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Phosphate Toxicity in CKD: The Killer among Us
#MMPMID26912542
Ritter CS
; Slatopolsky E
Clin J Am Soc Nephrol
2016[Jun]; 11
(6
): 1088-1100
PMID26912542
show ga
Maintenance of a normal serum phosphate level depends on absorption in the gut,
reabsorption and excretion by the kidney, and the flux between the extracellular
and skeletal pools. Phosphate homeostasis is a coordinated, complex system of
crosstalk between the bone, intestine, kidney, and parathyroid gland. Dysfunction
of this system has serious clinical consequences in healthy individuals and those
with conditions, such as CKD, in which hyperphosphatemia is associated with
increased risks of cardiovascular morbidity and mortality. The last half-century
of renal research has helped define the contribution of the parathyroid hormone,
calcitriol, fibroblast growth factor 23, and Klotho in the regulation of
phosphate. However, despite new discoveries and insights gained during this time,
what remains unchanged is the recognition that phosphate retention is the
initiating factor for the development of many of the complications observed in
CKD, namely secondary hyperparathyroidism and bone and cardiovascular diseases.
Controlling phosphate load remains the primary goal in the treatment of CKD. This
review discusses the clinical effects of dysregulated phosphate metabolism,
particularly in CKD, and its association with cardiovascular disease. The
importance of early control of phosphate load in the treatment of CKD is
emphasized, and the latest research in the treatment of phosphate retention is
discussed.
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