scholarly journals Egg Intake in Chronic Kidney Disease

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1945 ◽  
Author(s):  
Dina Tallman ◽  
Sharmela Sahathevan ◽  
Tilakavati Karupaiah ◽  
Pramod Khosla

Patients with chronic kidney disease (CKD) are often instructed to adhere to a renal-specific diet depending on the severity and stage of their kidney disease. The prescribed diet may limit certain nutrients, such as phosphorus and potassium, or encourage the consumption of others, such as high biological value (HBV) proteins. Eggs are an inexpensive, easily available and high-quality source of protein, as well as a rich source of leucine, an essential amino acid that plays a role in muscle protein synthesis. However, egg yolk is a concentrated source of both phosphorus and the trimethylamine N-oxide precursor, choline, both of which may have potentially harmful effects in CKD. The yolk is also an abundant source of cholesterol which has been extensively studied for its effects on lipoprotein cholesterol and the risk of cardiovascular disease. Efforts to reduce dietary cholesterol to manage dyslipidemia in dialysis patients (already following a renal diet) have not been shown to offer additional benefit. There is a paucity of data regarding the impact of egg consumption on lipid profiles of CKD patients. Additionally, egg consumption has not been associated with the risk of developing CKD based on epidemiological studies. The egg yolk also contains bioactive compounds, including lutein, zeaxanthin, and vitamin D, which may confer health benefits in CKD patients. Here we review research on egg intake and CKD, discuss both potential contraindications and favorable effects of egg consumption, and describe the need for further research examining egg intake and outcomes in the CKD and end-stage renal disease population.

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Ifeoma I. Ulasi ◽  
Chinwuba K. Ijoma

Background. The magnitude of the problem of chronic kidney disease (CKD) is enormous, and the prevalence keeps rising. To highlight the burden of CKD in developing countries, the authors looked at end-stage renal disease (ESRD) patients seen at the University of Nigeria Teaching Hospital (UNTH), Enugu, South-East Nigeria.Method. ESRD patients seen from 01/05/1990 to 31/12/2003 were recruited. Records from A&E Department, medical-out-patients, wards and dialysis unit were used.Results. A total of 1001 male versus 537 female patients were reviewed. About 593 male versus 315 female patients had haemodialysis. The mean age was years and 86.5% were <60 years. Primary renal disease could not be determined in 51.6% while hypertension and glomerulonephritis accounted for −17.2% and 14.6%, respectively. Death from renal causes constituted 22.03% of medical deaths.Conclusion. The prognosis for CKD patients in Nigeria is abysmal. Only few patients had renal-replacement-therapy (RRT). The prohibitive cost precludes many patients. This underscores the need for preventive measures to reduce the impact of CKD in the society.


Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1234
Author(s):  
Maria Cappuccilli ◽  
Camilla Bergamini ◽  
Floriana A. Giacomelli ◽  
Giuseppe Cianciolo ◽  
Gabriele Donati ◽  
...  

Cardiovascular morbidity and mortality are several-fold higher in patients with advanced chronic kidney disease (CKD) and end-stage renal disease (ESRD) than in the general population. Hyperhomocysteinemia has undoubtedly a central role in such a prominent cardiovascular burden. The levels of homocysteine are regulated by methyl donors (folate, methionine, choline, betaine), and cofactors (vitamin B6, vitamin B12,). Uremia-induced hyperhomocysteinemia has as its main targets DNA methyltransferases, and this leads to an altered epigenetic control of genes regulated through methylation. In renal patients, the epigenetic landscape is strictly correlated with the uremic phenotype and dependent on dietary intake of micronutrients, inflammation, gut microbiome, inflammatory status, oxidative stress, and lifestyle habits. All these factors are key contributors in methylome maintenance and in the modulation of gene transcription through DNA hypo- or hypermethylation in CKD. This is an overview of the epigenetic changes related to DNA methylation in patients with advanced CKD and ESRD. We explored the currently available data on the molecular dysregulations resulting from altered gene expression in uremia. Special attention was paid to the efficacy of B-vitamins supplementation and dietary intake of methyl donors on homocysteine lowering and cardiovascular protection.


