Hyperphosphatemia : Causes, Symptoms, Diagnosis & Treatment

Last Updated: 20/07/2022

Hyperphosphatemia is a pathological condition characterized by an increase in the concentration of phosphorus in the blood of more than 1.46 mmol / l. The causes may be kidney disease, pathology of the parathyroid glands, severe general somatic diseases. The brightness of the clinical picture varies from the complete absence of symptoms to pronounced signs of hypocalcemia. The diagnosis is made on the basis of the determination of the level of phosphorus in the blood serum. For treatment, restriction of the intake of phosphorus with food, forcing diuresis, and the introduction of drugs that bind phosphorus are used.

Phosphorus (P) is one of the main mineral components of bone tissue (about 85% of all P is found in bones). It is part of ATP, the main intracellular energy carrier. Phosphorus is an important element of the phosphate buffer, one of the regulators of the acid-base balance of the blood. The main proportion of cases of hyperphosphatemia occurs in patients suffering from chronic renal failure. Precise data on the prevalence of this disorder are not available.

Causes of hyperphosphatemia

There are many etiological factors that can cause hyperphosphatemia. Often, this pathological condition develops due to the simultaneous influence of several factors acting on different stages of phosphorus metabolism. The causes of hyperphosphatemia are listed below, grouped by mechanism of action (common to rare):

  • Violation of the excretion of phosphorus. Leading cause of hyperphosphatemia. Excretion from the body P is carried out mainly by the kidneys. This process is regulated by parathyroid hormone (PTH). Therefore, in the vast majority of cases, hyperphosphatemia occurs in acute and chronic renal failure, hypoparathyroidism, pseudohypoparathyroidism (tissue resistance to PTH).
  • Release of P from cells. The main amount of phosphorus is intracellular. Any disease or disorder accompanied by massive damage to cells and tissues can lead to an increase in the level of phosphorus in the blood, for example, hemolytic anemia, tumor lysis syndrome during chemotherapy (especially with leukemia, lymphoma), rhabdomyolysis with prolonged compression syndrome.
  • transcellular shift. The transition of phosphorus from cells to the extracellular space occurs with gross shifts in the acid-base balance towards acidosis (metabolic, ketoacidosis, lactic acidosis).
  • Excessive exogenous intake of phosphates. The introduction of large amounts of phosphate-containing solutions, parenteral nutrition with phospholipids, the use of phosphate-containing enemas can cause hyperphosphatemia.
  • Increased absorption and reabsorption. Some hormones (thyroxine, growth hormone) and vitamin D increase the absorption of phosphates in the small intestine. Therefore, pathologies such as thyrotoxicosis, acromegaly, vitamin D overdose, as well as granulomatosis with increased vitamin D synthesis (tuberculosis, sarcoidosis) are sometimes accompanied by hyperphosphatemia.

More rare causes include chronic adrenal insufficiency, cortical hyperostosis, familial (hereditary) form of hyperphosphatemia. An increase in the concentration of P occurs in infants who are fed cow's milk. The main provoking factor in the increase in the level of P in the blood in people suffering from chronic renal failure is the use of foods high in phosphorus (meat, fish, seafood, dairy products).


The main pathogenic effect of hyperphosphatemia is that this disorder causes significant changes in calcium metabolism. P inhibits the absorption of calcium in the intestine and the synthesis of vitamin D. Phosphates also bind calcium ions in the blood and form insoluble complexes with them. As a result, these salts are deposited in soft tissues (calcifications), including vascular endothelium and brain cells.

High phosphorus and hypocalcemia stimulate reactive hyperplasia of the parathyroid glands and increased production of parathyroid hormone. Secondary hyperparathyroidism develops, which is the leading pathogenetic link of mineral-bone disorders and patients suffering from CRF (renal osteodystrophy).




There is no single classification, as well as clear criteria for the division of hyperphosphatemia, in clinical practice. According to the rate of occurrence, acute and chronic hyperphosphatemia can be distinguished. False hyperphosphatemia is possible, which is observed with hyperthrombocytosis, hyperbilirubinemia, monoclonal gammopathy (multiple myeloma or macroglobulinemia).

Symptoms of hyperphosphatemia

In some cases, a completely asymptomatic course of this condition is possible. Clinical manifestations are mainly associated with hypocalcemia. Due to increased neuromuscular conduction, muscle cramps and spasms occur. Some patients complain of paresthesias (tingling sensation, crawling) of the extremities.

Due to the weakening of vascular tone and cardiac output, blood pressure decreases - the patient may experience dizziness, a feeling of increased and rapid heartbeat. Clinical signs of hypocalcemia are much more pronounced if the cause of hyperphosphatemia is chronic renal failure or hypoparathyroidism. Calcification of soft tissues causes skin itching, pain in the joints, aggravated by movement. Hard subcutaneous nodules form in the projection area of ​​the joints.


