OVERVIEW
Hyperphosphatemia is a pathological condition in which the level of blood phosphate is increased above the normal level. It is a disorder of phosphorus metabolism, in which there is an increase in phosphate intake, a decrease in phosphate excretion, or a disturbance in redistribution. It is a disorder of phosphate metabolism with increased phosphate intake and decreased phosphate excretion or redistribution. Early stages of the disease usually have no specific clinical symptoms and are rare.
Causes
1. Acute and chronic renal insufficiency is the most common cause of hyperphosphatemia. When the glomerular filtration rate is 0.3-0.5 ml/s or less, renal excretion of phosphorus decreases, blood phosphorus rises, secondary parathyroid hormone secretion increases, and bone salt release increases.
2. Increased release of phosphorus from bone Certain secondary hyperparathyroidism, due to enhanced osteolytic action of parathyroid hormone, increased release of phosphorus from bone, which can lead to elevated blood phosphorus; can also be seen in hypoparathyroidism (primary, secondary and pseudoparathyroidism), urinary excretion of phosphorus decreases leading to increased blood phosphorus.
3. Phosphorus into the extracellular fluid increased application of phosphorus-containing laxatives or enemas, vitamin D poisoning, phosphorus into the extracellular fluid increased; in addition, phosphorus from the intracellular to the extracellular, can also lead to an increase in extracellular fluid phosphorus, seen in acute acidosis, bone destruction, hyperthermia, malignant tumors (chemotherapy) and so on.
Questions you may be concerned about
What are the causes of hyperphosphatemia
The causes of hyperphosphatemia include under-excretion of phosphorus by the kidney, over-giving of phosphorus by exogenous sources, over-production of endogenous phosphorus, and pseudohyperphosphatemia.
1. Low renal phosphorus excretion: the most common cause of renal damage is the reduction of glomerular filtration rate, resulting in high blood phosphorus.
In addition to the reduction of glomerular filtration rate, the increase of proximal tubular phosphorus reabsorption will also lead to a decrease in phosphorus excretion, which can be seen in hypoparathyroidism, acromegaly, the application of bicarbonate phosphate compounds, and familial tuberculous calcium sedimentation disease.
2. Exogenous phosphorus oversupply: in some children given high-calcium milk, the application of phosphorus-containing laxatives or enemas (eg, sodium phosphate), vitamin D toxicity and transfusion of stored blood.
3. Excessive endogenous phosphorus production: seen in a large number of hemolysis, lymphoma or leukemia chemotherapy, rhabdomyolysis, lactic acidosis and diabetic ketoacidosis.
4. Pseudohyperphosphatemia: mainly seen in some patients with multiple myeloma. These patients often have a monoclonal protein in the blood can be tightly bound to phosphorus, and in the automatic biochemistry interferes with phosphorus detection, the application of sulfuric acid treatment or serum ultrafiltration can be exempted from this interference. In addition, hemolysis of the blood specimen may cause false hyperphosphatemia.
If hyperphosphatemia occurs, it is important to go to the hospital in time to identify the cause of the disease and follow the doctor’s instructions to standardize the treatment.
Symptoms
Hyperphosphatemia has no specific clinical symptoms. If hyperphosphatemia persists for too long, it can affect the stability of the internal environment of calcium; the combination of calcium and phosphorus can lead to ectopic calcification, and can inhibit intestinal calcium absorption, so that the blood calcium is lowered, which can be secondary to hypocalcemia, and a series of low-calcium symptoms, such as hand and foot twitching, and progressive impairment of kidney function caused by calcification of kidneys, and so on.
Examination
1. Blood electrolyte test: Increased serum phosphorus may be accompanied by decreased blood calcium or decreased serum pH value.
2. Renal function tests
(1) If renal function is normal, measure urinary phosphate excretion.
(2) If renal function is reduced, hyperphosphatemia due to renal failure should be considered.
3. Urinary phosphate Under normal renal function, increased urinary phosphate excretion should be considered as increased phosphate intake, tumor destruction, or hyperphosphatemia after tumor treatment; decreased urinary phosphate excretion should be considered as hypoparathyroidism.
4. Imaging examination Skeletal X-ray examination, may have osteoporosis manifestation.
Diagnosis
Hyperphosphatemia can be diagnosed according to history, clinical manifestations and laboratory tests.
1. Medical history: history of hyperphosphatemia, such as renal failure, chemotherapy, intravenous or oral phosphorus supplementation.
2. Clinical manifestations The clinical manifestations of hyperphosphatemia are metastatic calcification, hypocalcemia, and secondary hyperparathyroidism.
3. Laboratory tests Serum phosphorus concentration >1.61 mmol/L in adults and >1.90 mmol/L in children.
Treatment
1. General treatment If renal function is normal, saline should be given intravenously to expand extracellular volume and increase phosphate excretion through urine to reduce blood phosphate.
2.Drug treatment
(1) Calcium-phosphorus binding agents such as calcium carbonate, calcium acetate. The main adverse reaction is hypercalcemia, calcium acetate is better than calcium carbonate.
(2) Aluminum-containing phosphorus binding agent Aluminum-containing phosphorus binding agent is now eliminated, only for other methods can not control hyperphosphatemia, the course of treatment should be short. Such as aluminum hydroxide, the treatment course of 4 weeks, up to 12 weeks, aluminum hydroxide treatment can often cause constipation, and sometimes can also increase plasma aluminum levels, resulting in aluminum poisoning.
(3) Non-aluminum, non-calcium and phosphorus binding agents, such as sevelamer, lanthanum carbonate, niacin, colestipol, it should be noted that sevelamer, whether capsules or tablets, should be swallowed whole, not chewed.
3. Dialysis treatment For patients with chronic renal failure, plasma dialysis or peritoneal dialysis can be used to control plasma phosphate levels. The time and frequency of hemodialysis should be increased. Chronic hyperphosphatemia can also be effectively controlled by prolonging the time of hemodialysis (6-7 times/week, 8-10 hours of hemodialysis during sleep at night); the traditional hemodialysis of 3 times/week for 4 hours each time can not effectively remove blood phosphorus.