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Lu, E.M. Vitamin D Deficiency on Chronic Kidney Disease. Encyclopedia. Available online: https://encyclopedia.pub/entry/56251 (accessed on 17 April 2024).
Lu EM. Vitamin D Deficiency on Chronic Kidney Disease. Encyclopedia. Available at: https://encyclopedia.pub/entry/56251. Accessed April 17, 2024.
Lu, Emily Ming-Chieh. "Vitamin D Deficiency on Chronic Kidney Disease" Encyclopedia, https://encyclopedia.pub/entry/56251 (accessed April 17, 2024).
Lu, E.M. (2024, March 14). Vitamin D Deficiency on Chronic Kidney Disease. In Encyclopedia. https://encyclopedia.pub/entry/56251
Lu, Emily Ming-Chieh. "Vitamin D Deficiency on Chronic Kidney Disease." Encyclopedia. Web. 14 March, 2024.
Vitamin D Deficiency on Chronic Kidney Disease
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Vitamin D has important anti-inflammatory, anti-microbial properties and plays a central role in the host immune response. Due to the crucial role of the kidneys in the metabolism of vitamin D, patients with chronic kidney disease (CKD) are prone to vitamin D deficiency.

vitamin D chronic kidney disease periodontal disease

1. Introduction

Vitamin D deficiency is associated with various noncommunicable diseases, among which are chronic kidney disease (CKD) and periodontal disease. As well as its fundamental roles in calcium and phosphate homeostasis, vitamin D possesses important antibacterial, anti-inflammatory and host modulatory effects [1], which exert “renoprotective” and “perio-protective” effects.
CKD is a global health concern affecting 5–10% of the world population [2]. According to Kidney Disease Improving Global Outcomes (KDIGO), CKD is diagnosed on the basis of an estimated glomerular filtration rate (eGFR) and values less than 60 mL/min/1.73 m2 have been identified as the threshold for CKD [3][4], together with abnormalities of renal structure or function, present for more than 3 months with implications for health [4]. There are five stages in CKD, the higher the staging the lower the eGFR [4].
Periodontitis is a chronic multifactorial inflammatory disease with an overall prevalence of 11.2% and is the 6th most prevalent disease worldwide [5]. It is associated with dysbiosis of the oral flora, characterised by the progressive destruction of the periodontium, with loss of clinical attachment, loss of the alveolar bone, presence of periodontal pockets and gingival bleeding [6]. Periodontitis is a serious public health issue, as it can cause not only local symptoms, but it can also have a negative impact on the individual’s general health, contributing to the development, and to the worsening, of chronic non-communicable degenerative diseases, such as chronic kidney disease (CKD) [7].
Periodontal disease and CKD have shared pathophysiological mechanisms, namely an increased inflammatory state, impaired immune response, and oxidative stress [8]. Therefore, the occurrence of both conditions is likely to result in an amplification of adverse outcomes [9]. A recent large cohort study suggested a bidirectional, causal relationship between periodontal inflammation and renal function [10], such that a 10% increase in periodontal inflamed surface area (PISA) was associated with a 3.0% decrease in eGFR and a 10% decrease in eGFR led to a 25.0% increase in PISA [10].

2. Vitamin D Metabolic Pathways

Vitamin D is a fat-soluble hormone that can be obtained from two main sources. Firstly, it can be obtained from dietary sources such as fatty fish and mushrooms. It is found in the form of Ergocalciferol (D2) from plant sources or Cholecalciferol (D3) from animal sources [11]. Secondly, it can be obtained through the action of sunlight’s ultraviolet rays on skin in the form of 7-Dehydrocholesterol which is converted into the previtamin Cholecalciferol (D3) [12]. Due to the relatively small proportion of vitamin D from the diet, dermal synthesis accounts for 90% of vitamin D provision [13].

