Despite existing guidelines, dietary sodium intake among people worldwide often exceeds recommended limits. This article delves into the intricate relationship between sodium intake and kidney health, providing a detailed overview of sodium recommendations for individuals with kidney disease. We will explore the potential mechanisms of kidney injury caused by high sodium intake, its clinical implications, and the challenges in translating current guidelines into practice.
The Dangers of Excessive Sodium Intake
Research evidence is growing in both animal and human studies showing indirect and direct adverse consequences of high dietary sodium on the kidney. While sodium is essential for various bodily functions, excessive consumption can lead to detrimental health outcomes, especially for individuals with kidney disease. In patients with kidney disease, dietary sodium may have important effects on proteinuria, efficacy of antiproteinuric pharmacologic therapy, hypertension control, maintaining an optimal volume status, and immunosuppressant therapy. Dietary sodium intake is an important consideration in patients with all stages of chronic kidney disease, including those receiving dialysis therapy or those who have received a kidney transplant.
Sodium Intake in the United States
The United States guidelines for daily sodium intake generally recommend a limit of 2.3 grams (g) per day (1, 2). Despite guidelines, dietary sodium intake among people in the United States remains high. In the National Health and Nutrition Examination Survey (NHANES, 2005-06), individuals 50 years and older had daily sodium consumption between 3.1-3.9 g for males, and 2.4-3.0 g for females (3). male adults and 75% of female adults consume more than recommended. Though little is described about the actual sodium intake of patients with kidney disease, one small study of 60 patients showed those receiving dialysis consumed an average of 2.1 (SD: 1.3) grams of sodium per day and non-dialysis patients an average of 2.3 (SD: 1.1) grams (6).
Mechanisms of Kidney Injury
Potential models of kidney injury include indirect and direct mechanisms. Models of indirect mechanisms suggest a complex relationship between increased sodium load, increased blood pressure, and proteinuria (7). Increased blood pressure and proteinuria then lead to vascular and renal injury, potentially causing progression of disease, as shown in Figure A (8) (This model refers to sodium in the form of sodium chloride, i.e. Fig. Interplay between dietary salt, blood pressure, proteinuria and kidney disease progression. Reprinted with permission (8).One example of indirect mechanisms contributing to increasing blood pressure is seen in those individuals who are considered salt (where sodium is coupled specifically to a chloride anion) sensitive. Figure B shows pressure naturiesis curves for: 1.) normal, non hypertensive subjects, 2.) subjects with hypertension whose blood pressure is not significantly increased with salt loading (salt resistant) and, 3.) those with hypertension whose blood pressure changes significantly with salt loading (salt sensitive). Although actual changes in blood pressure are continuous, these different curves suggest the three subgroups adapt differently to sodium chloride intake (9). In one study, about 60% of patients with known essential hypertension were deemed salt sensitive (10). Fig. Pressure naturiesis curves for normal, salt resistant, and salt sensitive subjects. The salt sensitive show a significant change in mean arterial pressure associated with changes in salt loading. Reprinted with permission (9, 10).There is also evidence of high sodium intake affecting kidney and vascular systems directly, and independently of blood pressure (7). High dietary sodium increases oxidative stress in the mammalian kidney by increasing generation and decreasing the breakdown of reactive oxygen species (12, 13). Evidence supports a direct effect of sodium intake on endothelium, mediated through changes in shear stress, modulating the production of TGFβ1 and nitric oxide. Endogenous inhibitors of Na/K ATPase may also be implicated in renal injury models. Data suggest, that ouabain, in small doses, causes partial Na/K ATPase inhibition within renal epithelial cells, and acts as an inducer of regular, low frequency calcium oscillations. The oscillations lower the threshold for activation of calcium dependent transcription factor NF-Kβ (15), which has a role modulating the expression of immunoregulatory genes relevant in inflammatory disease and apoptosis (16, 17). Oubain itself may also contribute to hypertension. In patients with significantly decreased glomerular filtration rates, impaired renal excretion of sodium is implicated as a major culprit of hypertension, and some data supports that oubain plays a role in this process, by raising intracellular sodium, subsequently increasing intracellular stores of calcium in vascular smooth muscle through changes in Na/Ca exchange.