2019 ◽  
Vol 244 (6) ◽  
pp. 514-525 ◽  
Author(s):  
Mark A Bryniarski ◽  
Fares Hamarneh ◽  
Rabi Yacoub

Survival outcomes of patients with end stage renal disease are worse than those of many metastatic cancers. Kidney disease patients are often inflicted with higher rates of cardiovascular disease, in which nearly half of the mortalities are attributed to adverse cardiovascular events. Of the multifarious reasons for this detrimental impact, dysbiosis in the intestinal microbiome is surfacing as a potential participant. This is likely due to the numerous metabolic and inflammatory shifts found in chronic kidney disease, as well as environmental changes within the intestinal lumen. Studies are beginning to link microbiota alterations mediated by chronic kidney disease to negative cardiovascular outcomes. Here, recent findings connecting dysbiosis in chronic kidney disease and various cardiovascular insults are reviewed. Impact statement Negative alterations, or dysbiosis, in the intestinal microbial community balance in response to chronic kidney disease is emerging as a substantial and important factor in inducing and exacerbating multiple comorbid conditions. Patients with renal insufficiency experience a substantial increase in cardiovascular risk, and recent evidence is shedding light on the close interaction between microbiome dysbiosis and increased cardiovascular events in this population. Previous association and recent causality studies utilizing experimental animal models have enriched our understanding and confirmed the impact of microbial community imbalance on cardiac health in both the general population and in patients with renal impairment.


2020 ◽  
Vol 1 (2) ◽  
pp. 101-104
Author(s):  
Bando H ◽  
Kato Y

Maintenance of muscle mass and protein intake are closely related. Insufficient protein intake in each meal or a total of three meals causes a decrease in muscle mass. For the elderly, protein intake has been insufficient at breakfast and then a large amount of protein is necessary for stimulating muscle protein synthesis. Consequently, there is a need to more actively and consciously take protein in older age. There have been conflicting results concerning the effect of protein restriction diet on glomerular filtration rate (GFR) in patients with chronic kidney disease (CKD) from the data of various meta-analyses. A beneficial effect and also no significant effect was found. One of the perspectives suggested that protein restriction diet may make slower CKD progression in T1DM and non-DM subjects, but not for T2DM patients. However, further studies will be necessary in the future.


2018 ◽  
Vol 108 (5) ◽  
pp. 1145-1153 ◽  
Author(s):  
Ting-Yun Lin ◽  
Jia-Sin Liu ◽  
Szu-Chun Hung

ABSTRACT Background Obesity is a risk factor for de novo chronic kidney disease (CKD) in the general population. Obesity has been increasingly prevalent in patients with CKD and may lead to further progression of pre-existing CKD. However, whether obesity is associated with the development of end-stage renal disease (ESRD) in patients with CKD is not well understood. Objective We investigated the impact of obesity on ESRD (needing chronic dialysis treatment or pre-emptive renal transplantation) or all-cause mortality in patients with moderate to advanced CKD. Design A total of 322 patients with stages 3–5 CKD who were not yet on dialysis were prospectively followed for a median of 4.9 y. Obesity was defined by body mass index (BMI, in kg/m2) ≥30 or body fat percentage (BF%) >25% in men and >35% in women. BF% was assessed with the use of the Body Composition Monitor, a multifrequency bioimpedance spectroscopy device. Results In total, 100 participants progressed to ESRD and 39 participants died. Obesity, whether defined by BMI or BF%, was not associated with a significantly increased risk of ESRD in Cox proportional hazards models that adjusted for age, sex, diabetes mellitus, cardiovascular disease, estimated glomerular filtration rate, urine protein:creatinine ratio, high-sensitivity C-reactive protein, and use of renin-angiotensin-aldosterone system inhibitors or statins, accounting for the competing risk for mortality (subdistribution HR: 1.15; 95% CI: 0.62, 2.14 for BMI-defined obesity and subdistribution HR: 0.84, 95% CI: 0.54, 1.29 for BF%-defined obesity, respectively). Results were similar when BMI and BF% were analyzed as continuous or time-dependent variables. Whereas higher BMI was protective, higher BF% appeared to be associated with increased all-cause mortality. Conclusions Obesity did not confer an increased risk of ESRD in patients with moderate to advanced CKD. This trial was registered at http://www.clinicaltrials.gov as NCT03285074.


2019 ◽  
pp. 001857871989470
Author(s):  
Amanda Mertz ◽  
Danielle Cooney ◽  
Mahboob Rahman ◽  
Christopher Lacey ◽  
Christopher J. Burant ◽  
...  

