Disorders of Phosphate Metabolism: Hypophosphatemia and Hyperphosphatemia (original) (raw)
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Phosphate disorders and the clinical management of hypophosphatemia and hyperphosphatemia
Endocrinología, Diabetes Y Nutrición (english Edition), 2020
Serum phosphorus levels range from 2.5 and 4.5 mg/dl (0.81-1.45 mmol/l) in adults, with higher levels in childhood, adolescence, and pregnancy. Intracellular phosphate is involved in intermediary metabolism and other essential cell functions, while extracellular phosphate is essential for bone matrix mineralization. Plasma phosphorus levels are maintained within a narrow range by regulation of intestinal absorption, redistribution, and renal tubular absorption of the mineral. Hypophosphatemia and hyperphosphatemia are common clinical situations, although changes are most often mild and oligosymptomatic. However, acute and severe conditions that require specific treatment may occur. In this document, members of the Mineral and Bone Metabolism Working Group of the Spanish Society of Endocrinology and Nutrition review phosphate disorders and provide algorithms for adequate clinical management of hypophosphatemia and hyperphosphatemia.
Latest findings in phosphate homeostasis
Kidney International, 2009
The kidney is a key player in phosphate balance. Inappropriate renal phosphate transport may alter serum phosphate concentration and bone mineralization, and increase the risk of renal lithiasis or soft tissue calcifications. The recent identification of fibroblast growth factor 23 (FGF23) as a hormone regulating phosphate and calcitriol metabolism and of klotho has changed the understanding of phosphate homeostasis; and a bone-kidney axis has emerged. In this review, we present recent findings regarding the consequences of mutations affecting several human genes encoding renal phosphate transporters or proteins regulating phosphate transport activity. We also describe the role played by the FGF23-klotho axis in phosphate homeostasis and its involvement in the pathophysiology of phosphate disturbances in chronic kidney disease.
The Journal of physiology, 2014
The regulation of serum phosphate, an acknowledged risk factor for chronic kidney disease and cardiovascular mortality, is poorly understood. The discovery of fibroblast growth factor 23 (FGF23) as a key regulator of renal phosphate handling and activation of vitamin D has revolutionized our comprehension of phosphate homeostasis. Through as yet undetermined mechanisms, circulating and dietary phosphate appear to have a direct effect on FGF23 release by bone cells that, in turn, causes renal phosphate excretion and decreases intestinal phosphate absorption through a decrease in vitamin D production. Thus, the two major phosphaturic hormones, PTH and FGF23, have opposing effects on vitamin D production, placing vitamin D at the nexus of phosphate homeostasis. While our understanding of phosphate homeostasis has advanced, the factors determining regulation of serum phosphate level remain enigmatic. Diet, time of day, season, gender, age and genetics have all been identified as signifi...
Phosphate wasting disorders in adults
Osteoporosis International, 2018
A cause of hypophosphatemia is phosphate wasting disorders. Knowledge concerning mechanisms involved in phosphate wasting disorders has greatly increased in the last decade by the identification of phosphatonins, among them FGF-23. FGF-23 is a primarily bone derived factor decreasing renal tubular reabsorption of phosphate and the synthesis of calcitriol. Currently, pharmacological treatment of these disorders offers limited efficacy and is potentially associated to gastrointestinal, renal, and parathyroid complications; therefore, efforts have been directed toward newer pharmacological strategies that target the FGF-23 pathway. This review focuses on phosphate metabolism, its main regulators, and phosphate wasting disorders in adults, highlighting the main issues related to diagnosis and current and new potential treatments.
Hyperphosphatemia: Consequences and Management Strategies
The Journal for Nurse Practitioners, 2012
Phosphorus is an essential element of the body and has many important functions. Hyperphosphatemia, or elevated levels of phosphorus, is defined based on patients' clinical status and often occurs in patients with acute or chronic kidney diseases. Prolonged periods of hyperphosphatemia are associated with such consequences as vascular calcification, organ failure, and mortality. Management includes correcting the underlying cause, hydrating patients to increase phosphorus excretion, and administering oral phosphate binders. Nurse practitioners and pharmacists should work together to identify and avoid exogenous sources of phosphorus, optimize patients' pharmacological therapy, and monitor patients' electrolytes.