Population. A Stepwise Multiple-Choice System Approach
Nutrients 2019, 11(1), 36; https://doi.org/10.3390/nu11010036
Received: 24 November 2018 / Revised: 8 December 2018 / Accepted: 17 December 2018 / Published: 24 December 2018
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Abstract
Background: Protein restriction may retard the need for renal replacement therapy; compliance is considered a barrier, especially in elderly patients. Methods: A feasibility study was conducted in a newly organized unit for advanced kidney disease; three diet options were offered: normalization of protein [...] Read more.
Background: Protein restriction may retard the need for renal replacement therapy; compliance is considered a barrier, especially in elderly patients. Methods: A feasibility study was conducted in a newly organized unit for advanced kidney disease; three diet options were offered: normalization of protein intake (0.8 g/kg/day of protein); moderate protein restriction (0.6 g/kg/day of protein) with a “traditional” mixed protein diet or with a “plant-based” diet supplemented with ketoacids. Patients with protein energy wasting (PEW), short life expectancy or who refused were excluded. Compliance was estimated by Maroni-Mitch formula and food diary. Results: In November 2017–July 2018, 131 patients started the program: median age 74 years (min–max 24-101), Charlson Index (CCI): 8 (min-max: 2–14); eGFR 24 mL/min (4–68); 50.4% were diabetic, BMI was ≥ 30 kg/m2 in 40.4%. Normalization was the first step in 75 patients (57%, age 78 (24–101), CCI 8 (2–12), eGFR 24 mL/min (8–68)); moderately protein-restricted traditional diets were chosen by 24 (18%, age 74 (44–91), CCI 8 (4–14), eGFR 22 mL/min (5–40)), plant-based diets by 22 (17%, age 70 (34–89), CCI 6.5 (2–12), eGFR 15 mL/min (5–46)) (p < 0.001). Protein restriction was not undertaken in 10 patients with short life expectancy. In patients with ≥ 3 months of follow-up, median reduction of protein intake was from 1.2 to 0.8 g/kg/day (p < 0.001); nutritional parameters remained stable; albumin increased from 3.5 to 3.6 g/dL (p = 0.037); good compliance was found in 74%, regardless of diets. Over 1067 patient-months of follow-up, 9 patients died (CCI 10 (6–12)), 7 started dialysis (5 incremental). Conclusion: Protein restriction is feasible by an individualized, stepwise approach in an overall elderly, high-comorbidity population with a baseline high-protein diet and is compatible with stable nutritional status. Full article
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Open AccessArticle
Prevalence and Correlates of Sarcopenia among Elderly CKD Outpatients on Tertiary Care
Nutrients 2018, 10(12), 1951; https://doi.org/10.3390/nu10121951
Received: 1 November 2018 / Revised: 27 November 2018 / Accepted: 4 December 2018 / Published: 10 December 2018
Cited by 1 | PDF Full-text (1003 KB) | HTML Full-text | XML Full-text
Abstract
Background: Sarcopenia is a widespread concern in chronic kidney disease (CKD) as well in elderly patients and is one of the main reasons why low-protein diets for this population are controversial. The aim of this study was to assess the prevalence and correlates [...] Read more.
