Introduction
The increasing prevalence of chronic kidney disease (CKD) represents a major public health issue that incurs a substantial burden on the family and society. Despite dramatic improvements have been made in the treatment and management of CKD, it is still associated with a high morbidity and mortality rate. In addition to pharmacological treatments, lifestyle modifications, including dietary management, have been demonstrated to serve as a critical component in retarding CKD progression and reducing of mortality.1 Current guidelines generally recommend 0.60–0.80 grams of protein per kilogram of body weight per day for individuals with advanced CKD (stage 3 or higher) who are at high risk of malnutrition due to low appetite, chronic micro-inflammatory state, and acidemia-induced muscle breakdown.2 Therefore, dietary management that provides essential and adequate nutrient intakes while minimizing kidney burden is of critical importance.
The plant-based diet (PBD), characterized by a preponderance of plant-based foods with a comparatively lower proportion of animal-sourced foods, is gaining popularity due to its purported health effects and environmental sustainability.3 Observational studies have linked adherence to a healthful PBD pattern with a reduced prevalence of hypertension, diabetes, and cardiovascular disease (CVD).4–6 Although traditional viewpoint holds that animal proteins possess a higher biological value and thus superior to plant proteins,7 an increasing number of studies have indicated that a PBD is cross-sectionally associated with kidney function and may decrease the risk of diabetic nephropathy in patients with type 2 diabetes.8,9 Furthermore, a PBD represents the sole source of fiber capable of modulating gut microbiota and decreasing uremic toxins. Another notable advantage of PBD is its superior protein to phosphorus ratio compared to animal-based diets.10 To the best of our knowledge, the majority of previous studies have focused on the health effects of individual nutrients or nutrient quantities, with relatively less attention devoted to the assessment of diet quality.
We are aware that two earlier studies have already investigated the impact of PBD patterns on the mortality risk in patients with CKD.11,12 However, both studies included a predominantly advanced CKD cohort. It is currently unknown whether a PBD pattern also exerts a significant influence on the mortality risk of early stages of CKD, in which studies of nutritional management are relatively insufficient. To bridge this gap in the literature, our study examined the association between PBD indices and all-cause or cardiovascular mortality in a cohort of community-dwelling adults with predominantly early stages of CKD without comorbid CVD.
Methods
Data Source and Participant Selection
Publicly available data from the US 1999–2018 National Health and Nutrition Examination Survey (NHANES), an ongoing biennial cross-sectional survey, were used to conduct this mortality follow-up study. Ethical approval was obtained from the NCHS Research Ethics Review Board, and all participants provided informed consent. Based on the item 1 and 2 of Article 32 of the Measures for Ethical Review of Life Science and Medical Research Involving Human Subjects dated February 18, 2023, China, our study is exempted from ethical approval from our institution. Detailed descriptions of data acquisition can be found elsewhere.13
Adult participants with CKD, defined as an estimated glomerular filtration rate (eGFR) calculated from 2009 serum creatinine-based equation14 <60 mL/min/1.73m2 or a urinary albumin-to-creatinine ratio (uACR) >30 mg/g, were potentially eligible for inclusion. We further excluded participants for the following reasons: age < 20 years, pregnancy at the time of interview, with a history of malignancy or CVD (including self-reported stroke, heart attack, coronary heart disease, congestive heart failure, and angina pectoris), dialysis at the time of interview, missing data of PDI or follow-up, and those with missing covariates. As illustrated in Figure 1, a total of 4098 CKD subjects with complete data were included in the final analysis.
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Figure 1 The participant flow diagram. Abbreviations: CKD, chronic kidney disease; CVD, cardiovascular disease; NHANES, National Health and Nutrition Examination Survey; PDI, plant-based diet index.
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Assessment of PBD Indices
The dietary intake data were derived from the first-round (1999–2002 cycles) or the average of the first-round and second-round (2003–2018 cycles) 24-hour dietary recall, as appropriate. Details of the construction of PBD indices have been delineated previously.15 First, a total of 17 food groups were categorized into the healthy PBD (whole grains, fruits, vegetables, nuts, legumes, vegetable oils, and coffee), unhealthy PBD (fruit juices, refined grains, potatoes, sugar-sweetened beverages, sweets and desserts) and animal-based foods (animal fats, dairy products, eggs, fish or seafood, meat, and miscellaneous animal-based foods), primarily based on our current knowledge of the relationships between specific foods and certain chronic diseases. Consequently, the healthy PBD index (hPDI) and the unhealthy PBD index (uPDI) were generated by dividing each food intake into cohort-specific quintiles and assigning a score of 1 to 5. For the calculation of hPDI, positive scores were assigned to higher quintiles of healthy PBD (ie, the highest and lowest quintiles were assigned a score of 5 and 1, respectively), and higher quintiles of unhealthy and animal-based foods (ie, the highest and lowest quintiles were assigned a score of 1 and 5, respectively) received inverse scores. A similar approach was employed during the calculation of uPDI, wherein positive scores were assigned to unhealthy PBD and inverse scores were allocated to healthy and animal-based foods. To semiquantitatively assess the relative intake of plant-based foods and animal-based foods, a total PDI was scored by assigning positive scores to healthy and unhealthy PBD and negative scores to animal-based foods.