Clinical Implications of High Sodium Intake
In addition to being linked to cardiovascular morbidity and mortality (20), high sodium intake is associated with increased risk of incident hypertension (21). Blood pressure control, however, can be improved with sodium reduction. Follow up to the Dietary Approaches to Stop Hypertension (DASH) Trial showed that both sodium reduction and a diet rich in fruits, vegetables and low in fat (DASH diet) lower blood pressure.
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Proteinuria and CKD Progression
Reducing sodium intake in patients with chronic kidney disease (CKD) is important to maximize benefits of other therapies. Proteinuria is a marker of kidney disease and contributes to progression, therefore, controlling and reducing protein in the urine is a mainstay of treatment. High dietary sodium is related to increased urinary albumin excretion (23), and has been shown to abate the anti-proteinuric benefits of angiotensin converting enzyme (ACE) inhibitor therapy (24). As previously noted, hypertension is a potential indirect mechanism for risk of CKD progression due to increased dietary sodium intake.
End-Stage Renal Disease (ESRD)
Increased dietary sodium has implications in those with end stage renal disease (ESRD). Sodium accumulation is one of the consequences of renal failure, resulting in increased water intake, increases in the extracellular volume, and accompanying rise in blood pressure (27). At the beginning of maintenance hemodialysis, Scribner recommended dietary sodium restriction and ultrafiltration to control extracellular volume (28), citing research in nephrectomized dogs in which hypertension appeared to be influenced by the size of the extracellular space. Indeed, studies on humans show strict volume control is associated with improved control of hypertension, and prolonged survival in those on hemodialysis (29, 30). Volume homeostasis is an important predictor of outcome in peritoneal dialysis patients as well (32). In patients utilizing continuous peritoneal dialysis, excessive dietary sodium intake is cited as a major cause of extracellular volume expansion (33).
Kidney Transplant Patients
Lower sodium intake also benefits those with kidney transplants. In kidney transplant patients being treated for hypertension, low sodium intake in combination with antihypertensive therapy results in significantly decreased blood pressure versus those on therapy without sodium restriction (35).
Controversy Surrounding Sodium Intake
In reviewing this literature, it would take significant effort not to recognize that there exists some controversy regarding high dietary sodium and its clinical implications. On one hand is the evidence that high dietary sodium potentially leads to poor outcomes, as previously discussed. However, others suggest there is no proven benefit to restricting sodium intake and that it may not be a prudent use of resources to attempt to alter sodium intake, as it may be a predefined, physiologically set parameter in humans (37). Indeed, the largest world-wide observational study to examine blood pressure and sodium consumption did not find a significant relationship with median blood pressure or prevalence of high blood pressure across 48 centers. However, there was a weak association between sodium intake and rise in blood pressure with age (5); later re-analysis with a correction factor did confirm a strong, positive association of sodium intake with systolic pressure of individuals (38). One study looking at data from the NHANES III showed lower sodium intake had a modest association with higher mortality, and that cardiovascular disease was increased in the lowest quintile of sodium intake versus the highest (39). For one’s own conclusion, it is important to consider the attributes and limitations of study designs, especially when comparing randomized controlled trial findings to data from observational studies. As an example, the dietary sodium intake in the NHANES III population was determined by participant twenty four hour recall and not confirmed with 24 hour urine sodium excretion measurements. A final point for consideration is that a negative impact of dietary sodium on health outcomes may occur at extremes of intake.
Recommended Sodium Intake Levels
Based upon growing evidence showing associations of high dietary sodium with poor health outcomes, several organizations recommend a reduction in sodium intake (Table 1). For healthy people, the World Health Organization (WHO) recommends that sodium intake be reduced by 20% and ultimately to a goal of < 2.0 g sodium per day, except where lower levels have been set (40). The United States Department of Agriculture (USDA)(1), the Institute of Medicine (IOM)(2), and the American Heart Association (AHA) Nutrition Committee (41) recommend at most, a consumption of 2.3 g of sodium per day. Comparison of Daily Recommended Limits for Sodium Intake. AI to ensure nutrient adequacy, not to prevent chronic disease.AI not applicable to certain populations (e.g. Kidney disease is not specifically noted in these recommendations. However, guidelines from the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) state there is strong evidence to support the recommendation that non dialysis patients with CKD adhere to a goal of less than 2.4 g of sodium per day (42). Sodium restriction is not recommended for patients with salt-wasting nephropathies. According to Dr. Prest, people should consume around 2300 mg to maintain healthy blood pressure. For individuals with kidney disease or high blood pressure, 1500 mg may be more appropriate. Speak with your healthcare team to determine how much sodium is safe for you.
