|Year : 2021 | Volume
| Issue : 6 | Page : 1511-1522
|Dietary Acid Load and Chronic Kidney Disease
Maryam Hamidianshirazi1, Maryam Ekramzadeh2
1 Student Research Committee; Nutrition Research Center, Department of Clinical Nutrition, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
2 Nutrition Research Center, Department of Clinical Nutrition, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Shiraz, Iran; Division of Nephrology and Hypertension at the Lundquist Institute at Harbor-UCLA Center Torrance, California, USA, Iran
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|Date of Web Publication||27-Jul-2022|
| Abstract|| |
Chronic kidney disease (CKD) is a condition in which kidneys are damaged and can not function well, so this leads to the aggregation of excessive fluid and waste products in the blood. The acidity and alkalinity of urine are affected by our daily diet. Dietary proteins, especially amino acids containing sulfur (e.g., methionine and cysteine), are the major determinants of the dietary acid load because they can produce sulfate due to oxidation. Diet can affect the excreted acidity through the kidneys to maintain the acid-base balance. Diets with animal protein content contain more precursor acids than basic precursors compared to fruits and vegetables that produce more acid in the body than animal proteins and dramatically affect CKD and its progression. Acid-producing diets can cause high blood pressure through the kidneys, causing the production of the hormones angiotensin II, endothelin-1, and aldosterone. Metabolic acidosis can cause CKD and reduced bone tissue.
|How to cite this article:|
Hamidianshirazi M, Ekramzadeh M. Dietary Acid Load and Chronic Kidney Disease. Saudi J Kidney Dis Transpl 2021;32:1511-22
| Introduction|| |
Chronic kidney disease (CKD) is a health disorder. To change the cycle of kidney disease, patients with CKD and their physicians are looking for ways to reduce the risk of developing the end-stage renal disease (ESRD), death, and other complications of CKD. Diet modification is a possible solution to this issue. Metabolic acidosis is common among those who suffer from chronic renal insufficiency (CRI) and CKD. In fact, the accumulation of acid in the body depends on and is related to the level of kidney function, which might overcome the capacity of the failing kidney to compensate for the presence of concurrent factors preserving or impairing acid excretion. Numerous biochemical reactions bind hydrogen ions (H+) to the body. The acid load in the diet is another factor affecting physiological acid-base systems. Diet can impact the acid-base status that must be excreted from the kidney to keep the acid-base balance. Modern Western diets with higher animal protein content contain more precursor acids than basic precursors compared to fruits and vegetables. and dramatically lead to CKD and its progression. Protein-energy malnutrition is another common risk factor for CRI., Also, malnutritioninflammation complex syndrome (MICS) is prevalent in hemodialysis (HD). In fact, oxidative stress in patients is a possible cause of MICS. Intensive oxidative stress and inflammation can subsequently lead to malnutrition. In patients undergoing HD, malnutrition in the form of protein-energy wasting is very common, which is associated with adverse clinical outcomes, hospitalization, higher morbidity, and mortality.
In this study, using simplified terms as an appropriate method and summarizing the published literature, we will discuss the role of dietary acid load (DAL) in the progression of CKD and CKD-related morbidity, and the dietary determinants of the daily acid load.
Increased ammonia production per nephron as a compensatory way results in increased endothelin-1 and aldosterone in the kidneys. Each of these factors may have a role in tubular interstitial injury that can, in turn, lead to kidney failure. Aldosterone/endothelin activation in CKD plays a protective compensatory role in metabolic acidosis that causes tubule injury.
| The Role of Kidney in Maintaining Acid-base Balance and the Role of Metabolic Acidosis in Progressive Kidney Disease|| |
The homeostatic regulation of the acid-base state is critical for physiological function and clinical outcomes of acid-base disorders are well characterized. One of the most important kidney functions is to adjust the acid-base balance. Two main processes allow the kidney to prevent destroying the acid-base balance of the body’s base. These mechanisms act by reabsorbing thousands of millions of bicarbonates that are filtered daily. and produce new bicarbonate by acid secretion in the final urine by excreting titrable acids by producing and excreting ammonia into the urine. In fact, the accumulation of acid in the body depends on the degree of renal function and the acidic loads, which may also depend on the kidney compensating capacity and the presence of the factors responsible for maintaining or impairing acid excretion.
