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Hyperphosphatemia
Last reviewed: 23.04.2024
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Hyperphosphatemia is a serum phosphate concentration of more than 4.5 mg / dL (greater than 1.46 mmol / L). The causes include chronic renal failure, hypoparathyroidism, metabolic or respiratory acidosis. The clinical symptoms of hyperphosphataemia may be associated with concomitant hypocalcemia and may include tetanus. Diagnosis is based on the determination of serum phosphate levels. Treatment consists in limiting the consumption of phosphates and the introduction of antacids, binding phosphates, which include calcium carbonate.
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Causes of the hyperphosphataemia
Hyperphosphatemia usually develops as a result of decreased renal excretion of PO2. Progressive renal failure (GFR less than 20 ml / min) reduces excretion to an extent sufficient to increase the level of PO2 plasma. Disturbance of renal excretion of phosphate in the absence of renal failure is also observed in pseudohypoparathyroidism and hypoparathyroidism. Hyperphosphatemia also develops with excessive intake of PO2 by mouth and the excessive use of enemas containing PO2.
Hyperphosphatemia sometimes develops as a result of the massive release of PO2 ions into the extracellular space, which exceeds the excretory capacity of the kidneys. This mechanism most often develops in diabetic ketoacidosis (despite a general decrease in the PO2 content in the body), lesions, non-traumatic rhabdomyolysis, as well as with systemic infections and tumor disintegration syndrome. Hyperphosphatemia also plays a major role in the development of secondary hyperparathyroidism and renal osteodystrophy in patients on dialysis. Hyperphosphatemia may be false in hyperproteinemia (multiple myeloma or Waldenstrom's macroglobulinemia), hyperlipidemia, hemolysis, hyperbilirubinemia.
Symptoms of the hyperphosphataemia
In most patients, hyperphosphatemia is asymptomatic, but in the case of concomitant hypocalcemia , symptoms of the latter, including tetany, may be observed. Calcification of soft tissues is usually observed in patients with chronic renal failure.
Diagnosis of hyperphosphatemia is to determine the level of PO2 more than 4.5 mg / dl (> 1.46 mmol / l). If the etiology of the condition is not obvious (for example, rhabdomyolysis, tumor disintegration, renal failure, abuse of laxatives containing PO2), an additional study is needed to exclude hypoparathyroidism or pseudohypoparathyroidism, which is characterized by resistance of the target organ to PTH. Also, it is necessary to exclude the incorrect determination of the PO2 level by measuring the level of serum protein, lipids and bilirubin.
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Treatment of the hyperphosphataemia
The basis for the treatment of hyperphosphataemia in patients with renal failure is a decrease in PO2 consumption. It is recommended that you avoid foods that contain a large amount of PO2, and you also need to take phosphate binding drugs while eating. In connection with the likelihood of developing osteomalacia associated with the accumulation of aluminum, in patients with terminal stage of kidney disease, the use of carbonate and calcium acetate as antacids is recommended. Recently, the probability of developing vascular calcification due to excessive formation of Ca and PO2 binding products in patients who have a condition such as hyperphosphataemia and those on dialysis and receiving Ca-binding drugs has been revealed. For this reason, dialysis patients are recommended taking PO2 binding resin, sevelamer, at a dose of 800-2400 mg 3 times daily with meals.