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Dietary recommendations for patients with nondialysis chronic kidney disease

Dietary recommendations for patients with nondialysis chronic kidney disease
Authors:
Monique E Cho, MD
Srinivasan Beddhu, MD
Section Editor:
Gary C Curhan, MD, ScD
Deputy Editor:
Eric N Taylor, MD, MSc, FASN
Literature review current through: Dec 2022. | This topic last updated: Mar 28, 2022.

INTRODUCTION — Chronic kidney disease (CKD) is common in the United States and worldwide. CKD patients have a higher mortality than the general population [1]. Mortality is related in part to the progression of kidney disease and its complications, such as cardiovascular disease (CVD) and protein-energy wasting.

Dietary factors may have an effect on the progression of kidney disease and its complications. Among CKD patients, overnutrition results in sodium and volume overload, hyperkalemia, hyperphosphatemia, and accumulation of toxic metabolites of protein degradation. Undernutrition, on the other hand, exacerbates the risk for malnutrition and wasting.

Appropriate dietary interventions may have an effect on clinical outcomes in the CKD population. However, the optimal approach to nutrition is not known with certainty, and clinical trials have yielded conflicting results.

This topic review provides recommendations for nutrition for predialysis CKD patients. Recommendations for nutrition in the general public are discussed elsewhere. (See "Dietary assessment in adults" and "Geriatric nutrition: Nutritional issues in older adults".)

The approach to nutrition in dialysis patients is discussed elsewhere. (See "Assessment of nutritional status in patients on hemodialysis" and "Nutritional status and protein intake in peritoneal dialysis patients".)

OVERVIEW — The optimal diet for individual CKD patients varies depending upon the estimated glomerular filtration rate (eGFR), type of kidney disease (ie, proteinuric or nonproteinuric), and the presence of other comorbidities such as diabetes, hypertension, or heart failure. For most CKD patients, the optimal diet is one similar to the Dietary Approaches to Stop Hypertension (DASH) diet, which is low in sodium content and rich in fruits, vegetables, legumes, fish, poultry, and whole grains. (See "Diet in the treatment and prevention of hypertension", section on 'Dietary Approaches to Stop Hypertension trial'.)

However, among many patients, the diet needs to be modified further depending on specific laboratory values including serum potassium or serum phosphorus.

We do not suggest any dietary modification for patients with eGFR ≥60 mL/min/1.73 m2. Such patients should follow the same dietary recommendations as for the general population. (See "Healthy diet in adults".)

We suggest the following dietary guidelines for most patients with eGFR <60 mL/min/1.73 m2 who are not on dialysis:

A daily protein intake of 0.8 g/kg. We do not recommend very low-protein intake (<0.6 g/kg/day).

A diet rich in vegetables.

The sodium intake varies depending on individual patient clinical features. Among individuals who are hypertensive, volume overloaded, or proteinuric, we suggest a sodium intake of <2 g/day (ie, 5 g/day of salt [NaCl]).

For patients who are not hypertensive, volume overloaded, or proteinuric, sodium restriction to 2.3 g/day (5.75 g/day of salt [NaCl]) may be of benefit. There are no convincing studies of the general population that have proven that lowering sodium intake to <2.3 g/day lowers cardiovascular outcomes or all-cause mortality. The Institute of Medicine has concluded that there is insufficient evidence to recommend a different sodium intake for CKD patients as compared with the general United States population [2].

The potassium intake should be guided by serum potassium levels. If the potassium concentration is normal, we do not restrict dietary potassium. If the potassium concentration is high, dietary potassium intake should be restricted. (See "Treatment and prevention of hyperkalemia in adults", section on 'Prevention' and "Patient education: Low-potassium diet (Beyond the Basics)", section on 'How do I cut down on potassium?'.)

Some clinicians target a total calcium intake (both dietary and medication sources) ≤1500 mg/day, whereas others prefer a more stringent goal of ≤1000 mg/day.

Maximum phosphorus intake of 0.8 to 1 g/day, even if the serum phosphorus concentration is normal; this is because some studies suggest that dietary phosphorus intake may alter circulating fibroblast growth factor (FGF) 23 concentrations (see "Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)", section on 'Fibroblast growth factor 23'). The dietary phosphorus should be derived from sources of high biologic value, such as meats and eggs.

Maximum caloric intake of 25 to 35 kcal/kg/day.

Maximum fat intake <30 percent of daily energy intake, with saturated fat limited to <10 percent energy.

Daily dietary fiber intake of 25 to 34 g/day.

These recommendations, along with supporting studies, are individually discussed below.

PROTEIN INTAKE

Non-nephrotic patients — For patients with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 who do not have nephrotic syndrome, we suggest restricting daily protein intake to 0.8 g/kg. Nutritional studies in patients with reduced eGFR suggest that protein intake can be safely lowered to 0.6 g/kg/day [3-7] although a very low-protein diet has been associated with increased mortality over the long term [8]. A modest restriction is generally well tolerated and does not lead to malnutrition in patients with CKD, and metabolic acidosis is avoided.

Most clinical guidelines, including Kidney Disease: Improving Global Outcomes (KDIGO) and the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (KDOQI), suggest restriction of protein intake for CKD patients [9,10].

