Abstract
Chronic kidney disease (CKD) affects approximately 10% of adults worldwide. Dysregulation of phosphorus homeostasis which occurs in CKD leads to development of CKD-Mineral Bone Disorder (CKD-MBD) and contributes to increased morbidity and mortality in these patients. Phosphorus is regulated by multiple hormones (parathyroid hormone (PTH), 1,25-dihyxdroxyvitamin D (1,25D), and fibroblast growth factor 23 (FGF23)) and tissues (kidney, intestine, parathyroid glands, and bone) to maintain homeostasis. In health, the kidneys are the major site of regulation for phosphorus homeostasis. However, as kidney function declines, the ability of the kidneys to adequately excrete phosphorus is reduced. The hormonal changes that occur with CKD would suggest that the intestine should compensate for impaired renal phosphorus excretion by reducing fractional intestinal phosphorus absorption. However, limited studies in CKD animal models and patients with CKD suggest that there may be a break in this homeostatic response where the intestine fails to compensate. As many existing therapies for phosphate management in CKD are aimed at reducing absolute intestinal phosphorus absorption, better understanding of the factors that influence fractional and absolute absorption, the mechanism by which intestinal phosphate absorption occurs, and how CKD modifies these is a much-needed area of study.
Highlights
The Importance of Managing Phosphorus Homeostasis in Chronic kidney disease (CKD)1.1
Abnormalities in phosphorus homeostasis have been shown to occur early in CKD progression due to disease-mediated alterations in the hormonal regulators of phosphorus metabolism, well before clinical hyperphosphatemia is observed [2]. This is a central component of CKD-mineral bone disorder (CKD-MBD), which is a condition characterized by (1) abnormalities in laboratory values related to calcium and phosphorus metabolism, (2) increased vascular calcifications, and (3) bone disease, all of which interact and contribute to increased risk for cardiovascular events, bone fragility fractures, and death [3]
Foundation Kidney Disease Outcomes Qualities Initiative’s (KDOQI) clinical guidelines for CKD state that dietary phosphorus should be restricted to 800 to 1000 mg/day for CKD patients based on stage of disease and presence of elevated serum phosphate or parathyroid hormone (PTH) [1]
Summary
Chronic kidney disease (CKD) affects approximately 26 million American adults in the United. Foundation Kidney Disease Outcomes Qualities Initiative’s (KDOQI) clinical guidelines for CKD state that dietary phosphorus should be restricted to 800 to 1000 mg/day for CKD patients based on stage of disease and presence of elevated serum phosphate or parathyroid hormone (PTH) [1]. While this intake level still exceeds the 700 mg/day recommended daily allowance for most adults [8], it is still restrictive when compared to the average American phosphorus intake of ~1500 mg/day [9,10]. This review will provide an overview of phosphorus absorption, its role in phosphorus homeostasis, and what is currently known regarding phosphorus absorption in the context of CKD
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