Unbalanced diet such as high protein and low carbohydrate intake may cause mild metabolic acidosis and acid-base disorders. Metabolic acidosis is caused by an unbalanced dietaldosterone/endothelin activation in CKD and, thus, plays a protective compensatory role in metabolic acidosis that causes tubule injury. In addition, hyper aldosterone can accelerate glomeruli sclerosis. However, glomerular injury induced by metabolic acidosis has not been reported in animal models. Acid-base disorders and metabolic acidosis are caused by an unbalanced diet. Acidic diet rich in cheese, meat, eggs, and cereals has a high net acid load; however, alkaline precursors are abundant in fruits and vegetables. Kidney function can be impaired by the high DAL in contemporary diets through production of metabolic acidosis or even acidosis causing blood pressure in rats, which is consistent with net acid.,
| Definition of Chronic Kidney Disease|| |
CKD is a condition in which kidneys are damaged and cannot function well, so this leads to the aggregation of excessive fluid and waste products in the blood. In CKD, glomerular filtration rate (GFR) reaches <60 mL/min/1.73 m2.
In contrast, kidney dysfunction can be characterized as hypertension, edema, change in the quality of the urine, and delay in children’s growth. These changes are often evident with an increase in the serum creatinine, cysteine C, or urea nitrogen levels. Some types of kidney fibrosis are the most common pathological manifestations of CKD regardless of the cause of the disease. CKD can be classified according to GFR and albuminuria and is characterized by a continuous decrease in GFR and/or other symptoms of the kidney injury. Finally, patients with endstage kidney failure should be treated with HD or transplantation.
| Factors Affecting the Progression of Chronic Kidney Diseases and its Complications|| |
Net endogenous acid production (NEAP) reduces GFR in two ways. First, NEAP reduces the serum bicarbonate levels, which directly decreases the GFR or other pathways. In addition, NEAP decreases the GFR, but not through decreasing serum bicarbonate levels. NEAP is not directly associated with complications. Increased medullary kidney ammonia levels due to stimulation of ammonia production by the acid load on the diet activate an alternative complement pathway, which leads to progressive tubulo destructive injury. In addition, tubulinocytic injury is mediated by increasing endothelial production in CKD and then GFR is reduced due to metabolic acidosis. NEAP higher blood pressure via endothelial receptor. Vascular endothelial function properly is essential for blood flow.
| Nutrition and Chronic Kidney Diseases|| |
Unbalance diet (high protein, low carbohydrate) with an acidic load plays a role in the pathophysiology of CKD. The mortality rate of patients with ESRD is high despite rapid progress in the science and technology of renal replacement therapy. In kidney patients, dietary interventions are necessary and dietary recommendations vary considering the progress stage and the cause of the disease. In fact, understanding the nutritional principles are important to improve the nutritional status of CKD patients.
| Dietary Acid Load|| |
The alkaline diet, or acid-ash diet, has contributed to the fact that modern diets acidify the body and lead to the appearance of different diseases such as cancer, osteoporosis, CKD, and cardiovascular.,, A Western diet pattern is characterized by high consumption of foods containing animal products and beverages containing sugar and low consumption of fruits, vegetables, and grains. It has been hypothesized that Western-style diet can lead to low-grade metabolic acidosis and possibly cause metabolic disorders., A major source to DAL is dietary protein, which can especially be found in meat and fish. Sulfur-containing amino acids (e.g. methionine and cysteine) are important determinants of DAL because of sulfate production after oxidation. Diet DAL calculation is known as NEAP, which includes both acid and base and determines the total dietary capacity. Chronic disruptions at extracellular pH, such as higher NEAP, may activate compensatory mechanisms to restore acid-base balance. In fact, numerous studies have indicated a positive association between animal protein and CKD. It has been reported that net acid excretion (NAE) is reduced approximately one-third by fruit and vegetable consumption and is comparable to 0.5 mg/kg sodium bicarbonate administration. In addition, consumption of fruits and vegetables can reduce the DAL and also decrease proteinuria and blood pressure in patients with macroalbuminuric hypertensive nephropathy and stage 2 CKD, thus leading to the damage of CKD progression. Since the kidneys have an important role in acid-base homeostasis and acid excretion, it is important to understand the effect of DAL on patients with kidney disease.