Studies that have examined protein restriction have yielded inconsistent results [11-17].

Many early studies suggested that protein restriction may slow progression of CKD [16,18-23] although subsequent rigorous studies suggest that the benefit is modest [8,13,16,17,23-29]. The largest trial to date, the Modification of Diet in Renal Disease (MDRD) study, analyzed 585 patients with nondiabetic CKD and a mean GFR of 39 mL/min/1.73 m2 (all patients with GFR <55 mL/min/1.73 m2) [26]. Patients were randomly assigned to protein intakes of 1.3 or 0.58 g/kg/day with or without aggressive blood pressure (BP) control and followed for a mean of 2.2 years. The mean achieved protein intake was 1.11 g/kg/day for the usual-protein-diet group and 0.77 g/kg/day (approximately 45 to 60 g/day) for the low-protein-diet group [12]. This level of protein intake is substantially below the average protein intake in the United States of 90 to 100 g/day.

Despite good adherence, initially, there appeared to be little overall benefit with the low-protein diet. A biphasic response was noted: Patients treated with protein restriction had a greater fall in GFR (measured by iothalamate clearance) in the first four months (that may have reflected a reduction in intraglomerular pressure), followed by somewhat slower progression over the ensuing months (2.8 versus 3.9 mL/min/year) (figure 1). Interpretation of the MDRD trial is somewhat limited by this since the trial design did not account for this two-slope change in GFR in the moderate-protein-intake group. However, even in the later phase, the absolute benefit was approximately 1.1 mL/min/year. A similar lack of substantial benefit was noted in a second part of this study involving 255 patients with more advanced disease (mean GFR 19 mL/min/1.73 m2) who were randomly assigned to a low-protein diet (0.58 g/kg/day) or a very low-protein diet (0.3 g/kg/day) with a keto acid-amino acid supplement.

Other limitations to the trial are that it included very few diabetic patients (patients with insulin-requiring diabetes were excluded) and the rate of decline in GFR in the intervention and control groups was slower than expected, which may have resulted in decreased power to discern potential benefit. As the curves diverged at the end of the study, there is a possibility that longer-term follow-up of these patients would have revealed a slower progression in the moderate-protein-intake group.

A benefit of moderate protein restriction was suggested by a long-term follow-up analysis of the MDRD study, which was performed by linking the MDRD study to national registries [27]. In this 12-year study (1989 to 2000), the authors evaluated outcomes during the first six years after the trial ended (1989 to 1994), the next six-year period (1995 to 2000), and the total 12-year period. Analysis of outcomes after the first six years revealed a significant benefit of low-protein intake on kidney failure and all-cause mortality (hazard ratios [HRs] 0.68, CI 0.51-0.93 and 0.66, CI 0.50-0.87, respectively). However, there was no benefit of protein restriction when outcomes between 6 and 12 years were analyzed, but protein intake data were not available following the completion of the randomized study phase. Thus, it is possible that the early beneficial effects in the first six years dissipated after six years because the study participants were no longer on the intervention.

These data suggest the need for a longer follow-up period for future studies designed to assess the effects of protein restriction intervention. In the MDRD study, the average rate of GFR decline was 4 mL/min/1.73 m2 per year during the mean duration of 2.2 years, and relatively few patients developed kidney failure during this period. It is possible that the study duration was too short to fully appreciate the effect of protein restriction.

Since the initial MDRD report in 1994, several secondary analyses of the MDRD study, as well as other meta-analyses and controlled trials, have been published [11,12]. Systematic reviews suggest that protein restriction may be beneficial [30-34]. As an example, a Cochrane review limited to studies that used kidney death as an outcome measure (n = 10) demonstrated a protective effect of protein restriction despite heterogeneity among studies [30]. Kidney death in this review was defined as the need for starting dialysis, the death of the patient, or a kidney transplant. This analysis suggested that protein restriction decreases the number of patients reaching the defined outcome by approximately 32 percent. This equates to treating 2 to 56 patients with a low-protein diet to avoid one kidney death.

Overall, most experts believe that, despite the absence of observed benefit in the MDRD trial, the balance of evidence suggests a benefit of moderate dietary protein restriction [11,12]. Some of the MDRD investigators have proposed that the seemingly small benefit from protein restriction may be clinically important [12]. According to this reasoning, a patient with a GFR of 40 mL/min who is losing 4 mL/min per year will require dialysis in approximately eight years. However, if the rate of fall were only 3 mL/min per year, then 11 years would be required to reach the same endpoint. Thus, the absolute benefit would be three years without dialysis.

In addition, protein restriction may be particularly effective in diseases characterized by hyperfiltration, such as diabetes and certain glomerulopathies [16,21,22], although one study has suggested that the effects of protein restriction in advanced kidney disease due to polycystic kidney are similar to that due to other causes [12]. Polycystic kidney disease (PKD) is not characterized by hyperfiltration and tends to have a very different rate of progression compared with diabetic and other glomerulopathies.

