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Nutrients
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Nutritional Management in Kidney Disease
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Nutritional Management in Kidney Disease

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: 25 December 2025 | Viewed by 5009

Special Issue Editors

Prof. Dr. Yuji Kamijo

E-Mail Website
Guest Editor
Department of Nephrology, Shinshu University Hospital, Matsumoto 390-8621, Japan
Interests: nephrology; tubule; glomerulus; lipid metabolism; renal pathology; renal biochemistry; chronic kidney disease; acute kidney injury; dialysis; kidney transplantation; vascular access
Special Issues, Collections and Topics in MDPI journals
Dr. Katshuhito Mori

E-Mail Website
Guest Editor
Department of Nephrology, Osaka Metropolitan University Graduate School of Medicine, Osaka 545-8585, Japan
Interests: chronic kidney disease; nutrition; diabetes; glucose metabolism; insulin signaling; vascular calcification; hemodialysis
Special Issues, Collections and Topics in MDPI journals
Dr. Michihiro Hosojima

E-Mail Website
Guest Editor
Department of Clinical Nutrition Science, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan
Interests: nephrology; diabetology; metabolism and clinical nutrition; proximal tubule; megalin; low-protein diet; metabolic acidosis

Special Issue Information

Dear Colleagues,

Nutritional management is essential for the prevention and treatment of kidney disease. Traditionally, the main focus of nutritional management for kidney disease has been to restrict salt, calories, glucose, proteins, lipids, potassium, phosphate, etc. However, various nutrients are important for maintaining kidney function, and excessive restriction or disruption of nutrient balance may worsen the prognosis of kidney disease patients. In recent years, kidney disease patients have become more complex due to aging and comorbidities, and more appropriate nutritional management methods are needed. Furthermore, acute kidney injury and chronic kidney disease may require different nutritional management. For this Special Issue, we would like to discuss the clinical and basic topics that will help maintain normal function and metabolism in the kidney and that will develop new nutritional management methods to improve the prognosis of kidney disease patients (including dialysis and kidney transplant patients).

This Special Issue of Nutrients, entitled “Nutritional Management in Kidney Disease”, welcomes original research and reviews of the literature concerning this important topic.

Prof. Dr. Yuji Kamijo
Dr. Katshuhito Mori
Dr. Michihiro Hosojima
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • kidney disease
  • kidney function
  • metabolism
  • salt
  • calories
  • glucose
  • proteins
  • lipids
  • potassium
  • phosphate
  • trace elements

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Published Papers (4 papers)

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Research

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24 pages, 9204 KiB  
Article
Dietary Polyunsaturated Fatty Acid Deficiency Impairs Renal Lipid Metabolism and Adaptive Response to Proteinuria in Murine Renal Tubules
by Yaping Wang, Pan Diao, Daiki Aomura, Takayuki Nimura, Makoto Harada, Fangping Jia, Takero Nakajima, Naoki Tanaka and Yuji Kamijo
Nutrients 2025, 17(6), 961; https://doi.org/10.3390/nu17060961 - 10 Mar 2025
Viewed by 569
Abstract
Background/Objectives: Kidneys are fatty acid (FA)-consuming organs that use adenosine triphosphate (ATP) for tubular functions, including endocytosis for protein reabsorption to prevent urinary protein loss. Peroxisome proliferator-activated receptor α (PPARα) is a master regulator of FA metabolism and energy production, with high [...] Read more.
Background/Objectives: Kidneys are fatty acid (FA)-consuming organs that use adenosine triphosphate (ATP) for tubular functions, including endocytosis for protein reabsorption to prevent urinary protein loss. Peroxisome proliferator-activated receptor α (PPARα) is a master regulator of FA metabolism and energy production, with high renal expression. Although polyunsaturated fatty acids (PUFAs) are essential nutrients that are natural PPARα ligands, their role in tubular protein reabsorption remains unclear. As clinical PUFA deficiency occurs in humans under various conditions, we used a mouse model that mimics these conditions. Methods: We administered a 2-week intraperitoneal protein-overload (PO) treatment to mice that had been continuously fed a PUFA-deficient diet. We compared the phenotypic changes with those in mice fed a standard diet and those in mice fed a PUFA-deficient diet with PUFA supplementation. Results: In the absence of PO, the PUFA-deficient diet induced increased lysosomal autophagy activation; however, other phenotypic differences were not detected among the diet groups. In the PO experimental condition, the PUFA-deficient diet increased daily urinary protein excretion and tubular lysosomes; suppressed adaptive endocytosis activation, which was probably enhanced by continuous autophagy activation; and worsened FA metabolism and PPARα-mediated responses to PO, which disrupted renal energy homeostasis. However, these changes were attenuated by PUFA supplementation at the physiological intake level. Conclusions: PUFAs are essential nutrients for the tubular adaptive reabsorption response against urinary protein loss. Therefore, active PUFA intake may be important for patients with kidney disease-associated proteinuria, especially those with various PUFA deficiency-inducing conditions. Full article
(This article belongs to the Special Issue Nutritional Management in Kidney Disease)
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15 pages, 6483 KiB  
Article
Lactiplantibacillus plantarum 06CC2 Enhanced the Expression of Intestinal Uric Acid Excretion Transporter in Mice
by Shunsuke Nei, Tatsuya Matsusaki, Hibiki Kawakubo, Kenjirou Ogawa, Kazuo Nishiyama, Chuluunbat Tsend-Ayush, Tomoki Nakano, Masahiko Takeshita, Takuo Shinyama and Masao Yamasaki
Nutrients 2024, 16(17), 3042; https://doi.org/10.3390/nu16173042 - 9 Sep 2024
Cited by 2 | Viewed by 1527
Abstract
ATP-binding cassette transporter subfamily G member 2 (ABCG2) is responsible for the excretion of foreign substances, such as uric acid (UA) and indoxyl sulfate (IS), from the body. Given the importance of increased ABCG2 expression in UA excretion, we investigated the enhancement of [...] Read more.
ATP-binding cassette transporter subfamily G member 2 (ABCG2) is responsible for the excretion of foreign substances, such as uric acid (UA) and indoxyl sulfate (IS), from the body. Given the importance of increased ABCG2 expression in UA excretion, we investigated the enhancement of intestinal ABCG2 expression using Lactiplantibacillus plantarum 06CC2 (LP06CC2). Mice were reared on a potassium oxonate-induced high-purine model at doses of 0.02% or 0.1% LP06CC2 for three weeks. Results showed that LP06CC2 feeding resulted in increased ABCG2 expression in the small intestine. The expression level of large intestinal ABCG2 also showed a tendency to increase, suggesting upregulation of the intestinal excretion transporter ABCG2 by LP06CC2. Overall, LP06CC2 treatment increased fecal UA excretion and showed a trend towards increased fecal excretion of IS, suggesting that LP06CC2 treatment enhanced the expression of intestinal ABCG2, thereby promoting the excretion of UA and other substances from the intestinal tract. Full article
(This article belongs to the Special Issue Nutritional Management in Kidney Disease)
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Review