Outcome Ascertainment
Information regarding survival status was derived from the National Center for Health Statistics Public-Use Linked Mortality Files by linking to the National Death Index with a probabilistic matching algorithm. Follow-up time was censored at the recorded date of participant death, or at December 31, 2019 for those without a recorded death. The International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) codes were employed to determine the leading cause of death. In this context, CVD mortality was defined by the ICD-10 codes I00–I09, I11, I13, I20–I51, or I60–I69.16
Covariates
We incorporated a range of participant-level characteristics into the analysis, including demographics, socioeconomic status, clinical features, relevant laboratory results, and medication use. Specifically, we retrieved participants’ age (continuous), sex (men vs women), race (non-Hispanic white vs other), marital status (single vs non-single), poverty-income ratio (continuous), education level (less than high school vs high school vs higher than high school), body mass index (continuous, calculated as body weight in kilograms divided by height in meters squared), physical activity (none vs moderate vs vigorous), smoking (yes vs no), drinking (yes vs no), and total energy intake (continuous). The comorbidity variables included diabetes and hypertension. Laboratory tests included glycated hemoglobin, total cholesterol and triglycerides. Medication use assessed incorporated statins, angiotensin-converting enzyme inhibitors, and angiotensin II receptor blockers. The poverty-income ratio was calculated as annual household incomes divided by the family’s assigned poverty threshold. Smoking and drinking were defined as having smoked >100 cigarettes and consumed >12 drinks throughout their lifetime, respectively.
Statistical Analysis
Statistical analysis was performed in accordance with the analytic guideline that advocates appropriate weighting to obtain nationally representative estimates. Comparisons were made among total PDI tertiles (T1, lowest tertile; T2, medium tertile; T3, highest tertile) via the one-way analysis of variance or chi-squared test, as appropriate. The Kaplan–Meier survival curves were plotted to estimate the cumulative survival rate, which was then compared among different groups with the Log rank test. Following the assessment of the proportional hazard assumption using the Schoenfeld residual method, we examined the associations between total PDI, hPDI or uPDI with all-cause or CVD mortality using the Cox proportional hazards regression models, with results reported as hazard ratios (HRs) and 95% confidence intervals (95% CI). Potential non-linear associations between PBD indices and all-cause or CVD mortality were identified using the restricted cubic spline curves. In addition to the crude analysis without adjustments, two additional models adjusting for confounding factors were also generated. Model 1 was adjusted for participant’s age, sex, race, marital status, education level, and poverty-income ratio. Model 2 was further adjusted for body mass index, physical activity, smoking, drinking, hypertension, diabetes, glycated hemoglobin, total cholesterol, triglycerides, total energy intake, use of statins and angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, and eGFR and uACR. Subgroup analyses were also conducted stratified by participant’s age, sex, diabetes status, eGFR, and uACR. We conducted two sensitivity analyses: 1) in the first sensitivity analysis, participants who had deceased within 24 months of the follow-up were excluded to mitigate the risk of reverse causation; 2) in the second sensitivity analysis, we further adjusted for serum uric acid levels, dietary oxidative balance score,17 and dietary phosphorus to protein ratio.18 The statistical analyses were conducted using the R software (version 4.2.3), and a two-tailed P value < 0.05 was considered statistically significant.
Results
Baseline Participant Characteristics
Table 1 presents the characteristics of the 4098 participants (mean age 55.50 years, 40.38% men) and comparisons of participants stratified by total PDI tertiles. The mean eGFR and uACR for the entire cohort were 80.62 mL/min/1.73m2 and 153.12 mg/g, respectively. In comparison to the lowest total PDI tertile, those within the highest total PDI tertile were significantly older, more likely to be women, with higher educational attainment, more likely to be physically inactive, with a lower smoking prevalence, and a lower triglyceride level.
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Table 1 Comparison of Baseline Characteristics in Individuals with Chronic Kidney Disease Stratified by the Tertile of the Total Plant-Based Diet Index
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Kaplan–Meier Survival Analysis
During a median follow-up period of 102 (interquartile range 58–154) months, 1191 (19.52%) participants deceased, of which 397 were determined to be died of CVD causes. Specifically, the mortality rates were 23.40%, 20.31%, and 15.85% for the total PDI T1, T2 and T3 groups, respectively. Of these, 161 (6.92%), 135 (7.16%) and 101 (5.78%) were attributed to CVD mortality. Kaplan–Meier survival curves (Figure 2) based on the total PDI, hPDI and uPDI tertiles showed significant differences in all-cause mortality rate among the three uPDI subgroups. All-cause mortality in the T1, T2 and T3 groups stratified by total PDI and hPDI, and CVD mortality stratified by total PDI, hPDI and uPDI tertiles were not statistically significant.