Limiting protein intake is also associated with favorable laboratory and metabolic effects, including reduction of blood urea nitrogen levels, uremic toxins, and acid load, in addition to reduced phosphorus load with better control of metabolic bone disorders [35]. A modest protein restriction to 0.6 to 0.8 g/kg/day appears to be safe. The safety profile of a modest protein restriction was assessed in an analysis of patients who were enrolled in the MDRD study [4]. Patients were randomly assigned to a standard-protein diet (1.3 g/kg/day), a low-protein diet (0.58 g/kg/day), or a very low-protein diet (0.3 g/kg/day supplemented with a ketoacid-amino acid mixture at 0.28 g/kg/day) based upon their GFR. Patients assigned to the low-protein diet achieved a protein intake between 0.6 to 0.8 g/kg/day. Patients assigned to the very low-protein diet achieved a protein intake between 0.4 to 0.8 g/kg/day.

At a mean follow-up of 2.2 years, a low-protein intake was not associated with increased rates of mortality, hospitalization, or malnutrition.

We do not recommend very low-protein intake (<0.6 g/kg/day) in CKD patients due to the safety concerns. Significant health risks are associated with more severe restrictions over the long term. The MDRD study tested the effects of low-protein diet (0.58 g/kg/day) or a very low-protein diet (0.28 g/kg/day) with a keto acid-amino acid supplement in those with GFR between 13 to 24 mL/min/1.73 m2 on death/end-stage kidney disease (ESKD) outcome. While there were no statistically significant differences between the two groups during the trial, a longer-term, postintervention, observational follow-up showed a higher risk of death in those assigned to the very low-protein group (HR 1.92, 95% CI 1.15-3.20) [8].

An important limitation of these long-term observations is that measurements of protein intake or nutritional measurements were not performed beyond nine months after the original MDRD study ended; the number of patients that continued the prescribed diet is not known [36]. Despite this limitation, these observations suggest that important long-term safety risks are associated with the very low-protein diet among patients with advanced CKD.

Our recommendation varies somewhat from the 2020 National Kidney Foundation KDOQI guidelines, which suggest a low-protein diet (0.55 to 0.6 g/kg/day) or very low-protein diet (0.28 to 0.43 g/kg/day with keto acid/amino acid analogs supplementation) in nondiabetic adults with stage 3 to 5 CKD who are metabolically stable [10,16,17].

Patients with CKD who are on a protein-restricted diet should be carefully monitored, with close follow-up every three to six months for adequate caloric intake and evidence of protein malnutrition. We usually follow the body weight as well as serum albumin.

Three conditions must be met to avoid malnutrition:

Adequate caloric intake must be maintained (by increasing polyunsaturated fats and by avoiding processed carbohydrates).

At least 60 percent of the ingested protein must be of high biologic value or contain a high percentage of essential amino acids (table 1) [3].

Stimulation of skeletal muscle protein breakdown should be prevented to limit net nitrogen loss. Metabolic acidosis should be treated since metabolic acidosis stimulates skeletal muscle protein breakdown [3,37] (see "Pathogenesis, consequences, and treatment of metabolic acidosis in chronic kidney disease"). A protein-restricted diet may, of itself, help to prevent metabolic acidosis. A post-hoc analysis of the MDRD study showed that a reduction in protein intake resulted in increased serum CO2 after one year of follow-up [38].

Patients with nephrotic syndrome — We do not restrict protein intake among patients with nephrotic syndrome. The safety of a low-protein diet in nephrotic syndrome is uncertain. In some experimental models of nephrotic syndrome, the institution of a low-protein diet diminished hepatic albumin synthesis, which suggests protein deficiency [39,40]. However, in the same study, a low-protein diet also decreased protein excretion, presumably due to a fall in intraglomerular pressure. The net effect of these opposing factors was no change in the plasma albumin concentration [39,40]. Overall, studies have not demonstrated conclusive evidence of malnutrition with protein restriction in moderately nephrotic animals [41].

One study examined this issue in five stable patients with nephrotic syndrome [42]. Despite moderate proteinuria that averaged 7.2 g/day, nitrogen balance was maintained on a diet that provided 0.8 g/kg/day of protein plus 1 g of protein for each gram of proteinuria and 35 kcal/kg/day. Positive nitrogen balance was maintained by the inhibition of amino acid oxidation and protein degradation and by stimulation of protein synthesis during feeding.

These data suggest that protein restriction can be safely implemented in patients with moderate proteinuria, providing adequate caloric intake is maintained. However, these data do not define the minimum safe protein intake, nor do they prove that supplementing protein intake for the degree of proteinuria is necessary. In addition, the safety of protein restriction in patients with massive proteinuria (>15 g/day) or concurrent catabolic states (eg, due to corticosteroids or systemic lupus erythematosus) is uncertain, even with adequate caloric intake.

Source of protein intake — A diet rich in protein from plant sources may be beneficial among CKD patients. Observational data suggest that such a diet may reduce proteinuria [43-45], lower the incidence and slow the progression of CKD [45-52], decrease the production of uremic toxins [53-58], lower phosphorus intake, lower the endogenous production of acid [48,49,59,60], and potentially decrease mortality risk [61-63]. (See "Pathogenesis, consequences, and treatment of metabolic acidosis in chronic kidney disease", section on 'Choice of therapy'.)