| A Diet Containing Acid and Base|| |
Urine acidity and alkalinity can be influenced by diet. This condition is attributable to low consumption of fruits and vegetables and high consumption of animal products and salt. High citrate and malate in fruits and vegetables induce an alkalinizing effect syndrome with decreased hydrogen ions. Furthermore, plant proteins usually contain high amounts of glutamate (an anionic amino acid that uses hydrogen ions to neutralize) compared to animal proteins. Animal proteins and cereals contain sulfur-containing amino acids (methionine, homocysteine and cysteine) that oxidize to produce sulfate, a nonmetabolizable anion that determines the daily acid load. In meat and eggs, the content of these amino acids is 2-5 times higher than that of grains and legumes. Phosphate and chloride found in animal products and cereals are potent anions in potassium, making these nutrients more acidic than fruits and vegetables. The modern Western animal-based diet causes no compensation for the acidic load by fruits and vegetables, leading to metabolic acidosis without growing. People on an animal protein-based diet have a higher kidney acid excretion and acidic urinary pH compared to those on a vegetarian diet. Also, in people with an animal protein diet, excretion of urinary sulfate, phosphate, and uric acid is higher than those on the vegetarian diet. The following food list can be used as a guide to adjust the potential kidney acid load [Table 1].
Table 1. The food list as a guide influencing the potential renal acid load.
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| Various Types of Diet|| |
Healthy dietary patterns can be an effective way to reduce mortality in patients with CKD. The effects of the Mediterranean diet include better kidney function in the community, favorable cardiac metabolic characteristics, and improved dyslipidemia with CKD.,
Western diet compromises high-processed foods and cholesterol, high-protein, and excess salt intake. The Western-style diet is potentially acid-producing and may disrupt the kidneys through the toxicity of the ammonium tube and activation of the renin-angiotensin system. Findings from prospective studies using exploratory methods to define dietary patterns indicate that dietary patterns containing high amounts of fruit, vegetables, whole grains, and legumes and low amounts of red meat and beverages are useful for CKD prevention. The following table describes the types of diet and its progression in CKD [Table 2].
Table 2. Various types of diets as a guide influencing chronic kidney disease progression.
VLPDs: Very low-protein diet supplemented with amino acids and keto acids, NA: Not accessible, CRP: Creactive protein, NFkB: Nuclear factor-kappa beta, CKD: Chronic kidney disease, GFR: Glomerular filtration rate, DASH: Dietary approaches to stop hypertension.
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| Determination of Dietary Acid Load|| |
A detailed analysis of the acid generated from consuming foods may be useful to predict the effect of the diet on the acid-base status., The dietary acid levels were estimated through two trends in epidemiological studies. The intestinal absorption rate of 5 nutrients, including protein, potassium, phosphorus, magnesium, and calcium forms the basis of the probable renal acid load (PRAL). Second, the dietary acid levels are determined by NEAP, where the total amount of protein and potassium consumed is considered. A significant association between 24-h urinary NAE with PRAL and NEAP was confirmed in kidney transplant recipients. Therefore, both PRAL and NEAP may be effective indicators of DAL status in patients with CKD. Patients’ dietary patterns were assessed using a semiquantitative questionnaire that determined the dietary PRAL as a load of acid in kidney evaluation (LAKE)., The LAKE score is a fast screening that measures the diet's potential acid intake by assessing the consumption of grains, meat, fermented meat, eggs, cheese, potatoes, beans, fruits, vegetables, milk and other dairy products, and bread.,
| Dietary Acid Load Calculation|| |
Based on several nutrient intakes, the PRAL is calculated as follows:
Estimated PRAL: (mEq/d) = 0.49 × (g/d) + 037 × (mg/d) - 0.021 × potassium (mg/d) - 026 × magnesium (mg/d) - 0.013 × (mg/d).