Background: Sarcopenia is a widespread concern in chronic kidney disease (CKD) as well in elderly patients and is one of the main reasons why low-protein diets for this population are controversial. The aim of this study was to assess the prevalence and correlates of sarcopenia among elderly male patients affected by CKD followed up in an outpatient nephrology clinic, where moderate protein restriction (0.6–0.8 g/Kg/day) is routinely recommended to patients in CKD stage 3b-5 not on dialysis. Methods: This observational study included 80 clinically-stable male out-patients aged >60, affected by stage 3b-4 CKD. Forty patients aged ≥75 (older seniors) were compared to the other forty patients aged 60–74 (younger seniors). All patients underwent a comprehensive nutritional and functional assessment. Results: Older seniors showed lower serum albumin, hand-grip strength, body mass index (BMI), skeletal muscle mass, and resting energy expenditure. Protein intake was significantly lower in older seniors whereas energy intake was similar. Average daily physical activity was lower in the older seniors than in the younger ones. Sarcopenia was more prevalent in older than in younger seniors. Among older seniors, sarcopenic and non-sarcopenic ones differed in age and performance on the Six-Minute Walk test, whereas the estimated glomerular filtration rate (eGFR), biochemistry, dietary protein, and energy intakes were similar. Conclusions: Older senior CKD male patients have lower muscle mass, muscle strength, and physical capacity and activity levels, with a higher prevalence of sarcopenia than younger patients. This occurs at the same residual renal function and metabolic profile and protein intake. Energy intake was at the target in both subgroups. In this CKD cohort, sarcopenia was associated with age and physical capacity, but not with eGFR or dietary intakes. Full article
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Open AccessArticle
Does a Supplemental Low-Protein Diet Decrease Mortality and Adverse Events After Commencing Dialysis? A Nationwide Cohort Study
Nutrients 2018, 10(8), 1035; https://doi.org/10.3390/nu10081035
Received: 20 July 2018 / Revised: 3 August 2018 / Accepted: 6 August 2018 / Published: 8 August 2018
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Abstract
Background: A beneficial effect of a ketoanalogue-supplemented low-protein diet (sLPD) in postponing dialysis has been demonstrated in numerous previous studies. However, evidence regarding its effect on long-term survival is limited. Our study assessed the long-term outcomes of patients on an sLPD after commencing [...] Read more.
Background: A beneficial effect of a ketoanalogue-supplemented low-protein diet (sLPD) in postponing dialysis has been demonstrated in numerous previous studies. However, evidence regarding its effect on long-term survival is limited. Our study assessed the long-term outcomes of patients on an sLPD after commencing dialysis. Methods: This retrospective study examined patients with new-onset end-stage renal disease with permanent dialysis between 2001 and 2013, extracted from Taiwan’s National Health Insurance Research Database. Patients who received more than 3 months of sLPD treatment in the year preceding the start of dialysis were extracted. The outcomes studied were all-cause mortality, infection rate, and major cardiac and cerebrovascular events (MACCEs). Results: After propensity score matching, the sLPD group (n = 2607) showed a lower risk of all-cause mortality (23.1% vs. 27.6%, hazard ratio (HR) 0.77, 95% confidence interval (CI) 0.70–0.84), MACCEs (19.2% vs. 21.5%, HR 0.86, 95% CI 0.78–0.94), and infection-related death (9.9% vs. 12.5%, HR 0.76, 95% CI 0.67–0.87) than the non-sLPD group did. Conclusion: We found that sLPD treatment might be safe without long-term negative consequences after dialysis treatment. Full article
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Review

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Open AccessReview
Lipid Accumulation and Chronic Kidney Disease
Nutrients 2019, 11(4), 722; https://doi.org/10.3390/nu11040722
Received: 28 February 2019 / Revised: 25 March 2019 / Accepted: 26 March 2019 / Published: 28 March 2019
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Abstract
Obesity and hyperlipidemia are the most prevalent independent risk factors of chronic kidney disease (CKD), suggesting that lipid accumulation in the renal parenchyma is detrimental to renal function. Non-esterified fatty acids (also known as free fatty acids, FFA) are especially harmful to the [...] Read more.
Obesity and hyperlipidemia are the most prevalent independent risk factors of chronic kidney disease (CKD), suggesting that lipid accumulation in the renal parenchyma is detrimental to renal function. Non-esterified fatty acids (also known as free fatty acids, FFA) are especially harmful to the kidneys. A concerted, increased FFA uptake due to high fat diets, overexpression of fatty acid uptake systems such as the CD36 scavenger receptor and the fatty acid transport proteins, and a reduced β-oxidation rate underlie the intracellular lipid accumulation in non-adipose tissues. FFAs in excess can damage podocytes, proximal tubular epithelial cells and the tubulointerstitial tissue through various mechanisms, in particular by boosting the production of reactive oxygen species (ROS) and lipid peroxidation, promoting mitochondrial damage and tissue inflammation, which result in glomerular and tubular lesions. Not all lipids are bad for the kidneys: polyunsaturated fatty acids (PUFA) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) seem to help lag the progression of chronic kidney disease (CKD). Lifestyle interventions, especially dietary adjustments, and lipid-lowering drugs can contribute to improve the clinical outcome of patients with CKD. Full article
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Open AccessFeature PaperReview
Dietary Components That May Influence the Disturbed Gut Microbiota in Chronic Kidney Disease
Nutrients 2019, 11(3), 496; https://doi.org/10.3390/nu11030496
Received: 22 January 2019 / Revised: 20 February 2019 / Accepted: 22 February 2019 / Published: 27 February 2019
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Abstract
Gut microbiota imbalance is common in patients with chronic kidney disease (CKD) and associates with factors such as increased circulating levels of gut-derived uremic toxins, inflammation, and oxidative stress, which are linked to cardiovascular disease and increased morbimortality. Different nutritional strategies have been [...] Read more.