Purpose: Proton pump inhibitors (PPIs) are commonly used medications and are historically well tolerated. Recent studies have linked PPI use to the development of chronic kidney disease (CKD) and end-stage renal disease. This study investigated the impact of discontinuing PPIs on renal function in patients with CKD. Methods: We conducted a retrospective chart review of patients with established CKD, defined as 2 eGFR (estimated glomerular filtration rate) measurements of less than 60 mL/min/1.73 m2 at least 90 days apart, who were on a PPI from January 1, 2014 to December 31, 2014, with a medication possession ratio greater than or equal to 70%. We compared baseline eGFR to a final eGFR after at least 6 months of discontinuation or continuation of a PPI. After power analysis, we targeted an enrollment of 200 patients (100 in each group) to achieve a power of 0.80 and an alpha of 0.05. Summary: A total of 100 patients in the PPI discontinuation group and 97 patients in the PPI continuation group met the study inclusion criteria. Baseline eGFR in the PPI continuation group was 47.9 mL/min/1.73 m2 and 50.7 mL/min/1.73 m2 in the discontinuation group. Final eGFR in the PPI continuation group was significantly higher than baseline at 51.1 mL/min/1.73 m2 (+3.25 ± 12.8, P = .01). Final eGFR in the PPI discontinuation group was 51.8 mL/min/1.73 m2 (+1.09 ± 12.8, P = .3). The average time between baseline and final eGFRs was 270 days in the PPI continuation group and 301 days in the discontinuation group. There was no statistically significant difference in the change in eGFRs between groups (95% confidence interval [CI] = −5.48-2.03, P = .37). Conclusions: Proton pump inhibitor discontinuation after prolonged continuous use in patients with CKD was not associated with a significant change in renal function after 1 year.


2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Aamir Cheema ◽  
Tejwant Singh ◽  
Manreet Kanwar ◽  
Karuna Chilukuri ◽  
Viqar Maria ◽  
...  

Incidence of sudden cardiac death (SCD) in end-stage renal disease (ESRD) remains high. Limited data is available about whether implantable cardioverter-defibrillators (ICDs) can prevent arrhythmic death in patients with chronic kidney disease (CKD). The purpose of this retrospective study was to determine the impact of CKD on all-cause and sudden cardiac death in ICD recipients. We evaluated 441 consecutive patients who underwent ICD implantation at our center between 1994 and 2002. We found that mortality rate was higher in patients with eGFR<60 mL/min and those with ESRD on hemodialysis (43%,n=69/162and 54%,n=12/22, resp.) than in patients with eGFR≥60 mL/min (23%,n=58/257;P<.0005). The SCD rate was also higher in the patients with ESRD (50%) than in CKD patients not on dialysis (10.2%;P<.0005). Mortality rate for single-chamber ICDs was 56.8% in comparison with dual-chamber ICDs (38.1%) and for biventricular ICDs (5.0%) (P<.0005).


2021 ◽  
Vol 72 (1) ◽  
pp. 25-33
Author(s):  
Đurđa Jerotić ◽  
Marija Matić ◽  
Lana McClements

Both excessive production of reactive oxygen species (ROS) and impaired antioxidant function are found in patients with chronic kidney disease (CKD). Therefore, individual susceptibility towards CKD can be induced by functional variations of genes encoding antioxidant regulatory (nuclear factor erythroid 2 - related factor 2 (Nrf2)) and catalytic (superoxide dismutase (SOD2) and glutathione peroxidase (GPX1)) proteins. Several types of single nucleotide polymorphisms (SNPs) have been found within the genes encoding these proteins, with Nrf2 (-617C/A), SOD2 (Ala16Val) and GPX1 (Pro198Leu) conferring impaired catalytic activity. The most unexplored gene polymorphism in CKD susceptibility, progression and survival, with only two original studies published, is the Nrf2 (-617C/A) polymorphism. The results of these studies showed that there was no individual impact of this polymorphism on the susceptibility towards end stage renal disease (ESRD) development, oxidative phenotype and mortality. However, Nrf2 had a significant role in ESRD risk and survival, when combined with other antioxidant genes. The results regarding the impact of SOD2 (Ala16Val) and GPX1 (Pro198Leu) polymorphisms on either CKD or ESRD are still inconclusive. Namely, some studies showed that patients having variant SOD2 (Val) or GPX1 (Leu) allele were at increased risk of CKD development and progression, while other studies reported only weak or no association between these polymorphisms and CKD. Surprisingly, the only study that reported an association of GPX1 polymorphism with overall/cardiovascular survival in ESRD patients showed a significant impact of low activity GPX1 (Leu/Leu) genotype on better survival. In this review, we comprehensively and critically appraise the literature on these polymorphisms related to oxidative stress in CKD patients, in order to identify gaps and provide recommendations for further clinical research and translation. New developments in the field of antioxidant polymorphisms in CKD patients could lead to better stratification of CKD patients, based on a prognostic antioxidant gene panel, and provide a more personalised medicine approach for the need of antioxidant therapy in these patients.


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