ABSTRACT
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.
ABSTRACT
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a common complication in patients experiencing end-stage renal disease (ESRD). It includes abnormalities in bone and mineral metabolism and vascular calcification. Hyperphosphatemia is a major risk factor leading to morbidity and mortality in patients with chronic kidney disease. Increased mortality has been observed in patients with ESRD, with serum phosphorus levels of >5.5 mg/dL. Therefore, control of hyperphosphatemia is a major therapeutic goal in the prevention and treatment of CKD-MBD. The treatment of hyperphosphatemia includes decreasing intestinal phosphorus load and increasing renal phosphorus removal. Decreasing the intestinal load of phosphorus plays a major role in the prevention and treatment of CKD-MBD. Among the dietary sources of phosphorus, some of the commonly prescribed medications have also been reported to contain phosphorus. However, drugs are often ignored even though they act as a potential source of phosphorus. Similarly, although proteins are the major source of dietary phosphorus, reducing protein intake can increase mortality in patients with CKD. Recently, the importance of phosphorus/protein ratio in food have been reported to be a sensitive marker for controlling dietary intake of phosphorus. This review summarizes the progress in the research on phosphate content in drugs as an excipient and the various aspects of dietary management of hyperphosphatemia in patients with CKD, with special emphasis on dietary restriction of phosphorus with low dietary phosphate/protein ratio.