A randomized trial compared a very low plant-based protein diet (0.3 g/kg/day) supplemented with ketoanalogues (KD) with a mixed-source (plant- and animal-based) low-protein diet (0.6 g/kg/day) among 207 patients with a stable eGFR <30 mL/min/1.73 m2 [47]. The median achieved protein intake was 0.29 and 0.59 g/kg/day in the KD and low-protein diet groups, respectively. At 18 months of follow-up, compared with the low-protein diet group, fewer patients in the KD group reached the composite endpoint of >50 percent reduction in eGFR or initiation of kidney replacement therapy (KRT; 42 versus 13 percent, respectively). Compared with the low-protein diet group, fewer patients in the KD group required KRT (30 versus 11 percent).

However, caution is warranted in interpreting these results. While there were no differences between groups in anthropometric or biochemical parameters of nutrition during the duration of this study, in the long-term follow-up of the MDRD study, there was increased mortality among those randomized to a very low-protein diet (0.28 g/kg/day supplemented with a mixture of essential keto acids and amino acids) compared with a low-protein diet (0.58 g/kg/day) [8] (see 'Non-nephrotic patients' above). Long-term studies of very low plant protein diets that examine mortality as a predefined outcome are warranted.

Concerns have also been raised about delayed registration of this trial in the public trials registry until after enrollment of some participants.

Studies that compare protein sources but maintain comparable levels of moderate protein intake (0.6 to 0.8 g/day) are required before a recommendation could be made for a primarily plant-based source of dietary protein.

SALT INTAKE — Salt is nutritionally equivalent to sodium chloride: 1 g salt of contains 0.4 g (17 mEq) of Na ion. Understanding these units is important for making dietary recommendations to patients.

Among selected CKD patients with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 who have hypertension, volume overload, or increased protein excretion, we suggest a sodium intake of <2 g/day (5 g/day of salt).

The approach for patients with reduced eGFR who do NOT have hypertension, volume overload, or increased protein excretion is not clear. For most patients, we generally advise a mild sodium restriction of 2.3 g/day (5.75 g/day of salt [NaCl]). An exception is the occasional CKD patient who wastes sodium.

We suggest not reducing sodium to <1500 mg/day (ie, salt <3 g/day). We agree with the conclusion of the US Centers for Disease Control and Prevention-commissioned Institute of Medicine Committee that there is insufficient evidence to recommend sodium restriction to ≤1500 mg/day in high-risk groups (ie, including CKD patients) [2].

In addition, very low sodium intake has been associated with increased mortality. In the Prospective Urban Rural Epidemiology (PURE) study of 101,945 people in 17 countries, compared with the reference range of estimated sodium excretion of 4 to 5.99 g/day, an estimated sodium excretion that was below 3 g/day was associated with an increased risk of the composite outcome of death or cardiovascular event (odds ratio [OR] 1.27, 95% CI 1.12-1.44). In the same study, very high Na intake above 6 g/day was associated with 15 percent higher risk of death or cardiovascular event [64].

It is unlikely that a large, randomized, controlled trial to conclusively establish the effects of Na intake on cardiovascular mortality and all-cause mortality will ever be conducted.

Our recommendation for a modest sodium restriction is consistent with the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) guidelines for the management of CKD [9], the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (KDOQI) 2020 guidelines [10], and the U.S. Department of Agriculture and U.S. Department of Health and Human Services Dietary Guidelines for Americans 2020-2025 [65].

Among CKD patients, the benefits of salt restriction might include the following:

Lower blood pressure (BP)

Slower progression to end-stage kidney disease (ESKD)

Improved cardiovascular outcomes

These are discussed separately below.

Hypertension — Large, long-term, randomized, controlled trials that assess the efficacy and safety of salt restriction in the CKD population are largely absent. The guidelines for dietary sodium intake in CKD, therefore, are based on expert opinion, observational studies, and extrapolation from general population studies. Studies overall suggest that salt restriction reduces the risk of hypertension in the general population. (See "Salt intake, salt restriction, and primary (essential) hypertension".)

A moderate salt restriction also reduces the risk of hypertension among CKD patients in small studies [66-70]. A four-week randomized crossover of dietary sodium restriction (target <2 g/day versus usual diet) in stage 3 to 4 CKD resulted in a significant reduction in systolic BP (-10.8 mmHg; 95% CI -17 to -4.6) [68]. (See "Overview of hypertension in acute and chronic kidney disease", section on 'Benefits of sodium restriction'.)

However, in a six-month trial comparing self-management support plus standard care with standard care alone, differences in sodium excretion rates and ambulatory blood pressures between the groups at six months were not different, illustrating the difficulties in sustained sodium restriction [70].

