Annals of translational medicine · 2023
Regulatory effects of nutritional and metabolic disorders on vascular calcification in chronic kidney disease: a narrative review.
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Xiong Yuqin, Yu Yang, Su Baihai
Аннотация
BACKGROUND AND OBJECTIVE: Vascular calcification (VC) is common in chronic kidney disease (CKD) patients and is associated with poor cardiovascular outcomes. This study aims to review nutritive pro-calcifying factors of CKD.
METHODS: Electronic databases (PubMed, Embase, and the Cochrane Central Register of Controlled Trials) were searched from 2001 as at July 26, 2022, to select and summarize the basic and clinical studies reporting the effects of malnutrition or metabolic disorders on VC in CKD and the evolving treatments for these nutrient metabolic disorders.
KEY CONTENT AND FINDINGS: Hyperphosphatemia, calcium load, hypomagnesemia, iron deficiency, lipoprotein(a) abnormalities, protein malnutrition, and vitamin K deficiency secondary to CKD were closely associated with the occurrence and development of VC. Elevated phosphate and calcium levels were essential contributors to VC, yet current phosphate binders with good phosphate-lowering effects had not been shown to delay VC progression in CKD, and it remained challenging on how to identify and prevent calcium overload. Magnesium supplementation was the most promising treatment for mitigating VC, as supported by in vitro and in vivo studies and clinical trials. Correction of iron and vitamin K deficiency might contribute to VC attenuation, yet there was a lack of clinical evidence on CKD patients.
CONCLUSIONS: This review highlighted the effects of nutrient metabolism disorders on CKD-VC, and additional studies are needed to further address optimal nutrition strategies for mitigating VC in CKD.
METHODS: Electronic databases (PubMed, Embase, and the Cochrane Central Register of Controlled Trials) were searched from 2001 as at July 26, 2022, to select and summarize the basic and clinical studies reporting the effects of malnutrition or metabolic disorders on VC in CKD and the evolving treatments for these nutrient metabolic disorders.
KEY CONTENT AND FINDINGS: Hyperphosphatemia, calcium load, hypomagnesemia, iron deficiency, lipoprotein(a) abnormalities, protein malnutrition, and vitamin K deficiency secondary to CKD were closely associated with the occurrence and development of VC. Elevated phosphate and calcium levels were essential contributors to VC, yet current phosphate binders with good phosphate-lowering effects had not been shown to delay VC progression in CKD, and it remained challenging on how to identify and prevent calcium overload. Magnesium supplementation was the most promising treatment for mitigating VC, as supported by in vitro and in vivo studies and clinical trials. Correction of iron and vitamin K deficiency might contribute to VC attenuation, yet there was a lack of clinical evidence on CKD patients.
CONCLUSIONS: This review highlighted the effects of nutrient metabolism disorders on CKD-VC, and additional studies are needed to further address optimal nutrition strategies for mitigating VC in CKD.