Applied nutritional investigationBody adiposity predictors of vitamin D status in nondialyzed patients with chronic kidney disease: A cross-sectional analysis in a tropical climate city
Introduction
Overweight/obesity is commonly observed in the chronic kidney disease (CKD) population and follows the growing increase in worldwide prevalence. Overall, the proportion of the world's adult population with overweight/obesity is about 36.9% to 38% [1]. In Brazil, according to the 2008–2009 census, the scenario is not different. In adults >20 y, the prevalence of overweight was 50.1% in men and 48% in women, whereas the prevalence of obesity was 12.4% in men and 16.9% in women [2]. Obesity/overweight raises the risk for insulin resistance (IR), type 2 diabetes, hypertension, dyslipidemia [3], and vitamin D deficiency [4].
The definition of insufficiency and deficiency of vitamin D remains controversial, limited by the lack of a consensus regarding the cutoff point for serum 25-hydroxyvitamin D (25 [OH]D). However, there is a common understanding that low serum 25(OH)D concentration causes calcium malabsorption accompanied by negative calcium balance, secondary hyperparathyroidism, and bone disorders among other alterations [4], [5], [6], [7]. CKD is accompanied by alteration in bone mineral metabolism early in the evolution of the disease, and association with overweight/obesity might worsen this condition. Patients with CKD have a high burden of cardiovascular disease (CVD), and traditional risk factors only partially account for this risk. Multiple epidemiologic studies have demonstrated a survival benefit associated with higher serum concentration of 25(OH)D [4], [5], [6], [7].
There are few investigations concerning vitamin D status and its association with adiposity in nondialyzed CKD population, especially in those inhabiting a tropical area, where the ultraviolet index is high all year around [8], [9]. Additionally, data associating vitamin D with adiposity in patients with CKD are controversial and the majority of studies use body mass index (BMI) as body fat parameter [8], [10], [11], [12], [13]. However, BMI presents limitations in the accurate assessment of body fat [14], [15]. Furthermore, although the relation of body fat with IR is consistent, the association of vitamin D with IR is less explored in CKD population [16].
The hypotheses of this study are that the BMI is not a good body adiposity predictor of vitamin D deficiency, considering its known limitations to assess body adiposity; the total body adiposity, rather than central adiposity, is a predictor of vitamin D deficiency; the vitamin D deficiency is associated with IR, impaired homeostasis of parathyroid hormone (PTH), phosphorus, and lipids.
Thus, the aim of the present study was to describe the vitamin D status and to identify body adiposity predictors of vitamin D deficiency, in a nondialyzed CKD population under regular treatment, dwelling in a tropical city. A secondary objective was to examine the association of vitamin D status with clinical abnormalities commonly observed in CKD.
Section snippets
Study design and population selection
A cross-sectional observational study was carried out from October 2012 to December 2014. Nondialyzed patients with CKD, under regular treatment at the CKD interdisciplinary outpatient clinic at Pedro Ernesto University Hospital (Rio de Janeiro State University, Rio de Janeiro, Brazil) were included. Eligible participants were adults (≥18 y) with estimated glomerular filtration rate (eGFR) <60 mL/min and under regular treatment with a renal dietitian and nephrologist for ≥6 mo. We excluded
General sample population characteristics
The study included 244 patients with CKD, 54.9% (n = 134) were men. Demographic, nutritional, and biochemical variables are presented in Table 1. Overall, the patients were clinically stable and the majority was in CKD categories 3b and 4. The main baseline disease was hypertension (41.8%; n = 102) and 19.7% of patients had diabetes (n = 48), whereas the remaining consisted of others causes (27.4%; n = 67) and unknown (11.1%; n = 27). The number of patients who had the blood collected during
Discussion
The present cross-sectional study underlined that 25(OH)D status was sufficient (≥30 ng/dL) in 43% of the studied patients, in a high sunlight irradiation city. We found 37% classified as insufficient (20–30 ng/dL) and 20% (<20 ng/dL) as deficient. Most of the patients (∼60%) were overweight/obese, thus we sought among total and central body adiposity parameters as predictors of 25(OH)D deficiency. Total body adiposity, regardless whether evaluated by the reference method DXA or by the simple
Conclusions
Of nondialyzed patients with CKD, almost 50% presented sufficient concentration of 25(OH)D despite living in a tropical city, and the predictor of vitamin D deficiency was total body adiposity, independent of age and eGFR, regardless of whether it was assessed by a reference method DXA or by a simple anthropometric index BAI. Patients presenting with vitamin D deficiency showed higher serum phosphorus and higher prevalence of hyperparathyroidism. IR was not independently associated with 25(OH)D
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2020, American Journal of Kidney DiseasesCitation Excerpt :For most experts, vitamin D insufficiency is defined as serum 25(OH)D level between 20 and 29 ng/mL, deficiency is considered as 25(OH)D level < 20 ng/mL, and sufficiency as serum 25(OH)D level ≥ 30 ng/mL.343 A number of factors or conditions are implicated in suboptimal vitamin D status in patients with CKD, including aging, diabetes mellitus, obesity, reduced sun exposure, loss of urinary/dialysate vitamin D binding protein, impaired tubular 25(OH) reabsorption, and dietary restrictions.344-347 Considering the high prevalence of vitamin D deficiency/insufficiency in CKD/ESKD and the potential benefits of restoring vitamin D status, the K/DOQI348 (2003) and KDIGO349 (2017) clinical practice guidelines for CKD–mineral and bone disorder (CKD-MBD) have proposed ergocalciferol or cholecalciferol supplementation.
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The present study was supported by Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ). MIBS and RB contributed to the study conception and design, data collection, assembly, analysis and interpretation, manuscript drafting, and approval of the final version of the manuscript. VVdSC contributed to data collection, assembly, analysis, and interpretation, manuscript drafting, and approval of the final version of the manuscript. CCdaSL contributed to data collection, manuscript drafting, and approval of the final version of the manuscript. MRSTK contributed to study conception and design, data analysis and interpretation, manuscript drafting, and approval of the final version of the manuscript. The authors have no conflicts of interest to declare.