CKD progression — Very few studies have examined the effect of salt restriction on CKD progression. The limited available data suggest both direct and indirect benefit of sodium restriction on CKD outcomes, mostly regarding its synergistic effect to lower proteinuria in the setting of renin-angiotensin system inhibition:

A post-hoc analysis of the first and second Ramipril Efficacy in Nephropathy (REIN) trials suggested a potential benefit of sodium restriction [71]. During four years of follow-up, compared with those with a low-salt intake (<100 mEq/g urinary sodium/creatinine excretion), the risk of progression to ESKD was greater in those with high-salt intake (≥200 mEq/g urinary excretion; 6.1 versus 18.2 per 100 patient-years). A 100 mEq/g higher urinary sodium/creatinine excretion ratio was associated with a 40 percent increase in the risk of ESKD regardless of baseline proteinuria and other risk factors. However, the association between salt intake and the risk of ESKD disappeared after adjustment for changes in proteinuria, suggesting that, in CKD patients treated by angiotensin-converting enzyme (ACE) inhibitors, the increase in proteinuria is a primary mechanism by which high-sodium intake accelerates the progression of CKD toward ESKD.

In a posthoc analysis of the HALT-PKD trial, lower urinary sodium excretion was significantly associated with decreased kidney growth in those with eGFR >60 mL/min/1.73 m2. In polycystic kidney disease (PKD) patients with eGFR 25 to 60 mL/min/1.73 m2, urinary sodium excretion was significantly associated with increased risk for the composite endpoint of 50 percent reduction in eGFR, ESKD, or death (HR 1.08 for each 18 mEq urinary sodium excretion) and faster eGFR decline rate (-0.09 mL/min/1.73 m2/year for each 18 mEq urinary sodium excretion) [72]. Sodium restriction, therefore, is beneficial in the management of autosomal dominant PKD.

In the Chronic Renal Insufficiency Cohort (CRIC) study, compared with the lowest quartile of urinary sodium excretion (<117 mmol/24 hours), hazard ratios for the highest quartile of urinary sodium excretion (>195 mmol/24 hours) were 1.54 (95% CI, 1.23-1.92) for CKD progression, 1.45 (95% CI, 1.08-1.95) for all-cause mortality, and 1.43 (95% CI, 1.18-1.73) for the composite outcome of CKD progression and all-cause mortality [73].

However, despite these benefits, there are concerns that excessive lowering of sodium intake may adversely affect neurohormonal balance and lipids and generate proinflammatory milieu, which could enhance progression of disease among CKD patients [74]. A meta-analysis suggested that salt restriction increases plasma levels of renin, aldosterone, catecholamines, and lipids [75]. When salt intake is reduced, a fall in extravascular volume stimulates the renin-angiotensin-aldosterone axis and sympathetic system. These physiologic compensatory responses are more pronounced with sudden and large reduction in salt intake but become minimal with chronic, modest salt reduction. Nonetheless, it has been argued that these are only short-term responses, and, in the longer term, modest salt restriction over weeks results in only small increases in plasma levels of renin, aldosterone, and catecholamines, without any effect on the lipids [76].

Cardiovascular disease — The effect of salt restriction on cardiovascular outcomes has been difficult to ascertain definitively due to feasibility and logistic challenges. Evaluating cardiovascular morbidity and mortality requires a large sample size with extended follow-up. In addition, participants randomized to low-salt intake typically return to regular salt intake once the trial intervention phase ends, further limiting the ability to accurately assess the effect of long-term salt restriction.

Suggestive evidence for the cardiovascular protective effect of salt restriction in the general population is provided by the following:

A meta-analysis of observational studies suggests that a 5 g/day higher salt intake is associated with a 23 percent increase in stroke risk and a 17 percent increase in cardiovascular disease (CVD) [77].

An observational 10- to 15-year follow-up study of Trials of Hypertension Prevention (TOHP I and II) demonstrated that net sodium restriction of 33 to 44 mmol/day (0.75 to 1 g/day) in the intervention arm resulted in a 30 percent reduction lower cardiovascular event after adjustment for baseline sodium excretion and weight [78].

In an analysis of the CRIC study of CKD participants, adjusted hazard ratios of the highest as compared with the lowest quartile of sodium intake were 1.36 (95% CI, 1.09-1.70) for composite CVD events, 1.34 (95% CI, 1.03-1.74) for heart failure, and 1.81 (95% CI, 1.08-3.02) for stroke [79].

POTASSIUM INTAKE — Dietary potassium intake should be individualized based on the serum potassium. In general, potassium restriction is not required until the estimated glomerular filtration rate (eGFR) decreases to <30 mL/min/1.73 m2. However, there is variability between patients, and some patients with higher eGFRs and who are on angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) will require potassium restriction to maintain a normal serum potassium.

The National Kidney Foundation Kidney Disease Outcomes Quality Initiative (KDOQI) guideline recommends potassium intake between 2 to 4 g/day (51 to 102 mEq/day) for patients with CKD stages 3 to 4 (ie, eGFR 30 to 59 mL/min/1.73 m2), while recommending no restriction for those in earlier stages of CKD. However, we believe that dietary potassium recommendations need to be individually tailored based on the level of eGFR and serum potassium levels.

Our individualized approach towards potassium restriction among patients with CKD is based upon the beneficial effects of a normal to high potassium diet, which have been demonstrated in observational studies in the general population and in patients with CKD. Consumption of a potassium-rich diet is associated with a lower risk of incident CKD in the patients with normal kidney function and a slower decline in eGFR among patients with CKD [45,80]. Other benefits of high dietary potassium intake in the general population include a reduction in systolic BP [81-83], a lower risk of stroke, and higher bone mineral density [84-87].