Hyperphosphatemia can cause a large number of adverse effects. Especially often there are bone disorders. Developing secondary hyperparathyroidism stimulates the release of calcium ions from bone depots, which leads to osteoporosis and osteomalacia. The deposition of phosphorus-calcium salts on the walls of blood vessels accelerates the progression of atherosclerosis, the main cause of cardiovascular diseases (myocardial infarction, stroke).

The deposition of phosphates in the renal tubules contributes to the appearance of urolithiasis. With a prolonged course of hyperphosphatemia, calcification of the neurons of the basal ganglia occurs (parkinsonism, dystonia). Metastatic calcification of the periarticular tissues can significantly impede joint movement. Sometimes hypocalcemia provokes life-threatening arrhythmias, coronary spasm. Some patients develop cataracts.


Since end-stage renal failure is the leading cause of hyperphosphatemia, patients with this electrolyte disorder are most often under the supervision of nephrologists. During a general examination of the patient, attention is paid to traces of scratching on the skin, the presence of subcutaneous nodes that are hard on palpation, the identification of signs of latent tetany - the symptoms of Trousseau and Khvostek.

Help in recognizing this condition is provided by anamnestic information - diagnosed CRF, operations on the thyroid or parathyroid glands. The level of phosphorus is examined in the serum by biochemical analysis. Differential diagnosis is carried out in order to establish the etiological factor. For this, as well as to confirm the diagnosis, the following examination is prescribed:

  • Laboratory Research . In a biochemical blood test, an increase in the concentration of urea, creatinine is often noted, and almost always a decrease in the level of ionized calcium, less often a shift in pH to the acid side. In kidney disease, the glomerular filtration rate is calculated.
  • Testing for primary hypoparathyroidism. In patients, a decrease in the content of parathyroid hormone is detected in the blood, and an increased excretion of calcium in the urine. Ultrasound reveals atrophy or absence of the parathyroid glands. Testing for genetic forms of hypoparathyroidism may be required.
  • Densitometry. Bone densitometry (DEXA) shows a decrease in bone mineral density (T-score from -1 and below).
  • Echography. Ultrasound of the kidneys in some patients revealed stones in the renal pelvis. On ultrasound of the periarticular tissues, calcifications are noted.
  • CT scan. On CT of the brain, it is sometimes possible to visualize calcifications in the basal ganglia.
  • ECG. With severe hypocalcemia, the electrocardiogram reveals a prolongation of the QT interval, tachycardia of the "pirouette" type.

Ultrasound of the parathyroid glands


Treatment of hyperphosphatemia

Depending on the severity of the patient's condition, treatment can be carried out on an outpatient basis or in a hospital. Parenteral administration of solutions containing phosphates, if any, should be discontinued. The main condition for the normalization of the P level in the blood is the treatment of the underlying disease - the treatment of renal failure, the correction of acidosis, primary hypoparathyroidism, etc. The following measures are also prescribed:

  • Low phosphate diet. All patients must necessarily limit the intake of phosphates with food to 0.6-0.9 grams per day.
  • Phosphate binders. Phosphate-binding agents in the intestinal lumen are very effective, thereby limiting their absorption. These drugs include sevelamer, lanthanum carbonate, aluminum hydroxide. The latter should be used with caution in people with ESRD, as they are at high risk of aluminum toxicity in the form of osteomalacia and dementia.
  • Calcium and vitamin D preparations. Calcium acetate or calcium carbonate, active metabolites (alfacalcidol) and native forms of vitamin D (cholecalciferol) are used to correct hypocalcemia. Also, calcium preparations have a phosphate-binding effect.
  • Diuretics and crystalloids. With preserved kidney function, to accelerate the elimination of P from the body, intravenous isotonic solutions and diuretics - furosemide, mannitol are prescribed.
  • Hemodialysis. Hemodialysis in combination with the above measures is considered a mandatory procedure for removing excess phosphate from the systemic circulation in patients with chronic renal failure.

Forecast and prevention

With hyperphosphatemia, the prognosis is directly determined by the cause that caused it (extremely unfavorable for CRF and favorable for hypoparathyroidism). By itself, hyperphosphatemia can very rarely be the direct cause of death, and even in these cases, deaths are associated with severe hypocalcemia (cardiac arrhythmias, coronary vasospasm) that occurs against a background of elevated phosphate levels.

Prevention of hyperphosphatemia is the timely diagnosis and treatment of those diseases and conditions that can lead to it. To prevent this disorder, it is necessary to regularly monitor the concentration of phosphates in the blood plasma in risk groups - patients on hemodialysis, receiving chemotherapy, parenteral nutrition.

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