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.
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):
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).
Hyperphosphatemia
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).
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 ββthe 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:
Ultrasound of the parathyroid glands
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:
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.