Name: 高血磷症：成因、症狀、診斷、治療、病理一次看！ (Hyperphosphatemia causes, symptoms, diagnosis, treatment, pathology)
Uploaded: 2025-11-12T06:56:29.000Z
Duration: 12 min 37 s

With hyperphosphatemia, hyper means over.

講到高磷血癥，這裡的「高」就是指過量。

Phosphat refers to phosphate, and emia refers to the blood.

「磷酸」指的是磷酸鹽，而「血癥」就是指血液。

So hyperphosphatemia means having high phosphate levels in the blood, typically above 4.5 milligrams per deciliter.

所以高磷血癥的意思就是血液裡的磷酸鹽濃度偏高，通常會超過每分升 4.5 毫克。

Now, phosphate is made up of one central phosphorus atomic surrounded by four oxygen atoms in a tetrahedral arrangement, kind of like a mini pyramid, and

那磷酸鹽呢，它是由一個中心的磷原子，周圍環繞著四個氧原子，呈四面體排列，有點像個小金字塔，

In the body, about 85% of the phosphate is stored in the bones, where it combines with calcium to make a tough compound called hydroxyapatite, which is the stuff that makes bones hard.

在身體裡，大約有 85% 的磷酸鹽儲存在骨頭裡，它會跟鈣結合，形成一種堅硬的化合物叫做羥基磷灰石，這就是讓骨頭變硬的成分。

Of the remaining phosphate, a tiny amount is extracellular or outside the cells, like in the blood.

剩下的磷酸鹽，一小部分是在細胞外，像是血液裡。

And the majority is intracellular or inside cells, where it does all sorts of things.

大部分則是在細胞內，在那裡它會做各種事情。

It's responsible for phosphorylation, where it binds to fats and proteins.

它負責磷酸化，也就是結合脂肪和蛋白質。

It forms the high energy bonds of adenosine triphosphate, or ATP, which is the most common energy currency in the cell.

它構成了三磷酸腺苷（ATP）的高能鍵，ATP 是細胞中最常見的能量貨幣。

It's part of the DNA and RNA backbone that links individual nucleotides together.

它是 DNA 和 RNA 主鏈的一部分，將個別的核苷酸連接在一起。

And it's also part of cellular signaling molecules like cyclic adenosine monophosphate, or camp.

它也是細胞訊號分子的一部分，例如環磷酸腺苷（cAMP）。

The bottom line is that phosphate's really important now, because most of phosphate's locked up with calcium in the bones, the levels of phosphate are heavily tied with the levels of ionized calcium in the body.

總而言之，磷酸鹽現在非常重要，因為大部分磷酸鹽都鎖在骨頭裡的鈣中，磷酸鹽的水準與體內離子鈣的水準密切相關。

If calcium levels fall, the four parathyroid glands buried within the thyroid gland release parathyroid hormone, which frees up both calcium and phosphate ions from the bones.

如果鈣的水準下降，埋藏在甲狀腺裡的四個副甲狀腺就會釋放副甲狀腺荷爾蒙，將鈣離子和磷酸鹽離子從骨頭中釋放出來。

It does this by stimulating osteoclasts, the cells that break down bone to release hydrogen ions, which dissolves the hard mineralized hydroxyapatite.

它透過刺激蝕骨細胞來做到這一點，蝕骨細胞是分解骨頭以釋放氫離子的細胞，這會溶解堅硬的礦物質羥基磷灰石。

As soon as the positively charged calcium and negatively charged phosphate are released from the bones, they grab onto each other again, meaning that the ionized calcium level doesn't really go up much at all.

一旦帶正電的鈣和帶負電的磷酸鹽從骨頭中釋放出來，它們就會再次結合，這意味著離子鈣的水準實際上並沒有上升太多。

These two then make their way to the nephron of the kidney.

然後這兩者會進入腎臟的腎單位。

And at this point in the proximal convoluted tubule, phosphate usually gets reabsorbed back into the blood via sodium phosphate cotransporters.

在近端腎小管的這個階段，磷酸鹽通常會透過鈉磷酸鹽共轉運蛋白被重新吸收回血液中。

It turns out, though, that parathyroid hormone also shuts this down.

然而，事實證明，副甲狀腺荷爾蒙也會關閉這一過程。

So this means that phosphate's left in the lumen and eventually gets sent out in the urine, now that calcium's still in the lumen.

所以這表示磷酸鹽會留在管腔裡，最後隨著尿液排出，而鈣離子則還在管腔裡。

But parathyroid hormone also affects the distal convoluted tubule and increases calcium reabsorption.

但副甲狀腺荷爾蒙也會影響遠曲小管，增加鈣離子重吸收。

As a result of parathyroid hormone, phosphate is lost in the urine, while ionized calcium is kept in the blood.

