Dietary Phosphorus as a Marker of Mineral Metabolism and Progression of Diabetic Kidney Disease

Abstract

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease.

Joint associations among non-essential heavy metal mixtures and nutritional factors on glucose metabolism indexes in US adults: evidence from the NHANES 2011–2016

“…Phosphorus, an essential nutrient, plays a crucial role in regulating cell and tissue function and maintaining body homeostasis. 59 Our findings identified that a high intake of phosphorus (1418.60 mg per day, see ESI Table S4 †) augmented the relationship between Cd and HbA1c, W and HbA1c, Tl and HOMA-IR. For phosphorus-Cd-HbA1c, a U-shaped relationship between phosphorus consumption and diabetes was discovered in the overall Chinese adult population, 60 and animal studies found that high phosphorus intake may lead to increased oxidative stress, 61 which is also a mechanism of both the impacts of Cd exposure on human health and T2DM, 62,63 indicating that oxidative stress may be the common underlying mechanism of phosphorus, Cd, and diabetes.…”

Phosphate Dysregulation and Metabolic Syndrome

“…The absence of the amount of phosphate in the nutritional ingredient lists also contributes to dietary phosphate overload, even among health-conscious individuals. Hyperphosphatemia has been consistently detected in the advanced stage of both human and experimental models of diabetes mellitus [ 76 , 77 ].…”