For the residue, we adjusted both PRAL and protein and potassium for total energy consumption. Mean DAL scores were used for statistical analysis.,
Estimated NEAP (mEq/d): 54.5 [protein (g/day) /K (mEq/d)] - 10.2.
| The Effect of Dietary Acid Load on Glomerular Filtration Rate|| |
A proper kidney diet may be more effective in protecting the kidneys from injury. A healthy diet may prevent the GFR decreasing in the early stages of CKD., The incidence of metabolic acidosis increases with decreased kidney function, especially when GFRs are below 30−40 mL/min/1.73 m2. In an interventional randomized controlled trial, the effect of 36-month dietary acid reduction on eGFR and other kidney parameters was assessed by adding daily oral NaHCO3 (HCO3) or adding fruits and vegetables (F and V), which supported the hypothesis. This study indicated that consumption of fruits and vegetables in the basal diet would protect the kidneys in people with CKD and metabolic acidosis. In addition, decreases in dietary acid intake for one year through consumption of fruits and vegetables or oral NaHCO3 resulted in a higher plasma CO2 level, and a decrease in urinary indicators of kidney injury in patients with stage 4 CKD compared to the pre-treated state. Moreover, a lower plasma TCO2 and a higher rate of NAE were observed in the fruits and vegetables consumer group compared to the HCO3 group, and this is possibly due to higher alkali equivalents.
| The Effect of Dietary Acid Load on Phosphorus|| |
The main role of the kidneys is maintaining the internal milieu, such as maintaining the acid-base and phosphorus homeostasis. Acid-base balance is regulated by excretion acid in the kidney medulla.
Patients with kidney impairment lose the ability to excrete the phosphorus and, therefore, phosphatemia is a common failure in patients with advanced CKD and it is a strong predictor of mortality in the advanced stage. In addition, physiological adaptations lead to increased blood phosphorus levels in CKD stage 4-5 to counter the excess phosphorus levels. Consequently, secondary compensatory hypertension and increased fibroblast growth factor-23 occur to increase the urinary phosphorus excretion and maintain phosphorus balance.
There are three sources of phosphorus in foods (especially plant foods), including organic phosphorus (mostly in the form of phytates), animal protein-containing organic P, and processed foods enriched in additives and conservatives containing inorganic phosphorus. The phosphorus in plant foods has the lowest bioavailability (20%−40%) because humans do not have phytase degradation enzymes, while inorganic P is more available (100%).,
| The Role of Dietary Acid Load in Insulin Resistance in Chronic Kidney Disease|| |
The relationship between metabolic acidosis and insulin resistance has been demonstrated in diabetic patients with CKD. It has been shown that administration of oral sodium bicarbonate and/or a low-protein diet or a diet rich in fruits and vegetables can improve metabolic acidosis and insulin sensitivity in these patients. Therefore, reducing the DAL can improve the health status in diabetic patients. Increased magnesium excretion may also decrease insulin sensitivity due to higher acid load.
| Dietary Acid Load and Cardiovascular Risk Factors|| |
Cardiovascular disease is the leading cause of death among CKD patients. Increased consumption of protein causes the primary progression of cardiovascular diseases., DAL correlates with insulin resistance, so the insulin binding affinity for its receptor has been significantly reduced in individuals with metabolic acidosis. Thus, a very low degree of metabolic acidosis can lead to insulin resistance even in healthy individuals, resulting in hyperglycemia.,, Reducing metabolic acidosis can increase insulin sensitivity. The highest degree of DAL was associated with an increase in HOMA-IR values. Several mechanisms have been proposed due to the effect of DAL on blood pressure. A poor potassium diet can affect the vessels and be toxic to blood vessels. Potassium restriction results in a decrease in intracellular potassium and causes an increase in compensatory sodium in the cells to maintain the tone and volume. In a human study, 10 days with low potassium intake increased the systolic blood pressure by 5 mm Hg (P <0.02) and sensitivity to modified salt, resulting in hypertension. In contrast, hypertensive rats with a rich potassium diet had reduced blood pressure and stroke.