結果就是，副甲狀腺荷爾蒙會導致磷酸鹽從尿液中流失，而離子鈣則留在血液中。

So ionized calcium levels rise and phosphate levels fall.

所以離子鈣的水準會升高，而磷酸鹽的水準會下降。

With all that in mind, hyperphosphatemia can develop in a few ways.

考量到這一切，高磷血癥可能會有幾種形成方式。

The first possibility is as a result of acute or chronic kidney disease.

第一種可能性是急性或慢性腎臟疾病的結果。

And to illustrate this, we'll use some numbers.

為了說明這一點，我們會用一些數字。

So, let's say normally the glomerular filtration rate, or gfr, which is the fluid filtered into the kidney per unit time, is 180liters per day.

所以，假設正常情況下，腎絲球過濾率（GFR），也就是每單位時間過濾到腎臟的液體量，是每天 180 公升。

And the phosphate concentration of that blood is 0.04 grams per liter.

而血液中的磷酸鹽濃度是每公升 0.04 克。

That means that 7.2 grams of phosphate get filtered per day.

這表示每天有 7.2 克磷酸鹽被過濾。

And let's say 90% of that gets reabsorbed, or 6.48 grams.

假設其中 90% 會被重新吸收，也就是 6.48 克。

That leaves 10%, or 0.72 grams to get excreted per day.

這樣每天就只剩下 10%，也就是 0.72 克會被排出。

Now, with kidney disease, let's say the GFR falls to 28.8 liters per day, which means only 1.2 grams gets filtered and only 0.12 grams gets excreted in a day.

現在，如果腎臟疾病導致 GFR 下降到每天 28.8 公升，那每天就只剩下 1.2 克被過濾，也只剩下 0.12 克被排出。

And so where there was 0.72 grams being excreted per day, now there's only 0.12 grams.

所以，原本每天排出 0.72 克，現在只剩下 0.12 克。

And that means that the difference between these two stays in the blood every day.

這就意味著這兩者之間的差額每天都會留在血液裡。

And this contributes to hyperphosphatemia.

This number, 28.8 liters per day, or 20 milliliters per minute, is the point at which its thought excretion can't keep up with intake.

這個數字，每天 28.8 公升，或每分鐘 20 毫升，是認為排出量跟不上攝取量的臨界點。

In addition, the kidneys might be unable to reabsorb calcium, and so more gets excreted.

此外，腎臟可能無法重新吸收鈣，所以會有更多的鈣被排出。

Remember that in response to low calcium, the parathyroid gland releases parathyroid hormone.

請記得，為了回應低鈣血癥，副甲狀腺會釋放副甲狀腺素。

But since calcium just gets wasted, it keeps releasing parathyroid hormone.

不過因為鈣質就這樣被浪費掉了，副甲狀腺素就會持續釋放。

And this is called secondary hyperparathyroidism.

這就叫做次發性副甲狀腺功能亢進症。

Because the primary problem is with the kidneys.

This causes a continuous release of calcium and phosphate from the bones, kind of like an open tap.

這會造成鈣和磷酸鹽從骨頭裡不斷釋放，就像水龍頭開著一樣。

And while calcium is excreted due to impaired reabsorption, phosphates reabsorb due to impaired excretion.

而鈣質因為重吸收受損而被排出，磷酸鹽卻因為排洩受損而被重吸收。

So phosphate ends up building up in the blood.

所以磷酸鹽最後就會堆積在血液裡。

To make matters worse, all this loss from the bones makes them thin and weak, which is part of a process called reno osteodystrophy, which describes the overall bone changes that happen in people with chronic kidney disease.

更糟的是，骨頭的這些流失會讓骨頭變得又薄又弱，這也是腎骨失養症的一部分，它描述了慢性腎臟病患者發生的整體骨骼變化。

Related to this is pseudohypoparathyroidism, which is where the kidneys simply don't respond to parathyroid hormone because of a genetic defect in the parathyroid hormone receptor.

與此相關的是假性副甲狀腺功能低下症，這是因為副甲狀腺素接受器的基因缺陷，導致腎臟根本不回應副甲狀腺素。

Since Parathyroid hormone tells the kidneys to save calcium and get rid of phosphate.

因為副甲狀腺素會告訴腎臟要保留鈣質並排出磷酸鹽。

Calcium again gets lost in phosphate builds up in the blood, following the same pattern as kidney disease, including thinning of the bones.

鈣質又再次流失，磷酸鹽堆積在血液裡，這跟腎臟病的模式一樣，包括骨頭變薄。

Alright, so since again parathyroid hormone causes excretion of phosphate and reabsorption of calcium, then another cause of hyperphosphatemia is hypoparathyroidism.