However, the associations of potassium intake with CKD progression and mortality in CKD are controversial; a report from the Chronic Renal Insufficiency Cohort (CRIC) study observed a higher risk of CKD progression but not all-cause mortality with higher potassium intake [73]. Conversely, analyses of the Modification of Diet in Renal Disease (MDRD) cohort suggested that higher potassium consumption was associated with lower risk of all-cause mortality but not kidney failure [88].  

CALCIUM INTAKE — Some clinicians target a total calcium intake (both dietary and medication sources) ≤1500 mg/day whereas others prefer a more stringent goal of ≤1000 mg/day. The Kidney Disease Outcomes Quality Initiative (KDOQI) guideline (2020) suggests limiting total calcium intake (both dietary and medication sources) to 800 to 1000 mg/day for adults with CKD stage 3 to 4 not taking active vitamin D analogs [10,89]. The Dietary Guidelines for Americans 2020-2025 recommend a dietary calcium goal of 1000 mg/day in adults [65].

Calcium supplementation of 2 to 4 g/day results in suppression of parathyroid hormone levels in advanced CKD [90]. Administration of calcium-containing phosphorus binders in hemodialysis patients, however, results in increased vascular calcification [91], raising concerns about the safety of higher calcium intake in predialysis patients.

There are no randomized, controlled trials that established the safe levels of calcium intake in predialysis CKD.

However, in a calcium balance study, both normal individuals and patients with late-stage 3 and stage 4 CKD were in slightly negative to neutral calcium balance on an 800 mg calcium diet [92]. Normal individuals were in modest positive calcium balance on the 2000 mg diet, while patients with CKD on the same diet were in marked positive calcium balance. Furthermore, increased calcium intake significantly decreased 1,25-dihydroxy-vitamin D and intact parathyroid hormone levels but did not alter the serum calcium concentration.

These data suggest that a diet of 2000 mg/day of calcium in CKD patients might result in a positive calcium balance, with the extra calcium deposited in tissues, leading to metastatic calcification.

PHOSPHORUS INTAKE — We restrict dietary phosphorus intake to a maximum of 0.8 to 1 g/day or modify the phosphorous intake to normalize the serum level in patients with an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, although it is not clear that dietary restriction significantly alters the serum phosphate concentration among nondialysis CKD patients [9,89,93-95]. We do not restrict dietary phosphorus intake in CKD patients who have normal serum phosphate levels and parathyroid hormone (PTH) values. The management of hyperphosphatemia and secondary hyperparathyroidism is discussed elsewhere. (See "Management of hyperphosphatemia in adults with chronic kidney disease", section on 'Phosphate restriction' and "Management of secondary hyperparathyroidism in adult nondialysis patients with chronic kidney disease", section on 'Initial treatment' and "Management of secondary hyperparathyroidism in adult dialysis patients", section on 'Treat hyperphosphatemia'.) 

The average phosphorus intake in the United States population is 1300 mg/day. For healthy adults, Dietary Guidelines for Americans 2020-2025 recommend intake of 700 mg/day of phosphorus [65].

Higher serum phosphorus concentrations have been associated with increased cardiovascular risk, both in the general and CKD populations [96-98]. The association between serum phosphorus levels and cardiovascular risk is independent of eGFR and other cardiovascular disease (CVD) risk factors, even at modestly increased phosphorus concentrations.

A large meta-analysis of 14 studies showed an 18 percent risk of death for every 1 mg/dL increase in serum phosphorus (95% CI 1.12-1.25) in the CKD population [98].

Possible mechanisms underlying the increased cardiovascular risk include accelerated vascular calcification and arterial stiffness and induction of fibroblast growth factor (FGF) 23, which has been implicated in the development of left ventricular hypertrophy [99]. FGF-23 is also associated with increased risk of coronary heart disease, heart failure, and cardiovascular mortality independent of traditional cardiovascular risk factors and kidney function [100].

Because inorganic phosphate has much higher bioavailability compared with organic phosphate, sources rich in inorganic phosphate such as highly processed foods should be avoided as much as possible. Organic phosphate (ie, from unprocessed foods) must be hydrolyzed enzymatically in the gut before it can be absorbed. By contrast, foods that are highly concentrated in readily absorbable inorganic phosphate, such as preservatives used in processed and precooked meals, result in much greater absorption of phosphorus.

Dietary phosphate load is closely related to protein content. As noted above, using plant sources of protein may be beneficial for controlling phosphorus load (see 'Source of protein intake' above). Plant sources have the lowest bioavailability of phosphorus, with grains yielding only 50 percent bioavailability of phosphorus [101].

However, unlike the dialysis population, in nondialysis CKD patients with eGFR <60 mL/min/1.73 m2, the effect of dietary phosphorus restriction on the serum level is limited.

A small, crossover study in eight patients with a mean eGFR of 32 mL/min/1.73 m2 demonstrated that allocation to a vegetarian protein source to reduce absorbable phosphorus led to only a mild reduction in serum phosphorus (0.3 mg/dL) [59].