Gut microbiota imbalance is common in patients with chronic kidney disease (CKD) and associates with factors such as increased circulating levels of gut-derived uremic toxins, inflammation, and oxidative stress, which are linked to cardiovascular disease and increased morbimortality. Different nutritional strategies have been proposed to modulate gut microbiota, and could potentially be used to reduce dysbiosis in CKD. Nutrients like proteins, fibers, probiotics, and synbiotics are important determinants of the composition of gut microbiota and specific bioactive compounds such as polyphenols present in nuts, berries. and fruits, and curcumin, may also play a key role in this regard. However, so far, there are few studies on dietary components influencing the gut microbiota in CKD, and it is therefore not possible to conclude which nutrients should be prioritized in the diet of patients with CKD. In this review, we discuss some nutrients, diet patterns and bioactive compounds that may be involved in the modulation of gut microbiota in CKD and provide the background and rationale for studies exploring whether nutritional interventions with these dietary components could be used to alleviate the gut dysbiosis in patients with CKD. Full article
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Open AccessReview
Magnesium: A Magic Bullet for Cardiovascular Disease in Chronic Kidney Disease?
Nutrients 2019, 11(2), 455; https://doi.org/10.3390/nu11020455
Received: 31 January 2019 / Revised: 17 February 2019 / Accepted: 19 February 2019 / Published: 22 February 2019
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Abstract
Magnesium is essential for many physiological functions in the human body. Its homeostasis involves dietary intake, absorption, uptake and release from bone, swifts between the intra- and extracellular compartment, and renal excretion. Renal excretion is mainly responsible for regulation of magnesium balance. In [...] Read more.
Magnesium is essential for many physiological functions in the human body. Its homeostasis involves dietary intake, absorption, uptake and release from bone, swifts between the intra- and extracellular compartment, and renal excretion. Renal excretion is mainly responsible for regulation of magnesium balance. In chronic kidney disease (CKD), for a long time the general policy has been limiting magnesium intake. However, this may not be appropriate for many patients. The reference ranges for magnesium are not necessarily optimal concentrations, and risks for insufficient magnesium intake exist in patients with CKD. In recent years, many observational studies have shown that higher (in the high range of “normal” or slightly above) magnesium concentrations are associated with better survival in CKD cohorts. This review gives an overview of epidemiological associations between magnesium and overall and cardiovascular survival in patients with CKD. In addition, potential mechanisms explaining the protective role of magnesium in clinical cardiovascular outcomes are described by reviewing evidence from in vitro studies, animal studies, and human intervention studies with non-clinical endpoints. This includes the role of magnesium in cardiac arrhythmia, heart failure, arterial calcification, and endothelial dysfunction. Possible future implications will be addressed, which will need prospective clinical trials with relevant clinical endpoints before these can be adopted in clinical practice. Full article
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Open AccessReview
Folic Acid and Vitamin B12 Administration in CKD, Why Not?
Nutrients 2019, 11(2), 383; https://doi.org/10.3390/nu11020383
Received: 29 January 2019 / Revised: 9 February 2019 / Accepted: 11 February 2019 / Published: 13 February 2019
Cited by 1 | PDF Full-text (842 KB) | HTML Full-text | XML Full-text
Abstract
Patients affected by chronic kidney disease (CKD) or end-stage renal disease (ESRD) experience a huge cardiovascular risk and cardiovascular events represent the leading causes of death. Since traditional risk factors cannot fully explain such increased cardiovascular risk, interest in non-traditional risk factors, such [...] Read more.
