High Fitness Levels Offset The Increased Risk Of Chronic Kidney Disease Due To Low Socioeconomic Status: A Prospective Study Ⅱ

RESULTS Baseline Characteristics 

The overall mean (SD) age, SES, and CRF of study participants at baseline were 53 (5) years, 8.54 (4.24), and 30.3 (7.9) mL/kg/min, respectively (Table). Signifificant inverse correlations were observed among CRF and SES, age, alcohol consumption, body mass index, blood pressure, total cholesterol, and estimated GFR; whereas, significant positive correlations were observed with PA, high-density lipoprotein cholesterol, and creatinine. Values of CRF were significantly lower in men with preexisting diseases such as type 2 diabetes, hypertension, and coronary heart disease compared to those without as well as current smokers compared with nonsmokers.

CLICK HERE TO GET CISTANCHE FOR CKD TREATMENTS

Interplay Among SES, CRF, and Chronic Kidney Disease Risk

During a median (interquartile range) follow-up of 25.8 (18.0-28.0) years, 197 incident chronic kidney disease cases were recorded. In an analysis adjusted for model 2 covariates: age, systolic blood pressure, history of type 2 diabetes, smoking status, history of hypertension, history of coronary heart disease, total cholesterol, alcohol consumption, estimated GFR, and PA, low compared with high SES was associated with an increased risk of chronic kidney disease 1.55 (95% CI: 1.06-2.25; Figure 1), which remained similar on further adjustment for CRF (Figure 1). A multivariable restricted cubic spline curve showed that chronic kidney disease risk decreased continuously with increasing CRF across the range 25-46 mL/kg/min (P value for nonlinearity = .19; Figure 2). On adjustment for covariates in model 2, high CRF was associated with a decreased risk of chronic kidney disease compared with low CRF 0.66 (95% CI: 0.45-0.96), which remained similar on additional adjustment for SES (Figure 1). The association was signifificant when CRF was modeled per 1 SD increment (Figure 1).

Compared with men with high SES-high CRF, multivariable analysis (model 2) showed that men with low SES low CRF had an increased risk of chronic kidney 1.88 (95% CI: 1.23-2.87), with no evidence of an association for low SES-high CRF and chronic kidney disease risk 1.32 (95% CI: 0.85-2.05; Figure 1). Results of interaction analysis showed the RERI was 0.31 and the ratio of HRs was 1.14, indicating the presence of both additive and multiplicative interactions. disease Table Baseline participant characteristics and correlates of cardiorespiratory fitness

DISCUSSION 

Our results based on a general population-based prospective cohort study of middle-aged and older Caucasian men confirm the previously reported independent associations of low SES with increased chronic kidney disease risk and high CRF levels with lowered risk of chronic kidney disease. The association between CRF and chronic kidney disease was potentially consistent with a graded dose-response relationship across the range of CRF values 25-46 mL/kg/ min. New findings based on the joint associations of SES and CRF with chronic kidney disease risk showed that the risk of chronic kidney disease was increased in men with low SES and low CRF, but the increased risk of chronic kidney disease related to low SES was attenuated to null by high CRF levels. In interaction analysis, the association between the combined exposures (i.e., low SES and low CRF) and chronic kidney disease risk exceeded the sum or product of their associations considered separately.

Biological, behavioral, and psychosocial risk factors prevalent in socioeconomically deprived individuals are known to accentuate the relationship between low SES and chronic disease outcomes.38 These include lower levels of education, unhealthy lifestyles such as excessive alcohol consumption, limited access to health care, higher prevalence of comorbid conditions, and stress and depression. Social deprivation may also be associated with delayed presentation of, and lower rates of treatment, dose, and adherence to therapy for hypertension, diabetes, and metabolic syndrome, which are major risk factors for chronic kidney disease.5,6 Though CRF is determined by many nonmodifiable factors such as age, sex, and underlying disease states, with about half of its variation being heritable,39 it largely remains a modifiable risk factor. Increased PA and exercise training are well-documented methods for increasing CRF.40 Both aerobic and resistance training is effective for the beneficial modulation of dysglycemia, high blood pressure, obesity, dyslipidemia, and inflflammation,41 which are all involved in the pathophysiology of chronic kidney disease. Other specifific mechanisms postulated to underpin the protective effects of habitual PA on chronic kidney disease include improved endothelial dysfunction and alleviation of sympathetic overactivity.42-44

