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Nutrients Intakes and Chronic Kidney Disease

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

Deadline for manuscript submissions: closed (30 April 2019) | Viewed by 38410

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Dr. Maria Dolores Sanchez-Niño

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Nephrology and Vascular Pathology Lab, IIS-Fundacion Jimenez Diaz, Av Reyes Catolicos 2, 28040 Madrid, Spain
Interests: pathogenesis and treatment of renal injury with emphasis on acute kidney injury; podocyte injury, diabetic nephropathy and Fabry disease; cardiovascular injury and CKD; phosphate and aging, phosphate binders; dietary potassium and microbiota

Special Issue Information

Dear Colleagues,

Nutrient intake is a key contributor to kidney health and in the management of kidney disease. Kidney disease is characterized by spontaneous changes in nutrient intake. The quality and quantity of nutrients may impact on the composition and metabolic activity of the gut microbiota, which has emerged as key regulator of health and disease states. Intake of certain nutrients can generate uremic toxins, which injure the cardiovascular and other systems, while other nutrients may regulate the progression of chronic kidney disease. Certain drugs are prescribed to prevent the absorption of certain harmful nutrients and may interfere with the absorption of needed nutrients. Finally, some nutrients need to be supplemented in patients with kidney disease. This Special Issue is devoted to recent advances in the field of nutrient intake and progression of kidney disease or kidney disease manifestations and how these recent advances may contribute to redesign current therapeutic approaches and nutritional counseling to patients with kidney disease. Additionally, new avenues of research are to be highlighted.

Dr. Maria Dolores Sanchez-Nino
Guest Editor

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Keywords

Kidney
Acute Kidney Injury
Chronic Kidney Disease
Diabetes kidney disease
Fabry disease
Inflammation
Cell death
Systems biology
Nutrients and kidney disease

Published Papers (5 papers)

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Research

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10 pages, 617 KiB

Open AccessArticle

Questioning the Safety of Calcidiol in Hemodialysis Patients

by Ricardo Villa-Bellosta, Ignacio Mahillo-Fernández, Alberto Ortíz and Emilio González-Parra

Nutrients 2019, 11(5), 959; https://doi.org/10.3390/nu11050959 - 26 Apr 2019

Cited by 2 | Viewed by 3128

Abstract

Background. Epidemiological studies have suggested a survival benefit for hemodialysis patients on paricalcitol or calcitriol, but nutritional vitamin D supplementation of patients already on vitamin D receptor (VDR) activators is controversial. Methods. This observational retrospective cohort study was conducted with prospectively collected data from all consecutive patients with chronic kidney disease (CKD) who underwent hemodialysis under routine clinical practice conditions for two years. Results. Of the 129 patients, 89 were treated with calcidiol, paricalcitol, and/or calcitriol. The patients with any vitamin D formulation had higher serum concentrations of 25-hydroxy vitamin D and fibroblast growth factor-23 and tended to have higher mortality rates (42% vs. 25%, p = 0.07). On subgroup analysis, any calcidiol treatment or calcidiol combined with paricalcitol associated with significantly higher mortality rates than no treatment (47% and 62.5%, p = 0.043 and 0.008, respectively). The association between calcidiol/paricalcitol treatment and elevated mortality remained significant after adjusting for age, sex, diabetes, C-reactive protein, and hemodialysis vintage. Any calcidiol and calcidiol/paricalcitol treatment exhibited a dose-response relationship with mortality (p for trend: 0.002 and 0.005, respectively). Conclusions. These data draw attention to the hitherto unexplored safety of calcidiol supplementation in patients on hemodialysis, especially in those already on vitamin D. Until clinical trials demonstrate the safety and efficacy of this approach, caution should be exercised when prescribing these patients ≥0.5 calcidiol mg/month. Full article

(This article belongs to the Special Issue Nutrients Intakes and Chronic Kidney Disease)

