What Is Hyperphosphatemia?

Phosphate levels increase and exceed normal levels. Also known as hyperphosphatemia. A class of phosphorus metabolism disorders. There are usually no clinical symptoms.

Hyperphosphatemia

Introduction to Hyperphosphatemia

Phosphate levels increase and exceed normal levels. Also known as hyperphosphatemia. A class of phosphorus metabolism disorders. There are usually no clinical symptoms.

Causes of hyperphosphatemia

Disorders related to increased phosphate intake, decreased excretion, or redistribution. Increase intake. Such as oral or intravenous excess phosphate, and excessive vitamin D, increase intestinal phosphate absorption. Milk, soy-based milk substitutes, cereals contain higher levels of phosphorus. Reduced discharge. Parathyroid hormone reduces the reabsorption of phosphate by the kidneys. When parathyroid function is reduced, parathyroid hormone secretion is reduced, phosphate reabsorption is increased in the kidney, phosphate excretion is reduced, and blood phosphate is increased. In pseudohypoparathyroidism, the kidneys do not respond to the effects of parathyroid hormone. In acromegaly, excessive growth hormone secretion can increase reabsorption of phosphate by the kidneys. In patients with renal failure, the glomerular filtration function is reduced, and the excessive filtration of phosphate in the glomerulus is reduced. These can cause hyperphosphatemia. Disorders of redistribution of phosphate. In respiratory or metabolic acidosis, there is the release of cellular phosphate, which moves from the inside to the outside of the cell, causing the blood phosphate to rise. When tissue is destroyed, cell integrity is lost, and phosphate can be released from the inside to the outside of the cell, causing hyperphosphatemia. This can happen to patients with leukemia and other tumors after chemotherapy or radiation therapy. When a large amount of hemolysis occurs, the phosphate in the red blood cells is released from the cells, and hyperphosphatemia can also occur.

Clinical manifestations of hyperphosphatemia

Hyperphosphatemia has no specific clinical symptoms. If hyperphosphatemia persists for too long, it can affect the stability of calcium's internal environment; the combination of calcium and phosphorus can lead to ectopic calcification, and can inhibit intestinal calcium absorption, reduce blood calcium, and manifest hypocalcemia.

Hyperphosphatemia diagnosis

Before a clear diagnosis can be made, the hyperphosphatemia due to hemolysis of the blood sample must first be ruled out. Then follow the procedure below for identification. First check renal function. If renal function is normal, urinary phosphate excretion is measured. Increased urinary phosphate excretion. Consider increased phosphate intake, tumor destruction, or hyperphosphatemia after tumor treatment. Urinary phosphate excretion should be reduced, and hypoparathyroidism should be considered. If renal function declines, hyperphosphatemia due to renal failure is considered.

Hyperphosphatemia treatment

For hyperphosphatemia, if the kidney function is normal, the extracellular volume can be enlarged by supplying normal saline to increase the excretion of phosphate through the urine to reduce blood phosphate. Phosphate binding agents (such as aluminum hydroxide) can also be taken to reduce the absorption of intestinal phosphate. However, aluminum hydroxide treatment can often cause constipation, and there are fashions that can increase plasma aluminum levels, leading to aluminum poisoning. For patients with chronic renal failure, hemodialysis or peritoneal dialysis can be used to control plasma phosphate levels.

Hyperphosphatemia phosphate binder

Calcium-phosphorus binders: calcium carbonate, calcium acetate;
Aluminum-phosphorus binder: aluminum hydroxide;
Non-aluminum non-calcium-phosphorus binders: Sevelamer, lanthanum carbonate, niacin, and colestiran.

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