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Figure 2 Kaplan–Meier survival curves for the associations between total plant-based dietary index (PDI, A and B), healthy PDI (hPDI, C and D), unhealthy PDI (uPDI, E and F) and all-cause mortality or cardiovascular mortality in US adults with chronic kidney disease.
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Associations Between Total PDI, hPDI, uPDI and All-Cause or CVD Mortality
As shown in Tables 2 and 3, total PDI and hPDI, as either continuous or categorical variables, were not associated with all-cause or CVD mortality. In the fully adjusted Model 2, an one-unit increase in uPDI was associated with a 2% increased risk of all-cause mortality. Similarly, the HRs and 95% CIs for the uPDI T2 and T3 groups were 0.98 (0.79–1.20) and 1.45 (1.15–1.83), respectively (P for trend = 0.003), with the T1 group serving as the reference group. Correspondingly, the restricted cubic spline curves (Figure 3) also indicated a positive and linear relationship between uPDI and all-cause mortality.
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Table 2 Associations Between Total PDI, hPDI, uPDI and All-Cause Mortality in US Adults with Chronic Kidney Disease
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Table 3 Associations Between Total PDI, hPDI, uPDI and Cardiovascular Mortality in US Adults with Chronic Kidney Disease
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Figure 3 Restricted cubic spline curves for the associations between total plant-based dietary index (PDI, A and B), healthy PDI (hPDI, C and D), unhealthy PDI (uPDI, E and F) and all-cause mortality or cardiovascular mortality in US adults with chronic kidney disease.
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Subgroup Analysis
Subgroup analysis (Figure 4) showed that the associations between uPDI and all-cause mortality were more pronounced in women and non-diabetics than in men and diabetics. The relationship between uPDI and all-cause mortality remained consistent across the spectrum of participant’s age, eGFR, and uACR.
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Figure 4 Subgroup analyses of the association between unhealthy plant-based dietary index and all-cause mortality in US adults with chronic kidney disease. Abbreviations: CI, confidence interval; eGFR, estimated glomerular filtration rate; HR, hazard ratio; uACR, urinary albumin-to-creatinine ratio.
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Sensitivity Analysis
Both sensitivity analysis (Supplementary Tables 1–3) demonstrated that a higher uPDI was associated with increased all-cause mortality.
Discussion
This study demonstrated, for the first time, that a higher intake of unhealthy PBD is related to an increased risk of all-cause mortality, but not incident cardiovascular mortality, in a nationally representative sample of US community-dwelling adults with predominantly early-stage CKD, especially in women and in those without diabetes. The hPDI and total PDI did not appear to have a significant relation to mortality risk in this population. In addition, the sensitivity analysis indicated that the study results were robust and are unlikely to be affected by reverse causation. Taken together, these data indicated that intakes of unhealthy PBD seemed to outweigh adherence to healthy PBD in influencing mortality risk in US adults with early stage CKD.
The PBD has been previously shown to confer a range of potential health benefits, including weight management, blood pressure and glucose regulation, and a reduced risk of CVD.19 Furthermore, earlier studies have also linked PBD with decreased risk of specific chronic conditions, including metabolic syndrome, liver cirrhosis, and colorectal cancer.20–22 A recent meta-analysis of 14 studies further demonstrated that the pooled relative risks for all-cause, CVD, and cancer mortality were 0.85, 0.85 and 0.91, respectively, for a higher hPDI, and 1.18, 1.19 and 1.10, respectively, for a higher uPDI,23 underscoring the effects of PBD in mortality reduction. However, it should be noted that not all PBD are conducive to optimal health, and it is practically difficult to maintain a vegan diet for the majority of the US population. To overcome this limitation, Satija et al conceptualized a hierarchical dietary model consisting of total PDI, hPDI, and uPDI, which enabled the understanding of how gradually increasing plant foods, while decreasing animal foods, affects health.24
The applicability of findings from studies of PBD in the general population to CKD patients has not yet been established, as CKD patients often exhibit unique dietary patterns and nutrient needs. Cross-sectional studies, such as the Tehran Lipid and Glucose Study and the Multiethnic Study of Atherosclerosis, have all reported a decreased incidence of CKD with a PBD.25,26 Mechanistically, the beneficial effects of a plant-rich diet on kidney health may be related to its effect on inhibiting micro-inflammation, promoting intestinal mobility, modulating gut microbiota, reducing uremic toxin production, and providing nutrients of vitamins, minerals, fibers and phytochemicals.27