Patients affected by chronic kidney disease (CKD) or end-stage renal disease (ESRD) experience a huge cardiovascular risk and cardiovascular events represent the leading causes of death. Since traditional risk factors cannot fully explain such increased cardiovascular risk, interest in non-traditional risk factors, such as hyperhomocysteinemia and folic acid and vitamin B12 metabolism impairment, is growing. Although elevated homocysteine blood levels are often seen in patients with CKD and ESRD, whether hyperhomocysteinemia represents a reliable cardiovascular and mortality risk marker or a therapeutic target in this population is still unclear. In addition, folic acid and vitamin B12 could not only be mere cofactors in the homocysteine metabolism; they may have a direct action in determining tissue damage and cardiovascular risk. The purpose of this review was to highlight homocysteine, folic acid and vitamin B12 metabolism impairment in CKD and ESRD and to summarize available evidences on hyperhomocysteinemia, folic acid and vitamin B12 as cardiovascular risk markers, therapeutic target and risk factors for CKD progression. Full article
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Open AccessReview
Dietary Protein, Kidney Function and Mortality: Review of the Evidence from Epidemiological Studies
Nutrients 2019, 11(1), 196; https://doi.org/10.3390/nu11010196
Received: 3 January 2019 / Revised: 15 January 2019 / Accepted: 16 January 2019 / Published: 18 January 2019
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Abstract
The World Health Organization recommends a minimum requirement of 0.8 g/day protein/kg ideal weight. Low protein diets are used against kidney failure progression. Efficacy and safety of these diets are uncertain. This paper reviews epidemiological studies about associations of protein intake with kidney [...] Read more.
The World Health Organization recommends a minimum requirement of 0.8 g/day protein/kg ideal weight. Low protein diets are used against kidney failure progression. Efficacy and safety of these diets are uncertain. This paper reviews epidemiological studies about associations of protein intake with kidney function decline and mortality. Three studies investigated these associations; two reported data on mortality. Protein intake averaged >60 g/day and 1.2 g/day/kg ideal weight. An association of baseline protein intake with long-term kidney function decline was absent in the general population and/or persons with normal kidney function but was significantly positive in persons with below-normal kidney function. Independent of kidney function and other confounders, a J-curve relationship was found between baseline protein intake and mortality due to ≈35% mortality excess for non-cardiovascular disease in the lowest quintile of protein intake, a quintile where protein intake averaged <0.8 g/day/kg ideal weight. Altogether, epidemiological evidence suggests that, in patients with reduced kidney function, protein intakes of ≈0.8 g/d/kg ideal weight could limit kidney function decline without adding non-renal risks. Long-term lower protein intake could increase mortality. In most patients, an intake of ≈0.8 g/day/kg would represent a substantial reduction of habitual intake considering that average intake is largely higher. Full article
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Open AccessReview
Vitamin K in Chronic Kidney Disease
Nutrients 2019, 11(1), 168; https://doi.org/10.3390/nu11010168
Received: 16 November 2018 / Revised: 13 December 2018 / Accepted: 11 January 2019 / Published: 14 January 2019
Cited by 1 | PDF Full-text (282 KB) | HTML Full-text | XML Full-text
Abstract
Vitamin K is a composite term referring to a group of fat-soluble vitamins that function as a cofactor for the enzyme γ-glutamyl carboxylase (GGCX), which activates a number of vitamin K-dependent proteins (VKDPs) involved in haemostasis and vascular and bone health. Accumulating evidence [...] Read more.
Vitamin K is a composite term referring to a group of fat-soluble vitamins that function as a cofactor for the enzyme γ-glutamyl carboxylase (GGCX), which activates a number of vitamin K-dependent proteins (VKDPs) involved in haemostasis and vascular and bone health. Accumulating evidence demonstrates that chronic kidney disease (CKD) patients suffer from subclinical vitamin K deficiency, suggesting that this represents a population at risk for the biological consequences of poor vitamin K status. This deficiency might be caused by exhaustion of vitamin K due to its high requirements by vitamin K-dependent proteins to inhibit calcification. Full article
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Open AccessReview
The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD
Nutrients 2018, 10(12), 1890; https://doi.org/10.3390/nu10121890
Received: 13 September 2018 / Revised: 22 November 2018 / Accepted: 23 November 2018 / Published: 3 December 2018
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Abstract
In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D [...] Read more.
