Harm and Treatment of Hyperphosphatemia in Dialysis Patients

Hyperphosphatemia in Dialysis PatientsDue to the decrease of glomerular filtration rate (GFR), phosphorus excretion disorder occurs when the endogenous creatinine clearance rate is less than 60 ml/min.1.73 m2 in patients with chronic renal failure, and then blood phosphorus begins to rise. After Kidney Failure patients begin hemodialysis, the occurrence of hyperphosphatemia is more obvious due to the decrease of urine volume and the increase of protein diet intake.

Epidemiological investigation showed that the prevalence of hyperphosphorus in hemodialysis patients was 57.4%, and that in peritoneal dialysis patients was 47.4%, while the rate of reaching the standard of blood phosphorus was only 38.5%. For dialysis patients, it is recommended that the blood phosphorus level be maintained at 1.13-1.78 mmol/L. High blood phosphorus can cause a series of uremic complications such as bone disease, heart valve and vascular calcification, skin itching and so on. Large-scale meta-analysis showed that elevated serum phosphorus (greater than 1.78 mmol/L) in uremic patients led to an increased risk of death. For every elevated serum phosphorus of 1 mg/dL, all-cause mortality increased by 18% and cardiovascular mortality increased by 10%. With the popularization of dialysis therapy, it is urgent to prevent and treat hyperphosphorus and avoid complications.

There are three therapeutic strategies for hyperphosphorus in uremic patients.

First, to control phosphorus intake (limit to 800-1000 mg/d). Because organic phosphorus mainly binds to protein and distributes in cells, the content of blood phosphorus in protein-rich foods is also high. After dialysis, uremia patients are often suggested to increase protein intake, so it is easy to lead to high phosphorus. Besides, the absorption rate of protein phosphorus in plant is lower than that of animal. It was found that excessive restriction of phosphorus intake would lead to increased mortality due to malnutrition, and the intake of protein and phosphorus must be balanced. Therefore, it is appropriate to use the ratio of phosphorus (mg)/protein (g) to measure the phosphorus load in diet. Foods with low phosphorus content and rich protein content, such as egg protein, should be consumed as far as possible, while foods with high phosphorus content and low protein content should be consumed as little as possible. In addition, phosphorus is one of the main components of food additives, uremic patients should limit the intake of phosphorus-containing additives.

Second, increasing dialysis times or prolonging dialysis time can help remove phosphorus. Because phosphorus mainly distributes in cells and tissues, the transport rate from cells to extracellular is very slow. It often takes a long time of dialysis to achieve the goal of phosphorus reduction.

Third, the use of phosphorus binders reduces blood phosphorus levels mainly by reducing phosphorus absorption in the gastrointestinal tract. At present, the main phosphorus binders in clinical application are calcium-containing phosphorus binders, aluminum-containing phosphorus binders and non-calcium non-aluminium phosphorus binders.

If dialysis patients can not control the level of blood phosphorus by dietary phosphorus restriction and adequate dialysis, it is recommended to use calcium-containing phosphorus binder when the level of blood calcium is in the normal range or reduced.

If hypercalcemia persists or recurs, it is recommended to use non-calcium non-aluminum phosphorus binder.

Calcium carbonate and calcium acetate are commonly used in clinic.

In order to prevent potential hypercalcemia, it is suggested that the daily intake of elemental calcium from calcium-containing phosphate binders should not exceed 1500 mg, and the total daily intake of elemental calcium should be less than 2000 mg.

Because of the risk of aluminum poisoning, the application of aluminium-containing phosphorus binder is less, and long-term use should be avoided.

Non-calcium and non-aluminium phosphorus binders mainly include Sevelamer and lanthanum carbonate. Because they have no effect on blood calcium and parathyroid hormones, and can even reduce or delay vascular calcification, it has been widely recognized that non-calcium and non-aluminium phosphorus binders are the best choice for uremic patients with persistent high phosphorus version of vascular calcification.

It is suggested that phosphorus binders should be taken with meals, chewing to achieve the best effect of phosphorus reduction, and the dosage of phosphorus binders should be adjusted according to the amount of food containing phosphorus.

Now you know the harm and treatment of Hyperphosphatemia in dialysis patients. If you would like to know more detailed information on dialysis, please leave a message below or contact online doctor.

Declaration

***Please seek professional medical advise for the diagnosis or treatment of any ailment, disease or medical condition. This article is not intended to be a substitute for the advice of a licensed medical professional.***

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