2.1. Classical Pathway

The classical pathway for the activation of vitamin D involves two stages of hydroxylation. Firstly, the Vitamin D2 and D3 precursors are transported to the liver by vitamin D-binding protein (DBP) [14]. Precursors D2 and D3 are then converted into inactive 25-hydroxvitamin D (25(OH)D) by hydroxylation at the C25 position by 25-hydroxylase, coded by cytochrome P2R1 (CYP2R1) [15]. 25(OH)D acts as the main circulating and storage form of vitamin D in the body. 25(OH)D is then circulated in blood as the 25(OH)-DBP complex and undergoes glomerular filtration and uptake into the kidney proximal tubule cell by the receptor megalin. 25(OH)D-DBP then undergoes 1-α-hydroxylation by the Cytochrome P450 Family 27 Subfamily B Member 1 gene (CYP27B1) to its most activated state, 1,25-dihydroxyvitamin D (1,25(OH)2D), also known as calcitriol [15]. This is illustrated in Figure 1.
Figure 1. Vitamin ’s classical activation pathway in the human body. Sources of Vitamin D such as UV rays and diet deliver vitamin D in their precursor forms, D2 and D3. These precursors then bind to the Vitamin D-binding protein (DBP) at the site of synthesis and form the DBP-D protein complex. Vitamin D is then carried in the DBP-D complex through the blood plasma to the liver. Precursors D2 and D3 are hydroxylated into inactive 25-hydroxvitamin D [25(OH)D] by 25-hydroxylase, coded by the cytochrome P2R1 (CYP2R1) gene. 25(OH)D is taken up into the kidney from the blood and activated via 1-α-hydroxylation by the CYP27B gene to the 1,25-dihydroxyvitamin D (1,25(OH)2D) activated state. An increase in parathyroid hormone (PTH), reductions in phosphorous and calcium upregulates CYP27B gene activity, while an increase in fibroblast growth factor (FGF-23) downregulates CYP27B gene activity.
Calcitriol has wide ranging physiological and pharmacological effects [1]. Calcitriol is responsible for increasing intestinal calcium and phosphate absorption when serum calcium and phosphate levels are low. It also increases phosphorus resorption from bone and is involved in the production of antimicrobial peptides, epithelial defence mechanisms, host modulatory effects, the maintenance of the renin-angiotensin system, the inhibition of host tumour cells and suppression of parathyroid hormone (PTH) release [1]. Calcitriol exerts these affects by binding to intracellular vitamin D receptors (VDRs), which are steroid hormone nuclear receptors and function as transcription factors [16].
In health, the activation of the CYP27B gene is regulated by PTH, phosphorus, calcium, and fibroblast growth factor-23 (FGF-23) levels, and subsequently calcitriol levels [17]. Increased PTH levels combined with decreased phosphorus and calcium levels activate the CYP27B gene and lead to increased calcitriol levels [13]. Meanwhile, increased FGF-23 levels inhibit the CYP27B gene and decrease calcitriol levels [18].

2.2. Non-Classical Pathway

Aside from the classical metabolism of vitamin D and its role in calcium and phosphate homeostasis, a non-classical pathway of calcitriol synthesis appears to be present in various tissues, both including and peripheral to the kidneys. Additionally, 1-𝛼-hydroxylase (which is primarily expressed in the kidneys) may also be expressed in extrarenal cells and tissues [19]. Thus, the extra-renal production of calcitriol primarily functions as an autocrine or paracrine factor at extra-renal sites and thus plays a role in the non-classical actions of vitamin D [20][21].
Central to the non-classical function is the regulation of the renin–angiotensin–aldosterone system (RAAS). Calcitriol is regarded as a negative endocrine regulator of the renin gene, thereby inhibiting the RAAS and preserving renal function. The RAAS stimulates the production of renin, which cleaves angiotensin into angiotensin I, which is then processed into angiotensin II by the angiotensin-converting enzyme (ACE). Angiotensin II binds to the type 1 angiotensin II receptor (AT1R) to produce various deleterious effects for renal and cardiovascular tissues, including hypertension [22][23]. This is described in more detail in Figure 2.
Figure 2. Vitamin D deficiency leads to the progression of chronic kidney disease (CKD) and cardiovascular disease (CVD). Vitamin D deficiency leads to a decrease in VDR-mediated functions. VDR activation is responsible for stimulation of the juxtaglomerular apparatus, which usually suppresses the renin–angiotensin–aldosterone system (RAAS) and the secretion of renin. In the absence of VDR activation (created by vitamin D deficiency), intracellular calcium is not stimulated within the juxtaglomerular apparatus, and RAAS activity increases. Renin and subsequent angiotensin-II production will increase in turn. Renin cleaves angiotensinogen into angiotensin I, which is then converted into angiotensin II by the angiotensin-converting enzyme (ACE). Angiotensin-II can produce more downstream angiotensin sub-types.
There is also evidence that VDR activation by calcitriol may also downregulate other RAAS components aside from renin, including the Ang II type one receptor, renin receptor and transforming growth factor beta [24]. This can aid in the reduction of renal blood pressure and fibrogenesis. VDR activation by calcitriol could also have anti-inflammatory effects, via the suppression of nuclear factor-kB (NF-kB) activation. It also appears that VDR can form complexes with various transcription factors and engage in crosstalk with a wide range of cellular signals [25], thus illustrating the depth of the relationship between VDR activation and RAAS components.
The suppression of the NF-kB pathway by calcitriol has extra-renal consequences too. Its suppression of the pathway is twofold: calcitriol suppresses NF-kB nuclear migration and phosphorylation, and it downregulates IkB phosphorylation (a protein involved in NF-kB signalling) by suppressing ROS activity [26]. The NF-kB pathway promotes pro-inflammatory cytokine expression, and thus a reduction in NF-kB activity results in a reduction in inflammatory markers. Thus, the suppression of the NF-kB pathway in turn can prevent insulin resistance [27], have neuroprotective effects against ischaemic strokes [26], and protect against other inflammatory disorders. Therefore, both the inhibitions of the RAAS and the NF-kB pathway are responsible for the “reno-protective” effects of vitamin D [28].
It is also worth noting the role of vitamin D in muscle health, perhaps best characterised by the link between vitamin D deficiency and sarcopenia, a generalised degenerative skeletal muscle disorder [29][30]. Low serum 25(OH)D levels are associated with sarcopenia in haemodialysis patients [29]. This is explained by the fact that calcitriol binds to VDRs in skeletal myocytes, stimulating protein synthesis [31][32]. Patients suffering from renal failure have an increased risk for the development of sarcopenia, due to their accelerated protein catabolism, the dialysis procedure itself, as well as their low energy and protein intakes [33]. Therefore, replenishing vitamin D levels would facilitate the restoration of muscle health [33].

