Hyperphosphatemia

Overview
Hyperphosphatemia is an electrolyte disturbance in which there is an abnormally elevated level of phosphate in the blood. Often, calcium levels are lowered (hypocalcemia) due to precipitation of phosphate with the calcium in tissues.

Differential diagnosis of causes
It can be caused by hypoparathyroidism due to the lack of PTH effect of inhibiting renal reabsorption of phosophate.

Independent of parathyroid hormone (PTH) and serum 1,25-dihydroxyvitamin D level, fibroblast growth factor 23 (FGF23) regulates the sodium/phosphate cotransporter (NPT2a) by controlling renal expressions of key enzymes of vitamin D metabolism. Both NPT2a and NPT2c are regulated in a similar fashion by parathyroid hormone (PTH), FGF23, and dietary phosphate.

There are two rare autosomal recessive metabolic disorders characterized by hyperphosphatemia:

hyperphosphatemic familial tumoral calcinosis (HFTC)

and

hyperphosphatemia-hyperostosis syndrome (HHS).

The principal clinical features of HFTC are represented by ectopic periarticular calcifications associated with hyperphosphatemia. HFTC has been shown to result from mutations in two genes: GALNT3 and FGF23. The secretion of FGF23 requires O-glycosylation, which is selectively directed by GALNT3, to block processing of FGF23.

Hyperphosphatemia-hyperostosis syndrome (HHS) is also characterized by radiological evidence of cortical hyperostosis. HHS is caused by mutations in GALNT3. HHS and HFTC may be different manifestations of the same disorder.

Hyperphosphatemia is also commonly seen in chronic renal failure.

This can also be caused by taking oral sodium phosphate solutions prescribed for bowel preparation for colonoscopy in children.

Hyperphosphatemia can be induced by using hyperphosphate.

Treatment
High phosphate levels can be avoided with phosphate binders and dietary restriction of phosphate.

Signs and symptoms
Signs and symptoms include ectopic calcification, secondary hyperparathyroidism, and renal osteodystrophy. α-Klotho has been implicated in the renal and parathyroid response to hyperphosphatemia. In patients with end-stage renal disease (ESRD) the expression of osteopontin in vascular smooth muscle cells (VSMCs) is associated with hyperphosphatemia or azotemia.

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