Several randomized trials, including the Modification of Diet in Renal Disease (MDRD) study, did not show statistically significant reduction in the serum phosphorus concentration despite significant reduction in urinary phosphorus excretion by the use of oral phosphorus binders [102,103] or protein restriction [104].

This may relate to the fact that the studies relied on the morning fasting sample for phosphorus measurement, which may be less associated with dietary phosphorus absorption than afternoon measurements [105]. Morning fasting levels remain stable despite a wide fluctuation in dietary phosphorus absorption, making the morning value an insensitive marker for phosphorus overload.

It is possible that dietary protein restriction or use of phosphorus binders may reduce afternoon serum phosphorus levels; it remains unknown in the absence of randomized trials, however, if reduction of afternoon phosphorus levels translates into improved cardiovascular outcomes.

In an analysis of the National Health and Nutrition Examination Survey (NHANES) data, higher dietary phosphorus intake was not associated with mortality risk in moderate CKD [106].

Although the available literature does not provide evidence that dietary phosphorus restriction results in serum phosphorus level reduction in nondialysis CKD populations, the association between increased serum phosphorus levels and adverse cardiovascular outcomes remains robust.

Randomized trials are needed to establish the role of dietary phosphorus restriction in nondialysis CKD patients with eGFR <60 mL/min/1.73 m2.

CARBOHYDRATE AND FAT INTAKE — We suggest that patients with an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 who are not undergoing maintenance dialysis consume 25 to 35 kcal/kg/day [89].

Fat should be restricted to <30 percent of daily energy intake, with saturated fat limited to <10 percent energy.

Among CKD patients, obesity is associated with the development and progression of cardiovascular events [107] and mortality [108].

Observational studies suggest that higher body mass index (BMI) [109-111] and central adiposity [112,113] are also independent risk factors for progression of CKD and incidence of end-stage kidney disease (ESKD) [108,114,115].

The mechanism by which obesity may increase CKD progression is not known. Hemodynamic abnormalities observed in obese individuals include glomerular hyperfiltration [116], increased renal venous pressure [117], and glomerular hypertrophy [118]. Diets that contain excessive fat and carbohydrates are associated with accelerated inflammatory process and oxidative stress in the endothelium, leading to atherosclerosis [119].

Weight loss leads to improved blood pressure (BP) control [120,121] and the reduction of hyperfiltration and proteinuria [122,123]. Since hypertension, hyperfiltration, and proteinuria are all risk factors for progression of CKD, this suggests that weight loss in obese CKD patients may slow the progression of kidney disease. Further data to support restriction of excess caloric intake in the CKD population include:

High sugar intake and saturated fat intake are associated with albuminuria in cross-sectional studies [124,125]. In one prospective cohort study of Black Americans, a higher consumption of sugar-sweetened beverages was associated with an increased risk of incident CKD [126].

In the Nurse's Health Study, a Western dietary pattern characterized by higher intake of processed and red meats, refined grains, sweets, and dessert was associated with greater odds of moderately increased albuminuria (formerly called "microalbuminuria"; odds ratio [OR] 2.17, 95% CI 1.18-3.66) and rapid eGFR decline of ≥3 mL/min/1.73 m2 per year (OR 1.77, 95% CI 1.03-3.03) [127]. By contrast, also in the Nurses' Health Study, a Dietary Approaches to Stop Hypertension (DASH)-style diet (higher intake of fruits, vegetables, legumes, fish, poultry, and whole grains) was not associated with moderately increased albuminuria, but was associated with a lower risk of rapid eGFR decline (OR 0.55, 95% CI 0.38-0.80) [128]. In the same cohort, consumption of two or more servings per day of artificially sweetened soda was independently associated with a twofold higher odds for eGFR decline.

In another prospective observational study using the dietary data in the Chronic Renal Insufficiency Cohort (CRIC), greater adherence to several healthy dietary patterns (such as the alternate Mediterranean diet and the DASH diet) was associated with lower risk for CKD progression and all-cause mortality among people with CKD [129].

A prospective cohort study spanning 15 years demonstrated that doubling of relative energy intake, not BMI, is associated with an increased mortality risk of 48 percent in those with eGFR <60 mL/min/1.73 m2 [130].

Although data from randomized interventional trials are lacking, avoiding excessive caloric intake might reduce the risk of kidney disease progression and cardiovascular mortality in CKD individuals.

RECOMMENDED FIBER INTAKE — The recommended daily dietary fiber intake for CKD patients with estimated glomerular filtration rate (eGFR) ≤60 mL/min/1.73 m2 is 14 g per 1000 calories, which is the same as for the general population.

Dietary fiber is the nondigestible form of carbohydrates and lignin. Some of the best sources of dietary fiber are beans and peas but also include nuts, fruits, and whole grains. The US Department of Agriculture and US Department of Health and Human Services, in their updated Dietary Guidelines for Americans 2020-2025, has recommended a daily intake of 14 g per 1000 calories or up to 34 g of fiber for males and 28 g for females.