3. Impact of Vitamin D Deficiency on CKD

Vitamin D deficiency is associated with a higher risk of mortality, secondary and tertiary hyperparathyroidism [34]. Due to impaired renal function, the eGFR is reduced, and there is therefore a decline in the conversion of 25(OH)D to calcitriol, the active form of vitamin D. The latter reduces intestinal calcium absorption and, together with phosphate retention, contributes to the onset of secondary and tertiary hyperparathyroidism.
CKD Patients who are vitamin D deficient have high mortality rates [35] and an increased cardiovascular risk [36]. In addition, the elevation of FGF23, which is linked with vitamin D deficiency, is associated with the progression of CKD towards end-stage renal disease (ESRD), the occurrence of cardiovascular (CVS) events and increased mortality rates in patients with CKD [37][38].
The serum total 25(OH)D concentrations were predictive of renal outcomes, such as the doubling of serum creatinine in ESRD, and associated with disease progression and morality [39][40]. A meta-analysis of prospective studies demonstrated an increased relationship between all-cause mortality in patients with CKD and serum total 25(OH)D concentrations [41]. Conversely, a recent systematic review and meta-analysis concluded that higher levels of serum 25(OH)D were associated with lower risks of all-cause mortality [42].
Therefore, to ensure that patients with CKD avoid vitamin D deficiency and prevent complications such as secondary and tertiary hyperparathyroidism and other co-morbidities [43][44][45], the Kidney Disease Outcomes Quality Initiative (KDOQI) and Kidney Disease Improving Global Outcomes (KDIGO) group have suggested the use of vitamin D supplementation [44][45].

Vitamin D Supplementation in CKD Patients

Vitamin D supplementation is associated with the reduced risk of all-cause mortality [46] and cardiovascular mortality in patients in CKD, including those with ESRD [45][47]. In particular, therapies with calcitriol and analogues are associated with reduced mortality in CKD patients, particularly those suffering from SHPT [48].
CKD patients are deficient in vitamin D, even in the early stages of the disease [49]. Vitamin D plays a vital role not only in mineral homeostasis, but also in systemic health. As such, it is advised that vitamin D supplementation in CKD patients begins as soon as possible, to ensure a pool of vitamin D can be turned into calcitriol.
During the early stages of CKD, where there is still evidence of residual renal function, supplementation can be achieved for CKD patients with oral forms of inactive vitamin D3 or D2. Vitamin D3 (cholecalciferol) is the natural form synthesised in the dermis, whilst vitamin D2 (ergocalciferol) is a synthetic product made using fungi [50]. Another reason is that vitamin D2 is associated with higher catabolic processes, and therefore, the overall improvement in serum vitamin D levels is not as sustainable as that seen with D3. Therefore, vitamin D3 is superior to vitamin D2 in raising the total 25(OH)D and thus ideally used for supplementation [51].
It is important to appreciate that the renal production of calcitriol becomes suppressed during Stages 3–4 of CKD [52][53] that are characterised by the significant loss of renal 1-𝛼-hydroxylase, and the development of SHPT with declining kidney function. The current KDIGO guidelines recommend that calcitriol and vitamin D analogue supplementation should be reserved for predialysis CKD patients with severe and progressive hyperparathyroidism [2]. However, in line with the above points and existing clinical research [52][53][54], vitamin D supplementation (ideally with D3) should begin immediately after diagnosis to facilitate endogenous conversion into calcitriol and its positive downstream effects. 

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