Serum vitamin D levels and acute kidney injury: a systemic review and meta-analysis

Abstract

Numerous researches have evaluated the prevalence and clinical outcome of vitamin D deficiency in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). But the quantitative vitamin D status in acute kidney injury (AKI) patients and its relationship with prognosis remains controversial. We conducted this systemic review and meta-analysis to assess the quantitative difference of vitamin D status, including serum 25(OH) D and 1,25(OH)2D levels, between AKI patients and non-AKI controls, and further explore whether vitamin D status can be clearly correlated with the mortality of AKI. Major databases, including PubMed, Web of Science and EBSCO, were searched until 1st September 2021. All published observational studies related to vitamin D and AKI According to predefined inclusion and exclusion criteria were extracted. Meta-analyses were performed using Review Manager 5.3.5. Four studies including five cohorts were included with a total of 413 patients. The serum 25(OH)D levels showed no statistically significant difference in AKI patients and non-AKI controls. On the other hand, the serum 1,25(OH)2D levels were significant lower in AKI patients than in non-AKI controls (MD = − 17.79, 95% CI = − 32.73 to − 2.85, P = 0.02). As for the relationship between serum vitamin D status and AKI patients’ mortality, we were unable to give a consistent conclusion based on current limited and conflict study results. Our meta-analysis suggested that serum 1,25(OH)2D levels, rather than 25(OH)D, is significantly lower in AKI patients. The relationship between vitamin D status and clinical outcome of AKI remains controversial based on current evidence. Future comprehensive studies are required to confirm these relations and to elucidate potential mechanisms.

Phosphate Restriction Prevents Metabolic Acidosis and Curbs Rise in FGF23 and Mortality in Murine Folic Acid–Induced AKI

“…69,70 Although a recent metaanalysis revealed that patients with AKI typically have lower calcitriol levels compared with healthy controls, another study reported significantly higher plasma calcitriol and P i in nonsurvivors compared with survivors in critically ill patients with AKI. 71,72 In our AKI model, the rise in calcitriol was driven by PTH as the increase in renal Cyp27b1 mRNA expression and the concomitant increase in calcitriol was fully abrogated in Pth 2/2 mice.…”

Bone Dysregulation in Acute Kidney Injury

“…Alterations of vitamin D metabolism contribute to elevation of PTH, inflammation, cardiovascular disease, and mineral bone disease in CKD, but its impact on AKI is less well established [28]. While observational studies have found consistent lower 1,25 (OH) 2 vitamin D and less consistent lower 25 (OH) vitamin D in patients with AKI versus without AKI in acute settings, the relationship between these measurements and relevant clinical outcomes such as AKI progression, need of dialysis or death has not been confirmed [26, 29]. While one should still acknowledge the possibility that certain patients with AKI or CKD could benefit from vitamin D supplementation, identification of more specific clinical sub-phenotypes and mechanisms of action is needed to assist in the design of future clinical trials.…”

Vitamin D and chronic kidney disease: Insights on lipid metabolism of tubular epithelial cell and macrophages in tubulointerstitial fibrosis

“…Patients diagnosed with CKD have a progressive reduction of VitD levels ( LaClair et al, 2005 ; Nigwekar et al, 2012 ) and VitD deficiency is prevalent in 76.1% of stage 5 CKD patients submitted to the hemodialysis ( Del Valle et al, 2007 ; Cuppari and Garcia-Lopes, 2009 ; Zhang et al, 2022 ; Dhillon-Jhattu et al, 2023 ). Studies demonstrated in experimental models and in CKD patients a lower megalin expression in the kidneys ( Toi et al, 2019 ; Wen et al, 2022 ) and the absence of megalin in mice causes the inability of PTECs to capture the 25(OH)D3-VDBP complex, which in turn, are excreted in the urine, leading to a drastic reduction of plasma level of 25(OH)D3 and 1,25D3 ( Nykjaer et al, 1999 ; Negri, 2006 ).…”

“…CKD patients have a compromised VitD production that affects not only the kidney physiology, but also the systemic metabolism. Moreover, there is a diversity of studies that associate VitD deficiency and the development of pathological inflammation and renal fibrosis ( LaClair et al, 2005 ; Del Valle et al, 2007 ; Cuppari and Garcia-Lopes, 2009 ; Nigwekar et al, 2012 ; Wang et al, 2012 ; Zhang et al, 2022 ; Dhillon-Jhattu et al, 2023 ). Factors associated with the internalization of precursors for active VitD synthesis, such as endocytic receptors, are reduced in the injured kidneys, which could explain its low levels in CKD patients ( Toi et al, 2019 ; Wen et al, 2022 ).…”