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How to reduce the blood phosphorus of dialysis patients?
Most of the excess phosphorus is hidden in cells, and dialysis treatment can only effectively remove inorganic phosphorus from unbound proteins outside cells. At the same time, due to the slow transport speed of phosphorus from the inside to the outside of the cell, it is said that the efficiency of conventional dialysis for removing "a lot" of inorganic phosphorus hidden in the cell is extremely low, which eventually leads to incomplete phosphorus removal in conventional dialysis.
Phosphorus excretion in dialysis mainly depends on dialysis time rather than dialysis method.
Even hemofiltration or hemodiafiltration, even hemoperfusion, has no obvious advantage over ordinary hemodialysis in removing blood phosphorus.
Long-term dialysis is more helpful to reduce phosphorus.
The accumulated phosphorus is removed by the kidney in time when it is transferred from the cell, but the conventional intermittent dialysis has no obvious advantage no matter how advanced the filter is. This also explains from another angle why it is easier to control blood phosphorus in patients with certain residual renal function.
Therefore, it is unrealistic to solve the problem of hyperphosphatemia in dialysis patients by improving dialyzers or filters within the regular time of 12 hours per week. There has been a lot of evidence that long-term night dialysis can effectively control the blood phosphorus of dialysis patients and reduce or even stop using phosphorus binders.
What should we do?
Be sure to do regular dialysis for four hours three times a week, and don't often leave early without reason, let alone be absent without reason. Especially for patients with severe hyperphosphatemia, dialysis can be done four times a week in a short time to increase the dialysis clearance of phosphorus and reduce the harm of hyperphosphatemia as much as possible under the existing conditions.
Why is there secondary hyperparathyroidism?
Hyperphosphatemia can stimulate the body to "regulate" in many ways to inhibit persistent severe hyperphosphatemia. One of the main ways is that hyperphosphatemia stimulates parathyroid gland to secrete parathyroid hormone, which can promote kidney to excrete phosphorus, thus achieving the "original intention" of controlling blood phosphorus.
Unfortunately, the renal function of dialysis patients has been seriously reduced, the ability of glomerular filtration of phosphorus is very poor, and the response of renal tubules to parathyroid hormone is low. Therefore, it is not feasible for dialysis patients to promote phosphorus excretion by stimulating parathyroid secretion of parathyroid hormone. As a result, the self-regulation of phosphorus is out of control, resulting in the persistence or aggravation of hyperphosphatemia, further stimulating the "continuous" and "processing" of parathyroid hormone, resulting in the continuous increase of parathyroid hormone. That is, we often say that secondary hyperparathyroidism, referred to as "secondary hyperparathyroidism." Under the continuous "stimulation" of hyperphosphatemia, parathyroid gland continuously "gallops" to produce parathyroid hormone, and finally reaches the level of "complete forgetting", and produces parathyroid hormone uncontrollably, which leads to the serious exceeding of parathyroid hormone, and then causes systemic multi-system damage.
For blood phosphorus, persistent secondary hyperparathyroidism will lead to hyperkinetic osteopathy, which will lead to a large number of bone phosphorus dissolved into the blood, and further aggravate hyperphosphatemia. This repetition leads to the worsening of the vicious circle. This is the so-called "correction of imbalance"-high phosphorus originally requires parathyroid glands, which are busy tonifying kidney and discharging phosphorus. How can it be that renal failure is not corrected, but moving more will not help.
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