Abstract
Both vitamin D deficiency and cognitive impairment are common in patients with chronic kidney disease (CKD). Vitamin D exerts neuroprotective and regulatory roles in the central nervous system. Hypovitaminosis D has been associated with muscle weakness and bone loss, cardiovascular diseases (hypertension, diabetes and hyperlipidemia), inflammation, oxidative stress, immune suppression and neurocognitive impairment. The combination of hypovitaminosis D and CKD can be even more debilitating, as cognitive impairment can develop and progress through vitamin D-associated and CKD-dependent/independent processes, leading to significant morbidity and mortality. Although an increasingly recognized comorbidity in CKD, cognitive impairment remains underdiagnosed and often undermanaged. Given the association of cognitive decline and hypovitaminosis D and their deleterious effects in CKD patients, determination of vitamin D status and when appropriate, supplementation, in conjunction with neuropsychological screening, should be considered integral to the clinical care of the CKD population.
Highlights
Suboptimal vitamin D status, hypovitaminosis D, is extremely common [1]
It has been hypothesized that Chronic kidney disease (CKD) patients with inadequate vitamin D status could potentially experience an accelerated cognitive decline, there are scant adequately designed studies on this topic
We gathered the current evidence on occurrence rate, risk and role of hypovitaminosis D in non-dialysis and dialysis-dependent CKD patients with cognitive impairment (CI)
Summary
Suboptimal vitamin D status, hypovitaminosis D (vitamin D insufficiency and deficiency), is extremely common [1]. Vitamin D promotes neuron survival [59], inhibits oxidative pathways in the brain through reducing free radical formation [60] and increases antioxidant (γ-glutamyl transpeptidase) production [61], reverses oxidative stress associated mitochondrial dysfunction [62], down-regulates L-type calcium channels expression [63] and attenuates injurious effects of excitatory neurotoxins [64,65]. In a fully adjusted modal, 25(OH)D level was positively and progressively associated with a better memory function only in individuals carrying two APOE ε4 alleles, not in those carrying zero or one allele [31] These results are consistent with a role for varying genetic backgrounds in the susceptibility of vitamin D deficiency associated cognitive dysfunction
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