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Barriers to Reducing Sodium Intake
There are many potential barriers to reducing dietary sodium for patients with kidney disease. Figure C presents a suggested model of how decreasing daily sodium intake may lead to improved outcomes, and where some of the potential barriers may impact steps in this process.
Knowledge Gaps
There is some evidence showing limited patient knowledge about sodium content in food. For example, patients with heart failure who are less knowledgeable about sodium are more likely to have a higher weekly consumption of high-sodium foods and also increased readmission after hospitalization (47). Providers may also be unclear regarding the amount of sodium in foods. One study of providers showed their knowledge of the sodium content of common food items was no different than the knowledge of the general population (48). Patients commonly indicate that their health care provider (i.e. physician) counsels them to adhere to a low sodium diet, but usually does not offer the detailed advice needed to execute this important recommendation (49). At a minimum, patients should be instructed to reduce intake of processed, canned, and “fast” foods.
Food Industry Practices and Labeling
There is little regulation of the sodium content in foods, and since the US Food and Drug Administration (FDA) considers salt to be a substance “generally regarded as safe (GRAS)”, manufacturers are not limited in the amount of sodium added to processed foods. Interestingly, the American Medical Association has recommended twice to the FDA to revoke the GRAS status of salt without success. Since the majority of kidney patients are affected by hypertension and likely to be salt-sensitive, a low sodium diet is usually agreed upon as a worthy therapeutic effort. Interpretation of the sodium content in foods remains a challenge, especially in the United States. As mentioned earlier, most sodium in food is added during the manufacturing of processed foods. However, this remains hidden and elusive to most people. Even when foods are labeled with sodium content, limiting daily intake is a complex task. food label includes sodium content, however patients simply cannot navigate the dense information contained on it, nor can they calculate the total nutritional content of the food item (52). In the United Kingdom, the majority of the food industry has adopted a “traffic-light” type labeling system that indicates if the food is high (red-light), medium (yellow-light), or low (green-light) sodium content (4). Similar clear labeling efforts have been instituted in New Zealand and Australia. In Finland, sodium intake has decreased by nearly 40% attributed these efforts (53).
Palatability and Taste Perception
Limiting dietary sodium content to less than 1.3 g per day has been described as unpalatable and intolerable. The ability of patients with kidney disease to detect, or taste salt in food is often impaired (54). This may contribute to an increase in the dietary consumption of sodium to reach levels that are palatable. Habitual high dietary sodium consumption, diabetic nephropathy, and the use of diuretics also further increases the sodium taste threshold (55, 56).
Strategies for Reducing Sodium Intake
- Read food labels carefully: Kidney patients should look for products with no more than 6 to 10% of the daily value for sodium. Here are a few standard food labels that you may run into and what they mean:
- Sodium-free: Less than 5mg of sodium per serving.
- Very low-sodium: Less than 35mg per serving.
- Reduced-sodium: Sodium reduced by 25%.
- Light in sodium: Sodium reduced by 50%. Be wary, though. Many low sodium products contain potassium chloride as a substitute, which could cause harm if on a restricted potassium diet.
- Be aware of hidden sodium: Many poultry products are soaked in a saltwater solution.
- Cook at home more often: This allows you to control the amount of sodium in your food.
- Use herbs and spices to add flavor: Some flavorful spices and seasonings include Chili powder, Smoked paprika, Lemon zest, Dried oregano, Italian seasoning.
- Make your own chicken and vegetable stock.
- Look for pasta and other products without added salt or sodium, and don’t salt your pasta water.
- Cut back on convenience foods and prepackaged or frozen meals.
The Role of Healthcare Professionals
For patients receiving dialysis, the dietitian has been noted to be the most trusted and informative source to guide adherence to both sodium and fluid restrictions (58). In the care of all stages of kidney disease, increasing education and awareness through a multidisciplinary team may better empower patients and guide their dietary self-care. As of 2010, the Center for Medicare and Medicaid Services reimbursement will further support face-to-face educational services provided by qualified professionals, to patients with chronic kidney disease. Sessions may be provided individually, or in a group and may include up to six visits (59). The Patient resource “Sodium and Your CKD Diet: How to Spice Up Your Cooking” offers helpful, straightforward advice on integrating daily sodium intake goals into menu options (60).
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