In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients. Full article
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Open AccessFeature PaperReview
Energy-Dense Diets and Mineral Metabolism in the Context of Chronic Kidney Disease–Metabolic Bone Disease (CKD-MBD)
Nutrients 2018, 10(12), 1840; https://doi.org/10.3390/nu10121840
Received: 16 October 2018 / Revised: 8 November 2018 / Accepted: 20 November 2018 / Published: 1 December 2018
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Abstract
The aim of this paper is to review current knowledge about the interactions of energy-dense diets and mineral metabolism in the context of chronic kidney disease–metabolic bone disease (CKD-MBD). Energy dense-diets promote obesity and type II diabetes, two well-known causes of CKD. Conversely, [...] Read more.
The aim of this paper is to review current knowledge about the interactions of energy-dense diets and mineral metabolism in the context of chronic kidney disease–metabolic bone disease (CKD-MBD). Energy dense-diets promote obesity and type II diabetes, two well-known causes of CKD. Conversely, these diets may help to prevent weight loss, which is associated with increased mortality in advanced CKD patients. Recent evidence indicates that, in addition to its nephrotoxic potential, energy-dense food promotes changes in mineral metabolism that are clearly detrimental in the context of CKD-MBD, such as phosphorus (P) retention, increased concentrations of fibroblast growth factor 23, decreased levels of renal klotho, and reduction in circulating concentrations of calcitriol. Moreover, in uremic animals, a high fat diet induces oxidative stress that potentiates high P-induced vascular calcification, and these extraskeletal calcifications can be ameliorated by oral supplementation of vitamin E. In conclusion, although energy-dense foods may have a role in preventing undernutrition and weight loss in a small section of the CKD population, in general, they should be discouraged in patients with renal disease, due to their impact on P load and oxidative stress. Full article
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Open AccessReview
Biotic Supplements for Renal Patients: A Systematic Review and Meta-Analysis
Nutrients 2018, 10(9), 1224; https://doi.org/10.3390/nu10091224
Received: 15 June 2018 / Revised: 28 August 2018 / Accepted: 29 August 2018 / Published: 4 September 2018
Cited by 2 | PDF Full-text (1835 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Intestinal dysbiosis is highly pervasive among chronic kidney disease (CKD) patients and may play a key role in disease progression and complications. We performed a systematic review and meta-analysis to evaluate effects of biotic supplements on a large series of outcomes in renal [...] Read more.
Intestinal dysbiosis is highly pervasive among chronic kidney disease (CKD) patients and may play a key role in disease progression and complications. We performed a systematic review and meta-analysis to evaluate effects of biotic supplements on a large series of outcomes in renal patients. Ovid-MEDLINE, PubMed and CENTRAL databases were searched for randomized controlled trials (RCTs) comparing any biotic (pre-, pro- or synbiotics) to standard therapy or placebo. Primary endpoints were change in renal function and cardiovascular events; secondary endpoints were change in proteinuria/albuminuria, inflammation, uremic toxins, quality of life and nutritional status. Seventeen eligible studies (701 participants) were reviewed. Biotics treatment did not modify estimated glomerular filtration rate (eGFR) (mean difference (MD) 0.34 mL/min/1.73 m2; 95% CI −0.19, 0.86), serum creatinine (MD −0.13 mg/dL; 95% confidence interval (CI) −0.32, 0.07), C-reactive protein (MD 0.75 mg/dL; 95% CI −1.54, 3.03) and urea (standardized MD (SMD) −0.02; 95% CI −0.25, 0.20) as compared to control. Outcome data on the other endpoints of interest were lacking, sparse or in an unsuitable format to be analyzed collectively. According to the currently available evidence, there is no conclusive rationale for recommending biotic supplements for improving outcomes in renal patients. Large-scale, well-designed and adequately powered studies focusing on hard rather than surrogate outcomes are still awaited. Full article
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