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15 pages, 8456 KiB

Open AccessArticle

Dietary Chrysin Suppresses Formation of Actin Cytoskeleton and Focal Adhesion in AGE-Exposed Mesangial Cells and Diabetic Kidney: Role of Autophagy

by Eun-Jung Lee, Min-Kyung Kang, Yun-Ho Kim, Dong Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, Su Yeon Oh and Young-Hee Kang

Nutrients 2019, 11(1), 127; https://doi.org/10.3390/nu11010127 - 09 Jan 2019

Cited by 14 | Viewed by 5395

Abstract

Advanced glycation end products (AGE) play a causative role in the development of aberrant phenotypes of intraglomerular mesangial cells, contributing to acute/chronic glomerulonephritis. The aim of this study was to explore mechanistic effects of the flavonoid chrysin present in bee propolis and herbs on actin dynamics, focal adhesion, and the migration of AGE-exposed mesangial cells. The in vitro study cultured human mesangial cells exposed to 33 mM glucose and 100 μg/mL AGE-bovine serum albumin (AGE-BSA) for up to 5 days in the absence and presence of 1–20 μM chrysin. The in vivo study employed db/db mice orally administrated for 10 weeks with 10 mg/kg chrysin. The presence of ≥10 μM chrysin attenuated mesangial F-actin induction and bundle formation enhanced by AGE. Chrysin reduced the mesangial induction of α-smooth muscle actin (α-SMA) by glucose, and diminished the tissue α-SMA level in diabetic kidneys, indicating its blockade of mesangial proliferation. The treatment of chrysin inhibited the activation of vinculin and paxillin and the induction of cortactin, ARP2/3, fascin-1, and Ena/VASP-like protein in AGE-exposed mesangial cells. Oral administration of chrysin diminished tissue levels of cortactin and fascin-1 elevated in diabetic mouse kidneys. Mesangial cell motility was enhanced by AGE, which was markedly attenuated by adding chrysin to cells. On the other hand, chrysin dampened the induction of autophagy-related genes of beclin-1, LC3 I/II, Atg3, and Atg7 in mesangial cells exposed to AGE and in diabetic kidneys. Furthermore, chrysin reduced the mTOR activation in AGE-exposed mesangial cells and diabetic kidneys. The induction of mesangial F-actin, cortactin, and fascin-1 by AGE was deterred by the inhibition of autophagy and mTOR. Thus, chrysin may encumber diabetes-associated formation of actin bundling and focal adhesion and mesangial cell motility through disturbing autophagy and mTOR pathway. Full article

(This article belongs to the Special Issue Nutrients Intakes and Chronic Kidney Disease)

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13 pages, 843 KiB

Open AccessArticle

Age Modifies the Association of Dietary Protein Intake with All-Cause Mortality in Patients with Chronic Kidney Disease

by Daiki Watanabe, Shinji Machida, Naoki Matsumoto, Yugo Shibagaki and Tsutomu Sakurada

Nutrients 2018, 10(11), 1744; https://doi.org/10.3390/nu10111744 - 13 Nov 2018

Cited by 18 | Viewed by 5318

Abstract

Whether the effect of a low-protein diet on progression to end-stage renal disease (ESRD) and mortality risk differs between young and elderly adults with chronic kidney disease (CKD) is unclear. We conducted a retrospective CKD cohort study to investigate the association between protein intake and mortality or renal outcomes and whether age affects this association. The cohort comprised 352 patients with stage G3-5 CKD who had been followed up for a median 4.2 years, had undergone educational hospitalization, and for whom baseline protein intake was estimated from 24-h urine samples. We classified the patients into a very low protein intake (VLPI) group (<0.6 g/kg ideal body weight/day), a low protein intake (LPI) group (0.6–0.8 g), and a moderate protein intake (MPI) group (>0.8 g). Compared with the LPI group, the MPI group had a significantly lower risk of all-cause mortality (hazard ratio: 0.29; 95% confidence interval: 0.07 to 0.94) but a similar risk of ESRD, although relatively high protein intake was related to a faster decline in the estimated glomerular filtration rate. When examined per age group, these results were observed only among the elderly patients, suggesting that the association between baseline dietary protein intake and all-cause mortality in patients with CKD is age-dependent. Full article