好的，所以既然副甲狀腺素會造成磷酸鹽排出和鈣質再吸收，那麼高磷血癥的另一個原因就是副甲狀腺功能低下症。

When the parathyroid glands don't produce enough parathyroid hormone in the first place, this results in the same situation of increased reabsorption of phosphate and decreased reabsorption of calcium.

當副甲狀腺一開始就沒有產生足夠的副甲狀腺素時，這就會導致磷酸鹽的再吸收增加，鈣質的再吸收減少，情況就跟前面一樣。

This can happen following a thyroid gland removal surgery where the parathyroids are accidentally taken out too, or radiation treatment for cancer of the head and neck.

這可能發生在甲狀腺切除手術後，副甲狀腺也被意外移除，或是頭頸部癌症的放射線治療。

Also, people with the genetic disease Digeorge syndrome are often born with parathyroid glands that are too small and can't produce enough parathyroid hormone.

另外，患有狄喬治氏症候群這種基因疾病的人，通常天生副甲狀腺就太小，無法產生足夠的副甲狀腺素。

Alternatively, phosphate levels can rapidly increase in the blood from excessive intake and absorption through the gastrointestinal tract or bloodstream via intravenous fluids.

或者，磷酸鹽濃度也會因為攝取過量，以及透過腸胃道或靜脈輸液進入血液，而快速升高。

One cause is taking too much of a phosphate based laxative either orally or rectally as an enema.

其中一個原因是口服或灌腸使用過量的磷酸鹽瀉藥。

A final cause of hyperphosphatemia relates to the fact that most phosphate in the body is within the cells.

高磷血癥的最後一個原因，跟體內大部分磷酸鹽都存在細胞內有關。

Anytime a lot of cells die, the phosphate gets spilled into the bloodstream, causing hyperphosphatemia.

只要有大量細胞死亡，磷酸鹽就會釋放到血液中，造成高磷血癥。

This includes things like crush injuries, like when a piano falls on someone's legs, or tumorlysis syndrome, which is cancer treatment that causes lots of tumor cells to die all at once.

這包括像是嚴重的創傷，像是鋼琴砸到腿，或是腫瘤溶解症候群，這是癌症治療導致大量腫瘤細胞瞬間死亡。

Or rhabdomyolysis which is rapid destruction of skeletal muscle cells.

或是橫紋肌溶解症，這是骨骼肌細胞的快速破壞。

Another situation is when living cells get affected by respiratory acidosis, which is when the carbon dioxide levels rise because a person isn't breathing or ventilating it out of the lungs quickly enough that carbon dioxide can diffuse into a cell and react with water to form carbonic acid, which quickly breaks into a proton and bicarbonate.

另外一種情況是，當活細胞受到呼吸性酸中毒影響時，這表示二氧化碳水準升高，因為人體無法足夠快地將二氧化碳排出肺部，二氧化碳會擴散到細胞內並與水反應形成碳酸，碳酸會迅速分解成質子和碳酸氫根。

The bicarbonate goes back into the blood in exchange for a chloride ion, leaving behind a proton, and

碳酸氫根會與氯離子交換回到血液中，留下質子，

all this ends up lowering the cellular ph.

這一切最終會降低細胞的 pH 值。

Now, normally, glycolysis in the cell uses up a lot of phosphate, but

現在，正常情況下，細胞內的醣解作用會消耗大量磷酸鹽，但是

this lower ph in the cell tends to inhibit glycolysis.

細胞內較低的 pH 值會抑制醣解作用。

So as a result, the cells don't pull as much phosphate out of the blood and this allows levels in the blood to rise somewhat.

是以，結果是細胞從血液中提取的磷酸鹽量減少，這會讓血液中的磷酸鹽水準有所升高。

Similarly, in diabetic ketoacidosis, there are low levels of insulin, and

類似地，在糖尿病酮酸中毒中，胰島素水準較低，

although the exact mechanism is unclear, this reduces the amount of phosphate that cells extract from the blood, which causes it again to build up in the blood.

雖然確切機制尚不清楚，但這會減少細胞從血液中提取的磷酸鹽量，導致血液中的磷酸鹽再次堆積。

In this case though, it's a slower process since there's also an osmotic diuresis or increased urination from the hyperglycemia or high blood sugar.

不過，這種情況是一個較慢的過程，因為同時也存在滲透性利尿，或因高血糖（血糖過高）導致排尿增加。

Mild hyperphosphatemia doesn't usually cause symptoms, but severe hyperphosphatemia can make neurons more excitable.

輕微的高磷血癥通常不會引起症狀，但嚴重的高磷血癥會使神經元更容易興奮。

This can trigger the spontaneous firing of neurons in tetany or the involuntary contraction of muscles.

這可能會引發肌張力障礙時神經元的自發性放電，或肌肉的不自主收縮。

This can end up causing trvostech sign which is when the facial muscles twitch after the facial nerve is lightly finger tapped 1cm below the zygomatic process.

