Animal Protein Kidney Disease

All articles published by are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by , including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https:///openaccess.

Feature papers represent the most advanced research with significant potential for high impact in the field. A Feature Paper should be a substantial original Article that involves several techniques or approaches, provides an outlook for future research directions and describes possible research applications.

Editor’s Choice articles are based on recommendations by the scientific editors of journals from around the world. Editors select a small number of articles recently published in the journal that they believe will be particularly interesting to readers, or important in the respective research area. The aim is to provide a snapshot of some of the most exciting work published in the various research areas of the journal.

Kidney Disease Grocery List Low Sodium Potassium Protein

By Matthew Snelson Matthew Snelson Scilit Preprints.org Google Scholar 1, *, † , Rachel E. Clarke Rachel E. Clarke Scilit Preprints.org Google Scholar 1, 2, † and Melinda T. Coughlan Melinda T. Coughlan Scilit Preprints.org Google Scholar 1, 3, *

Diet is one of the largest modifiable risk factors for chronic kidney disease (CKD)-related death and disability. CKD is largely a progressive disease; however, it is increasingly appreciated that hallmarks of chronic kidney disease such as albuminuria can regress over time. The factors driving albuminuria resolution remain elusive. Since albuminuria is a strong risk factor for GFR loss, modifiable lifestyle factors that lead to an improvement in albuminuria would likely reduce the burden of CKD in high-risk individuals, such as patients with diabetes. Dietary therapy such as protein and sodium restriction has historically been used in the management of CKD. Evidence is emerging to indicate that other nutrients may influence kidney health, either through metabolic or haemodynamic pathways or via the modification of gut homeostasis. This review focuses on the role of diet in the pathogenesis and progression of CKD and discusses the latest findings related to the mechanisms of diet-induced kidney disease. It is possible that optimizing diet quality or restricting dietary intake could be harnessed as an adjunct therapy for CKD prevention or progression in susceptible individuals, thereby reducing the burden of CKD.

Chronic kidney disease (CKD) is a broad term given to a range of disorders characterised by impaired kidney structure and function [1]. Chronic conditions such as diabetes, obesity, hypertension or cardiovascular disease can lead to the development of CKD; however, it can also occur in the absence of disease due to aging, exposure to toxins or infection [1]. The current diagnostic criterion for CKD is a glomerular filtration rate (GFR) of <60 mL/min per 1.73 m

Chronic Kidney Disease

Or a urinary albumin to creatinine ratio of >30 mg/g [2]. Based on this definition, CKD is estimated to affect more than 10% of the global population [3]. A GFR of <60 mL/min per 1.73 m

Is associated with an increased risk of cardiovascular disease (CVD) mortality and all-cause mortality [4]. Given these observations, CKD is poised to become a major burden to health care systems globally, particularly as populations continue to age.

The kidney plays a central role in maintaining homeostasis in the body, and is often the target organ of inflammatory, metabolic and systemic vascular disorders [5]. Nutrition and dietary patterns are implicated in the development of chronic metabolic diseases, and are modifiable factors that can be utilised to prevent or slow the progression of CKD. The modern Western diet, composed of foods that are high in fat, protein, sugar and sodium and low in fibre, is considered to be a key driver behind the current epidemic of chronic diseases [6, 7]. In comparison, balanced diets consisting of moderate fat and high in whole grain carbohydrates are associated with reduced risk of disease and improved mortality [7]. Dietary therapy has historically been used in the management of CKD and guidelines exist surrounding the intake of protein and sodium for patients with CKD [8]. Adherence to current dietary guidelines can reduce the incidence, or slow the progression of CKD and improve mortality [9]. Evidence is emerging to suggest that there are many other nutrients that can potentially influence kidney health either through metabolic or haemodynamic effects, or via the modification of gut homeostasis including changes to gut microbiota. The purpose of this review is to summarise the key recommendations to date, and to provide an overview of recent literature pertaining to potential novel modifiable dietary components that may be useful in the treatment of CKD.

Is High Protein Intake A Real Concern For Healthy Kidneys?