Western diet-induced systemic metabolic increases ammonia genesis via exertion cortisol. Diet-induced insulin resistance can independently promote cardiovascular disease in different pathways, disrupt the function of coronary microcirculation, stimulate conduction function, and increase erythema. The American Heart Association encourages adequate consumption of fruits and vegetables because nutritional imbalances are a risk factor for CVD. Recently, the acid-base imbalance has been suggested as a risk factor for metabolic disorders. According to studies, using dietary approaches to stop hypertension (DASH), i.e. DASH diet, delays acidosis with decreased serum bicarbonate without an incidence of hyperkalemia.
| The Influence of Dietary Acid Load on the Survival of Chronic Kidney Disease Patients|| |
Consumption of plant foods affects CKD patient’s survival through its effect on blood pressure. In addition, a plant-based diet reduces the urinary parameters of kidney injury, the production of potential uremic toxins by altering the intestinal flora and body weight, so it improves the cardiovascular outcomes.,,, Modification of metabolic acidosis is achieved through oral alkaline consumption of sodium bicarbonate through foods rich in fruits and vegetables. A very low protein diet with sufficient consumption of fruits and vegetables modifies metabolic acidosis and reduces the NEAP. Excessive consumption of sweetened beverages has been associated with albuminuria, CKD, and a faster decrease in GFR in the community. Healthy lifestyles including no smoking habits, low BMI, high physical activity, and diet quality reduce the incidence of mortality in people with stage 3−5 CKD. It was shown that HD patients who received more protein lived longer. Also, a post-hemodialysis (HEMO) study showed that patients without protein restriction in their diet had a better survival rate than those using protein-restricted diet. The probability of survival without ESRD was higher (but not high) among those with lower red meat consumption (quartiles 1 and 2) than those with higher consumption (quartiles 3 and 4). In addition, replacing one serving of red meat with one serving of chicken, fish, eggs, or soybeans and legumes was associated with a significant reduction in ESRD risk. Adopting a Mediterranean diet was associated with a better kidney function, while low adherence led to a lower survival rate among patients with CKD., A low-protein diet limited the survival of patients with advanced CKD. Patient survival was higher in vegan supplemented diet (low-protein diet supplemented with keto analogs; LPD-KA), while kidney survival was better on a diet based on aproteic commercial food (low-protein diet supplemented “aproteic” commercial food; LPD-ACF).
| Conclusion|| |
Based on the previous findings, it seems that dietary acid reduction protects the kidneys in CKD patients. Some studies have suggested that there is less potassium, fewer fruits and vegetables, and more protein in high-acid load diets. Metabolic acidosis occurs in patients with CKD due to reduced kidney mass and impaired kidney acid excretion. Chronic metabolic acidosis is a common complication in CKD patients. It has also been shown that excessive dietary acid intake can impair the kidney function through induction of metabolic acidosis or subclinical acid retention. Acidosis metabolic promotes CKD via ammonia-induced activation of the endothelial pathway. Based on evidence from clinical trials, consumption of fruits and vegetables delay the progression of CKD via acid and base balance. However, there is no definitive evidence for optimal evidence-based practice guidelines. It is anticipated that ongoing trials will further improve evidence-based metabolic acidosis in other cases.
| Acknowledgment|| |
The authors would like to thank Shiraz University of Medical Sciences, Shiraz, Iran and also the Center for Development of Clinical Research of Nemazee Hospital as well as Dr. Amir Yousef Farahmandi for editorial assistance
Conflict of interest: None declared.
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Nutrition Research Center, Department of Clinical Nutrition, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
Source of Support: None, Conflict of Interest: None
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