這可能會導致特魯索徵象，也就是輕觸顴弓下方 1 公分處的顏面神經時，顏面肌肉會抽搐。

It can also cause trousseau sign, which is where a blood pressure cuff occludes the brachial artery.

這也可能導致特魯索氏徵象，也就是血壓袖帶壓迫肱動脈。

And that pressure on the nerve is enough to make it fire, resulting in a muscle spasm that makes the wrist and metacarpophalangeal joints flex.

而對神經的壓力足以使其放電，導致肌肉痙攣，使手腕和掌指關節屈曲。

It can also cause symptoms like tingling around the mouth, seizures and bone pain.

這也可能引起口周麻木、癲癇和骨痛等症狀。

The high levels of phosphate also cause it to find and stick to calcium, which forms bone like crystals containing calcium and phosphate in places that they shouldn't be, like just beneath the skin, in the walls of blood vessels, in the joints or in the kidneys where they can form kidney stones.

高濃度的磷酸鹽也會使其尋找並結合鈣質，形成不該出現的鈣質和磷酸鹽的骨狀結晶，例如皮膚下方、血管壁、關節或腎臟，進而形成腎結石。

With long term hyperphosphatemia, the whole kidney can eventually turn into bone, which is called nephrocalcinosis.

長期高磷血癥會導致整個腎臟最終變成骨頭，這稱為腎鈣質沉著症。

In other words, flesh literally turning to bone.

換句話說，就是肉體真的變成骨頭。

This widespread calcification of healthy tissues is called metastatic calcification.

這種健康組織廣泛的鈣化稱為轉移性鈣化。

In this case, metastatic means that the tissue rapidly changes from one thing to another, rather than referring to cancer.

在這種情況下，轉移性指的是組織快速地從一種狀態轉變成另一種狀態，而不是指癌症。

Diagnosis of hyperphosphatemia is based on the phosphate levels being above 4.5 milligrams per deciliter.

高磷血癥的診斷是根據磷酸鹽水準高於每分升 4.5 毫克來判斷。

And treatment often involves decreasing phosphate intake.

而治療通常會減少磷酸鹽的攝取。

And this is accomplished by avoiding foods that contain a lot of phosphate, like dairy, meat and soda.

這是透過避免攝取含有大量磷酸鹽的食物來達成，像是乳製品、肉類和汽水。

In other words, no more pepperoni pizza with coke.

換句話說，就是不能再吃含可樂的義大利臘腸披薩了。

To decrease the amount of phosphate that's absorbed from the gastrointestinal tract, people can be given medications called phosphate binders.

為了減少從胃腸道吸收的磷酸鹽量，可以給予病患稱為磷酸鹽結合劑的藥物。

Now you can also try to increase excretion of phosphate.

現在你也可以嘗試增加磷酸鹽的排洩。

And in people with healthy kidneys, a combination of intravenous saline and a loop diuretic like furosemide can increase excretion.

對於腎臟健康的人來說，靜脈輸液和像福莫替康這類的利尿劑可以增加排洩。

And it essentially overwhelms the proximal convoluted tubule of the nephron with so much fluid that it's unable to reabsorb solutes, including phosphate.

它基本上讓腎元近端腎小管充滿大量液體，使其無法重新吸收包括磷酸鹽在內的溶質。

Alright, as a quick recap, hyperphosphatemia describes high phosphate levels in the blood above 4.5 milligrams per deciliter, and

好的，快速總結一下，高磷血癥是指血液中的磷酸鹽水準高於每分升 4.5 毫克，而

this can result from increased absorption and intake, decreased excretion, or a shift of phosphate from the inside of cells to the bloodstream.

這可能是因為吸收和攝入增加、排洩減少，或是磷酸鹽從細胞內部轉移到血液中。

High levels of phosphate ions in the blood also like to bind with calcium, which forms bone like crystals, which can slowly turn into bony structures.

血液中高濃度的磷酸鹽離子也很喜歡與鈣結合，形成類似骨頭的晶體，這些晶體會慢慢變成骨骼結構。

That was a long one, so hopefully you stuck through it and learned a little bit about hyperphosphatemia.

這一段有點長，希望你堅持看完了，也學到了一點關於高磷血癥的知識。

One exciting thing is that we're almost done with all the renal videos, which is really cool because there is a ton of them and we're almost done.

令人興奮的是，我們快要完成所有關於腎臟的影片了，這真的很棒，因為腎臟的影片很多，我們快完成了。

So once that's done, we can move on to another topic and start hashing those out.

所以一旦完成，我們就可以轉到另一個主題，開始深入探討。

Other than that, special thanks goes to Charles B.

Davis for writing the script with this one, as well as Rishi for editing the script.

Davis 寫了這集的腳本，還有 Rishi 負責編輯腳本。

I did the audio as well as the illustrations.