Dietary protein restriction has been recommended for individuals with CKD for decades. Early experimental evidence in a number of rodent models of kidney disease, including models of diabetic nephropathy and spontaneously hypertensive rats, consistently demonstrated that low protein diets ameliorate the progression of glomerular dysfunction [10, 11]. Evidence that protein restriction was beneficial in improving albuminuria in patients with kidney disease was first described in 1986 [11, 12]. Current recommendations for protein intake in individuals with CKD stages 1–4 is 0.8 g/kg body weight, and avoidance of high protein intake (>1.3 g/kg/day) [13]. The key benefits of protein restriction are primarily thought to arise from the amelioration of proteinuria and it has been proposed that an even lower protein intake of 0.6–0.8 g/kg bodyweight in patients with CKD stages 3–5 may be desirable [11, 14]. Further dietary protein reduction, using a very low protein diet supplemented with ketoanalogues of essential amino acids (0.35 g/kg/day) has been shown to reduce blood pressure in CKD patients [15, 16]. Other factors that occur due to excess protein metabolism, such as increased GFR [17], metabolic acidosis [11] and oxidative stress [18], are also thought to contribute to kidney damage associated with high protein intake [11]. Despite substantial experimental evidence to indicate that dietary protein restriction prevents the development of proteinuria and renal fibrosis [19, 20, 21], many clinical studies in humans have failed to find the same level of renal protection [11, 22, 23, 24]. The Modification of Diet in Renal Disease (MDRM) study found that a low protein diet (0.58 g protein/kg/day) did not significantly improve glomerular filtration rate in CKD patients when compared to a standard protein diet (1.3 g/kg/day) at a two-year follow-up [24]. This is likely because of the extreme differences in protein content used in experimental diets, but may also be due to the effect of other factors associated with protein foods, such as energy, water, sodium and phosphorous, that may affect kidney function [11]. Protein energy wasting is a major complication of kidney disease [25], particularly in later stages. A long-term follow-up of patients from the MDRM study found that assignment to a very low protein diet supplemented with a mixture of essential keto acids and amino acids (0.28 g protein + 0.28 keto and amino acids/kg/day) was associated with a significantly greater risk of death compared to a low protein diet (0.58 g/kg/day) [26]. Though it was not clear whether this finding may be due to the reduced mean energy intake that occurred with the very low-protein diet, or the possible toxicity of the keto acids and amino acids supplement [26]. Consequently, effective strategies to improve GFR or reduce proteinuria without jeopardising protein balance are a high priority in advancing CKD treatment.

Growing evidence suggests that the source of protein (plant or animal) may be more important than the quantity of protein consumed (Figure 1). One reason for this is the tendency for excess meat intake to disrupt the acid-base balance. Metabolic acidosis is a common occurrence in CKD patients and results in low circulating bicarbonate—a risk factor for the progression of nephropathy [27, 28] and is associated with increased mortality [29]. Protein from animal sources is composed of sulphur-containing amino acids which, when oxidized, generate sulphate, a non-metabolizable anion that contributes to total body acid load [30]. Protein from plant sources contains higher levels of glutamate, an anionic amino acid that upon metabolism consumes hydrogen ions to remain neutral, thereby reducing acidity levels [30]. Plant foods are also generally higher in anionic potassium salts, which also result in the consumption of hydrogen ions upon metabolism and reduction in acid load [30]. In response to an increase in acid load the kidney adapts by increasing ammonium ion excretion in order to expel excess hydrogen ions, therefore increasing the demand for ammonia production [30]. This stimulates the breakdown of glutamine and other amino acids promoting protein catabolism and muscle wasting [31] while also leading to renal hypertrophy [32]. Metabolic acidosis also promotes protein muscle wasting via the activation of the ATP-dependent ubiquitin-proteasome system [33]. In response to a high acid load, the kidney also undergoes functional changes including promotion of glomerular hyperfiltration and renal vasodilation, features typical of early diabetic kidney disease [30]. Results of the Chronic Renal Insufficiency Cohort Study suggest that consumption of a greater