Both SES and CRF are powerful determinants of various chronic disease outcomes. The current findings are clinically relevant as they add to the increasing evidence on the plentiful health benefits of CRF and its ability to attenuate or offset the adverse effects of other major risk factors. Previous investigations have shown that higher CRF levels can offset the increased risk of diagnosed chronic obstructive pulmonary disease, hypertension, heart failure, and mortality due to low SES.16,17,21,22 The beneficial effects of PA and exercise are well documented and are observed across most organ systems, and these include enhancement of resilience, the immune system, and longevity.45 The World Health Organization recommended in 2020 that all adults should aim for 150-300 minutes of moderate-intensity PA per week or 75-150 minutes of vigorous-intensity PA per week or an equivalent combination of moderate-intensity and vigorous-intensity PA per week.46 These guidelines have evolved from previous guidelines.47 Despite guideline recommendations and population-wide strategies to promote PA levels, most populations do not adhere to PA recommendations. Promoting habitual PA and exercise training (which confers good CRF) is a critical intervention that can reduce the incidence and prevalence of common chronic diseases including chronic kidney disease. Populations at high risk of these chronic diseases including the socioeconomically deprived need more education on the substantial benefits of PA. Furthermore, access to PA resources that are both feasible and attractive for these populations also needs to be widened.

Strengths of the current study include the novelty, being the first evaluation of the separate and joint associations of SES and CRF with chronic kidney disease risk as well as formal investigation of the interactions between SES and CRF levels in relation to chronic kidney disease; the use of a population-based prospective cohort design comprising a relatively homogeneous sample of men with normal kidney function at baseline; the long-term follow-up duration of the cohort that was adequate for the ascertainment of the outcome under investigation; and employment of directly measured CRF as assessed using peak oxygen uptake during CPX (gold standard measure). Limitations deserving consideration included the use of self-administered questionnaires in assessing SES, which may be prone to misclassification bias; inability to generalize findings to women and other populations; lack of data on medications (eg, regular use of nonsteroidal anti-inflflammatory drugs) during follow-up, which may have impacted on kidney function; and the potential for biases such as residual confounding, reverse causation, and regression dilution bias because of the observational cohort design.

CONCLUSIONS

In middle-aged and older Caucasian males, SES and CRF are each independently associated with the risk of incident chronic kidney disease. There exists an interplay among SES, CRF, and chronic kidney disease risk, including significant additive and multiplicative interactions between SES and fitness levels in relation to chronic kidney disease and high fitness levels appear to offset the increased risk of chronic kidney disease related to low SES.

References 

1.. Couser WG, Remuzzi G, Mendis S, Tonelli M. The contribution of chronic kidney disease to the global burden of major noncommunicable diseases. Kidney Int 2011;80:1258–70. 

2. Chronic Kidney Disease Prognosis Consortium, Matsushita K, van der Velde M, et al. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Lancet 2010;375:2073–81.

3. World Health Organization. Fact sheets. The top 10 causes of death. Available at: https://www.who.int/news-room/fact-sheets/detail/thetop-10-causes-of-death. Accessed September 10, 2021. 

4. Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med 2004;351:1296–305.

5. Saran R, Li Y, Robinson B, et al. US renal data system 2014 annual data report: epidemiology of kidney disease in the United States. Am J Kidney Dis 2015;66: [Svii, S1-305. 

6. Kurella M, Lo JC, Chertow GM. Metabolic syndrome and the risk for chronic kidney disease among nondiabetic adults. J Am Soc Nephrol 2005;16:2134–40. 

7. Hawkins NM, Jhund PS, McMurray JJ, Capewell S. Heart failure and socioeconomic status: accumulating evidence of inequality. Eur J Heart Fail 2012;14:138–46. 

8. Adler NE, Ostrove JM. Socioeconomic status and health: what we know and what we don't. Ann N Y Acad Sci 1999;896:3–15. 

9. Zeng X, Liu J, Tao S, Hong HG, Li Y, Fu P. Associations between socioeconomic status and chronic kidney disease: a meta-analysis. J Epidemiol Community Health 2018;72:270–9. 

10. Wilund KR, Thompson S, Viana JL, Wang AY. Physical activity and health in chronic kidney disease. Contrib Nephrol 2021;199:43–55.

Supportive Service:

Email:wallence.suen@wecistanche.com 

Whatsapp/Tel:+86 15292862950

Shop:

https://www.xjcistanche.com/cistanche-shop