To the best of our knowledge, the results of our study differ from those of several previous studies on the associations of PBD indices with mortality risk specifically in CKD patients.11,12 In a report of 2539 CKD participants from the Chronic Renal Insufficiency Cohort Study, Amir et al found that the highest tertile of total PDI and hPDI exhibited a 26% and 21% reduced risk of all-cause mortality.12 Analogous findings have also been observed in an analysis of 4807 CKD patients from the UK Biobank.11 It is noteworthy that both studies exclusively focused on all-cause mortality, without investigating CVD mortality. This study bridged this knowledge gap by demonstrating that total PDI, hPDI, and uPDI were all unrelated to CVD mortality. While the current study, along with the two aforementioned studies, has all observed a deleterious effect of uPDI on mortality risk in CKD patients, this study diverges from others in its finding of no associations between total PDI, hPDI, and mortality risk. The potential explanation for this discrepancy may be attributed to variations in participant characteristics, such as the severity of CKD. Specifically, the mean eGFR of the included patients in this study is 80.62 mL/min/1.73m2, which is significantly higher than that reported by Amir et al (43.4 mL/min/1.73m2) and by Thompson et al (59.5 mL/min/1.73m2).11,12 More importantly, this study excluded participants with known diagnoses of CVD, whereas the other two studies did not. Consequently, the subjects in our study may represent a highly selected population with a more favorable cardiometabolic profile. This finding underscored that the consumption of unhealthy PBDs may exert a more substantial influence on the mortality risk in early-stage CKD without CVD than the adherence to a healthy PBD.
Our study showed that an unhealthy PBD has the potential to markedly elevate all-cause mortality risk, even among individuals with only mild CKD. An unhealthy PBD is typically high in refined and ultra-processed foods and less in healthy plants and animal-sourced foods. Its association with all-cause mortality in CKD patients may be attributable to its low micronutrient content, high caloric content, hyperorexia associated with high fat intake, and unfavorable effects of added sugars.28
Subgroup analysis indicated that the association between uPDI and all-cause mortality in CKD patients were sex-specific that was only observed in women and non-diabetics. Similarly, Wang et al reported a stronger reverse relationship between hPDI and the aging process in females.29 The potential explanation for these observed discrepancies include the differential influence of estrogen, which has been demonstrated to enhance fat transportation in women and promote serum triglyceride levels.30 The consumption of sugar-sweetened beverages, a component of the uPDI, has been demonstrated to increase the risk of metabolic syndrome in women, but not in men,31 possibly due to the fact that triglycerides and lipoproteins in women appear to be more sensitive to changes in dietary carbohydrates or fats than in men.32 The attenuated effect of uPDI on all-cause mortality in individuals with diabetes may reflect post-diagnosis dietary improvements, as patients often adopt healthier eating habits after being diagnosed. Nevertheless, these findings underscore the importance of avoiding unhealthy plant-based diets, particularly in those without diabetes, to mitigate mortality risk.
Notable strengths of this study include large sample size and national representation, thus facilitating external generalization of study results to US CKD patients with similar characteristics. We contend that our analysis has broadened previous research by incorporating predominantly those with only mild renal impairment. Moreover, we have also adjusted for dietary oxidative balance score, dietary phosphorus intake, and uric acid, as previous studies have demonstrated that these factors could also influence outcomes in CKD.33,34 There are, however, several limitations inherent in this study that should be pointed out. First, the dietary information was collected through self-report, which may introduce recall bias. Second, dietary patterns were collected using the 24-hour recall method, which may not always be a precise reflection of habitual dietary patterns or potential dietary changes over time. Third, PBD indices negative scored all animal-based foods, whereas animal-sourced proteins are generally preferred over plant-sourced proteins for protein bioavailability and malnutrition prevention.35 Finally, the observational nature of the study may be susceptible to residual confounding that may deviate results.
In conclusion, this population-based study showed that higher adherence to an unhealthy PBD is associated with an augmented risk of all-cause mortality in US adults with predominantly early stages of CKD, particularly in women and non-diabetics. Our results underscore the critical importance of avoiding unhealthy PBD in the management of early stages of CKD. In the future, further interventional studies are warranted to ascertain whether reducing unhealthy PBD may indeed improve outcomes in patients with early stages of CKD.
Data Sharing Statement
The dataset used for the current analysis are publicly available from the National Health and Nutrition Examination Survey at https://www.cdc.gov/nchs/nhanes/.
Ethical Approval and Consent to Participate
The NHANES has been approved by the NCHS Research Ethics Review Board. Informed consent was obtained from all participants.
Funding
There is no funding to report.
Disclosure
All the authors have declared no competing interests.
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