The rationale for the above dietary fiber intake recommendation is based on numerous clinical studies to demonstrate protective effects against cardiovascular disease (CVD), diabetes mellitus, cancer, and all-cause mortality. (See "Healthy diet in adults".)

While there are limited data, dietary fiber intake appears to provide similar, if not greater, benefits in the CKD population:

An analysis of National Health and Nutrition Examination Survey (NHANES)-III data (including 14,543 participants and 5.8 percent with eGFR <60 mL/min/1.73 m2), showed that, for each 10 g/day higher total fiber intake, the odds of increased serum C-reactive protein was decreased by 38 percent in those with CKD and by 11 percent in those without kidney disease [131]. Furthermore, the dietary fiber intake was inversely correlated with mortality only in those with CKD, suggesting that fiber intake may be more important for individuals with CKD.

A six-week study of 13 CKD patients (mean eGFR of 30 mL/min/1.73 m2) demonstrated that the addition of fiber (23 g/day) was associated with a significant reduction in serum creatinine by a mean of 0.24 mg/dL (p<0.05) from the baseline value [132]. The change in eGFR corresponded to an increase by approximately 3 mL/min/1.73 m2 from the baseline.

Based on the available data and extrapolating from the general population, therefore, fiber intake is likely protective against CKD progression and mortality, and every effort should be made to encourage higher fiber intake in the CKD population. Because potassium is high in fruits and vegetables, many CKD and dialysis patients are counseled against taking these. This may further compromise dietary fiber intake in the CKD population. However, fruits and vegetables that are low in potassium might be consumed in moderation.

The overall nutritional recommendations are described in the table (table 2).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic kidney disease in adults".)

SUMMARY AND RECOMMENDATIONS

The optimal diet for individual chronic kidney disease (CKD) patients varies depending upon the estimated glomerular filtration rate (eGFR), type of kidney disease (ie, proteinuric or nonproteinuric), and the presence of other comorbidities such as hypertension or heart failure. For most CKD patients, the optimal diet is one similar to the Dietary Approaches to Stop Hypertension (DASH) diet, consisting of fruits, vegetables, legumes, fish, poultry, and whole grains. (See 'Introduction' above and 'Overview' above and "Diet in the treatment and prevention of hypertension", section on 'Dietary Approaches to Stop Hypertension trial'.)

We do not suggest any dietary restriction for patients with eGFR ≥60 mL/min/1.73 m2. Such patients should follow the same dietary recommendations as for the general population. (See 'Overview' above and "Healthy diet in adults".)

Among patients with eGFR <60 mL/min/1.73 m2 who are not on dialysis and do not have nephrotic syndrome, we restrict daily protein intake to approximately 0.8 g/kg. A modest protein restriction may slow the progression of CKD and is associated with other benefits including reduced blood urea nitrogen, uremic toxins, decreased acid load, and decreased phosphorus intake. A diet rich in protein from plant sources may be beneficial among CKD patients. (See 'Protein intake' above.)

The optimal dietary salt intake is not known. Our approach is based upon expert opinion, observational studies, and extrapolations from general population studies and depends on the individual patient characteristics:

Among patients with eGFR <60 mL/min/1.73 m2 who have hypertension, volume overload, or increased protein excretion, we restrict sodium intake to <2 g/day (5 g/day of salt).

Among patients with reduced eGFR who do NOT have hypertension, volume overload, or increased protein, we use a more mild sodium restriction to 2.3 g/day (5.75 g/day of salt [NaCl]). (See 'Salt intake' above.)

Dietary potassium intake should be individualized based on the serum potassium. In general, potassium restriction is not required until the eGFR decreases to <30 mL/min/1.73 m2. (See 'Potassium intake' above.)

Among all patients with eGFR <60 mL/min/1.73 m2, we restrict total calcium intake (both dietary and medication sources) to 1000 mg/day. Some clinicians prefer a more stringent goal of ≤1000 mg/day. Data suggest that a diet of 2000 mg/day of calcium in CKD patients may cause a positive calcium balance, with the extra calcium deposited in tissues, leading to metastatic calcification. (See 'Calcium intake' above.)

The optimal dietary phosphorus intake is not known. Our approach depends upon the serum phosphorus concentration. Among patients with a normal serum phosphate concentration, we restrict dietary phosphorus intake to 0.8 to 1 g/day. Sources rich in inorganic phosphate, such as highly processed foods, should be avoided as much as possible. (See 'Phosphorus intake' above.)

Among patients with eGFR <60 mL/min/1.73 m2, we suggest caloric intake of 25 to 35 kcal/kg/day. Higher body mass index (BMI) and central adiposity are independent risk factors for end-stage kidney disease (ESKD), cardiovascular events, and mortality.

Fat should be restricted to <30 percent of daily energy intake, with saturated fat limited to <10 percent energy. (See 'Carbohydrate and fat intake' above.)

The recommended daily dietary fiber intake for CKD patients with eGFR <60 mL/min/1.73 m2 is 5 to 38 g/day, which is the same as for the general population. (See 'Recommended fiber intake' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Ajay K Singh, MD, who contributed to earlier versions of this topic review.

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Topic 7178 Version 34.0

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