Dietary protein restriction has been recommended for individuals with CKD for decades. Early experimental evidence in a number of rodent models of kidney disease, including models of diabetic nephropathy and spontaneously hypertensive rats, consistently demonstrated that low protein diets ameliorate the progression of glomerular dysfunction [10, 11]. Evidence that protein restriction was beneficial in improving albuminuria in patients with kidney disease was first described in 1986 [11, 12]. Current recommendations for protein intake in individuals with CKD stages 1–4 is 0.8 g/kg body weight, and avoidance of high protein intake (>1.3 g/kg/day) [13]. The key benefits of protein restriction are primarily thought to arise from the amelioration of proteinuria and it has been proposed that an even lower protein intake of 0.6–0.8 g/kg bodyweight in patients with CKD stages 3–5 may be desirable [11, 14]. Further dietary protein reduction, using a very low protein diet supplemented with ketoanalogues of essential amino acids (0.35 g/kg/day) has been shown to reduce blood pressure in CKD patients [15, 16]. Other factors that occur due to excess protein metabolism, such as increased GFR [17], metabolic acidosis [11] and oxidative stress [18], are also thought to contribute to kidney damage associated with high protein intake [11]. Despite substantial experimental evidence to indicate that dietary protein restriction prevents the development of proteinuria and renal fibrosis [19, 20, 21], many clinical studies in humans have failed to find the same level of renal protection [11, 22, 23, 24]. The Modification of Diet in Renal Disease (MDRM) study found that a low protein diet (0.58 g protein/kg/day) did not significantly improve glomerular filtration rate in CKD patients when compared to a standard protein diet (1.3 g/kg/day) at a two-year follow-up [24]. This is likely because of the extreme differences in protein content used in experimental diets, but may also be due to the effect of other factors associated with protein foods, such as energy, water, sodium and phosphorous, that may affect kidney function [11]. Protein energy wasting is a major complication of kidney disease [25], particularly in later stages. A long-term follow-up of patients from the MDRM study found that assignment to a very low protein diet supplemented with a mixture of essential keto acids and amino acids (0.28 g protein + 0.28 keto and amino acids/kg/day) was associated with a significantly greater risk of death compared to a low protein diet (0.58 g/kg/day) [26]. Though it was not clear whether this finding may be due to the reduced mean energy intake that occurred with the very low-protein diet, or the possible toxicity of the keto acids and amino acids supplement [26]. Consequently, effective strategies to improve GFR or reduce proteinuria without jeopardising protein balance are a high priority in advancing CKD treatment.

Growing evidence suggests that the source of protein (plant or animal) may be more important than the quantity of protein consumed (Figure 1). One reason for this is the tendency for excess meat intake to disrupt the acid-base balance. Metabolic acidosis is a common occurrence in CKD patients and results in low circulating bicarbonate—a risk factor for the progression of nephropathy [27, 28] and is associated with increased mortality [29]. Protein from animal sources is composed of sulphur-containing amino acids which, when oxidized, generate sulphate, a non-metabolizable anion that contributes to total body acid load [30]. Protein from plant sources contains higher levels of glutamate, an anionic amino acid that upon metabolism consumes hydrogen ions to remain neutral, thereby reducing acidity levels [30]. Plant foods are also generally higher in anionic potassium salts, which also result in the consumption of hydrogen ions upon metabolism and reduction in acid load [30]. In response to an increase in acid load the kidney adapts by increasing ammonium ion excretion in order to expel excess hydrogen ions, therefore increasing the demand for ammonia production [30]. This stimulates the breakdown of glutamine and other amino acids promoting protein catabolism and muscle wasting [31] while also leading to renal hypertrophy [32]. Metabolic acidosis also promotes protein muscle wasting via the activation of the ATP-dependent ubiquitin-proteasome system [33]. In response to a high acid load, the kidney also undergoes functional changes including promotion of glomerular hyperfiltration and renal vasodilation, features typical of early diabetic kidney disease [30]. Results of the Chronic Renal Insufficiency Cohort Study suggest that consumption of a greater