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22 pages, 4332 KiB  
Review
Assessing Creatine-Related Gene Expression in Kidney Disease: Can Available Data Give Insights into an Old Discussion?
by Matheus Anselmo Medeiros, Bento João Abreu and João Paulo Matos Santos Lima
Nutrients 2025, 17(4), 651; https://doi.org/10.3390/nu17040651 - 12 Feb 2025
Viewed by 1328
Abstract
The impact of creatine supplementation on individuals with kidney disease or pathological conditions with an increased risk of developing kidney dysfunction remains an active discussion. However, the literature on gene expression related to cellular creatine uptake and metabolism under altered renal function is [...] Read more.
The impact of creatine supplementation on individuals with kidney disease or pathological conditions with an increased risk of developing kidney dysfunction remains an active discussion. However, the literature on gene expression related to cellular creatine uptake and metabolism under altered renal function is scarce. Therefore, the present study utilized comprehensive bioinformatics analysis to evaluate the expression of creatine-related genes and to establish their relationships to normal and disturbed renal conditions. We identified 44 genes modulated explicitly in response to creatine exposure from a gene enrichment analysis, including IGF1, SLC2A4, and various creatine kinase genes. The analysis revealed associations with metabolic processes such as amino acid metabolism, indicating a connection between creatine and tissue physiology. Using the Genotype-Tissue Expression Portal, we evaluated their basal tissue-specific expression patterns in kidney and pancreas tissues. Then, we selected several pieces of Gene Expression Omnibus (GEO) transcriptomic data, estimated their expression values, and established relationships to the creatine metabolism pathways and regulation, shedding light on the potential regulatory roles of creatine in cellular processes during kidney diseases. These observations also highlight the connection between creatine and tissue physiology, emphasizing the importance of understanding the balance between endogenous creatine synthesis and creatine uptake, particularly the roles of genes such as GATM, GAMT, SLC6A8, and IGF1, under several kidney dysfunction conditions. Overall, the available data in the biological databases can provide new insights and directions into creatine’s effects and role in renal function. Full article
(This article belongs to the Special Issue Nutritional Management in Kidney Disease)
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33 pages, 1650 KiB  
Review
Lifestyle Factors and the Microbiome in Urolithiasis: A Narrative Review
by Antonios Koudonas, Stavros Tsiakaras, Vasileios Tzikoulis, Maria Papaioannou, Jean de la Rosette, Anastasios Anastasiadis and Georgios Dimitriadis
Nutrients 2025, 17(3), 465; https://doi.org/10.3390/nu17030465 - 27 Jan 2025
Viewed by 994
Abstract
Urolithiasis represents one of the most common urologic diseases, and its incidence demonstrates, globally, an increasing trend. The application of preventive measures is an established strategy to reduce urolithiasis-related morbidity, and it is based mostly on the adaptation of lifestyle factors and pharmacotherapy. [...] Read more.
Urolithiasis represents one of the most common urologic diseases, and its incidence demonstrates, globally, an increasing trend. The application of preventive measures is an established strategy to reduce urolithiasis-related morbidity, and it is based mostly on the adaptation of lifestyle factors and pharmacotherapy. Furthermore, other research areas demonstrate promising results, such as the research on the microbiome. In the current review, we searched for the latest data on lifestyle–based prevention and microbiome alterations in urolithiasis patients. The majority of the proposed lifestyle measures are already included in the urological guidelines, while additional factors, such as vitamin D supplementation, seem to have a putative positive effect. From the microbiome studies, several microbial composition patterns and metabolic pathways demonstrated an inhibiting or promoting role in lithogenesis. Up to the present, stone prevention has not shown satisfying results, which suggests that lifestyle measures are not adequate. Moreover, microbiome studies are prone to bias, since microbes are strongly affected by numerous clinical factors, while the analysis procedures are not standardized yet. Analysis standardization and data pooling from extensive registration of clinical and microbiome data are essential steps in order to improve the existing prevention strategy with targeted microbiome manipulations. Full article
(This article belongs to the Special Issue Nutritional Management in Kidney Disease)
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