(This article belongs to the Special Issue Nutrients Intakes and Chronic Kidney Disease)

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Review

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24 pages, 1214 KiB

Open AccessReview

Dietary Care for ADPKD Patients: Current Status and Future Directions

by Sol Carriazo, Maria Vanessa Perez-Gomez, Adrian Cordido, Miguel Angel García-González, Ana Belen Sanz, Alberto Ortiz and Maria Dolores Sanchez-Niño

Nutrients 2019, 11(7), 1576; https://doi.org/10.3390/nu11071576 - 12 Jul 2019

Cited by 27 | Viewed by 7505

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic nephropathy, and tolvaptan is the only therapy available. However, tolvaptan slows but does not stop disease progression, is marred by polyuria, and most patients worldwide lack access. This and recent preclinical research findings on the glucose-dependency of cyst-lining cells have renewed interest in the dietary management of ADPKD. We now review the current dietary recommendations for ADPKD patients according to clinical guidelines, the evidence base for those, and the potential impact of preclinical studies addressing the impact of diet on ADPKD progression. The clinical efficacy of tolvaptan has put the focus on water intake and solute ingestion as modifiable factors that may impact tolvaptan tolerance and ADPKD progression. By contrast, dietary modifications suggested to ADPKD patients, such as avoiding caffeine, are not well supported and their impact is unknown. Recent studies have identified a chronic shift in energy production from mitochondrial oxidative phosphorylation to aerobic glycolysis (Warburg effect) as a contributor to cyst growth, rendering cyst cells exquisitely sensitive to glucose availability. Therefore, low calorie or ketogenic diets have delayed preclinical ADPKD progression. Additional preclinical data warn of potential negative impact of excess dietary phosphate or oxalate in ADPKD progression. Full article

(This article belongs to the Special Issue Nutrients Intakes and Chronic Kidney Disease)

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26 pages, 2969 KiB

Open AccessFeature PaperReview

Vegetable-Based Diets for Chronic Kidney Disease? It Is Time to Reconsider

by Aleix Cases, Secundino Cigarrán-Guldrís, Sebastián Mas and Emilio Gonzalez-Parra

Nutrients 2019, 11(6), 1263; https://doi.org/10.3390/nu11061263 - 04 Jun 2019

Cited by 86 | Viewed by 16456

Abstract

Traditional dietary recommendations to renal patients limited the intake of fruits and vegetables because of their high potassium content. However, this paradigm is rapidly changing due to the multiple benefits derived from a fundamentally vegetarian diet such as, improvement in gut dysbiosis, reducing the number of pathobionts and protein-fermenting species leading to a decreased production of the most harmful uremic toxins, while the high fiber content of these diets enhances intestinal motility and short-chain fatty acid production. Metabolic acidosis in chronic kidney disease (CKD) is aggravated by the high consumption of meat and refined cereals, increasing the dietary acid load, while the intake of fruit and vegetables is able to neutralize the acidosis and its deleterious consequences. Phosphorus absorption and bioavailability is also lower in a vegetarian diet, reducing hyperphosphatemia, a known cause of cardiovascular mortality in CKD. The richness of multiple plants in magnesium and vitamin K avoids their deficiency, which is common in these patients. These beneficial effects, together with the reduction of inflammation and oxidative stress observed with these diets, may explain the reduction in renal patients’ complications and mortality, and may slow CKD progression. Finally, although hyperkalemia is the main concern of these diets, the use of adequate cooking techniques can minimize the amount absorbed. Full article

(This article belongs to the Special Issue Nutrients Intakes and Chronic Kidney Disease)

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