本周，查房時(shí)教授提問(wèn)：腹透病人一天丟失蛋白多少？

答：太棒了，這個(gè)我看過(guò)，大概10g，合并感染時(shí)增加50%，

再問(wèn)：既然如此，腹透病人丟失蛋白多于腎綜病人（尿中）丟失蛋白，為什么在臨床中低蛋白/低白蛋白血癥在腎綜病人中出現(xiàn)卻多于腹透？

答：囧

低白蛋白血癥是腎病綜合征的四大特點(diǎn)之一，在內(nèi)科學(xué)時(shí)我們就牢牢記住了這一點(diǎn)。

往往我們提到低蛋白血癥很自然的與「大量蛋白尿」聯(lián)系在一起，但是遇到這樣的問(wèn)題，就有點(diǎn)困惑了。

試圖從生成障礙、代謝增加、體內(nèi)激素水平等方面解釋?zhuān)Ч患眩?/p>

檢索中外文獻(xiàn)，試圖發(fā)現(xiàn)是否人關(guān)注過(guò)兩者比較，無(wú)收獲。

想找有沒(méi)有人研究低蛋白血癥/營(yíng)養(yǎng)不良狀態(tài)的因素，同樣無(wú)滿意收獲。

倒是有一些關(guān)于腹透病人低蛋白血癥的原因的研究：

回頭翻翻教科書(shū)，The Kidney 還是不負(fù)所托，大致如圖

尿中丟失與低白蛋白血癥的存在聯(lián)系，但是關(guān)系存在矛盾且不能完全解釋。

低白蛋白血癥的重要機(jī)制。肝臟本身具有強(qiáng)大的儲(chǔ)備能力，其最高較正?？缮仙?倍。

在腎綜病人中可以發(fā)現(xiàn)白蛋白合成較平時(shí)上升，但并不足彌補(bǔ)丟失，且遠(yuǎn)未達(dá)到上限。

白蛋白代謝每天約6-10%的白蛋白，約10g白蛋白代謝在血管內(nèi)皮細(xì)胞，但是腎病綜合征的病人，大量蛋白尿，蛋白尿除了從尿中排，還有很大一部分被腎小球?yàn)V過(guò)后在小管重吸收后代謝掉了。

如上圖，24小時(shí)尿蛋白定量可能僅僅反映了蛋白丟失的冰山一角。

存在但不主要地位。

教授提問(wèn)的問(wèn)題基本明白了，有所收獲，下一步是不是可以嘗試，如何通過(guò)改善肝臟內(nèi)滲透壓感受器的反饋來(lái)糾正低白蛋白血癥？似乎是個(gè)有意思的問(wèn)題。

The Kidney 「9th edition」

Extracorporeal Losses.

The magnitude of hypoalbuminemia tends to increase with increasing proteinuria, but the relationship is inconsistent. Urinary losses alone should not lead to hypoalbuminemia because the liver can easily augment albumin synthesis and thus compensate for such losses. Evidence for enhanced intestinal albumin loss, or in-creased albumin catabolism, in the nephrotic syndrome is not strong.[66] As discussed later, renal albumin catabolism is in-creased, thereby contributing to the greater tendency to hypoalbuminemia.

Hepatic Albumin Synthesis.
Hepatic albumin synthesis is not impaired and, in fact, may be significantly increased in the nephrotic syndrome. [67] [68] In nephrotic rats, hepatic release of albumin is enhanced, and the relative synthetic rate of albumin is markedly increased, with a comparable increase in albumin mRNA. [69] [70] Oncotic pressure may play a role in albumin synthesis, as albumin gene expression varies inversely with oncotic pressure in experimental models.[71] That a transcriptional process is mainly responsible is suggested by findings that both steady-state levels and transcription rates of albumin mRNA are increased in the livers of nephrotic rats.[72] However, the increase in hepatic albumin synthesis is inadequate for the degree of hypoalbuminemia; thus, the albumin synthetic response rate is relatively impaired.

Albumin Catabolism.
In some hypoalbuminemic states, albumin catabolic rates are reduced.[73] In contrast, the possibility that hypoalbuminemia might be exacerbated by a maladaptive increase in albumin catabolism was suggested by Katz and associates,[74] who speculated that the increased urinary albumin load might up-regulate tubular albumin catabolism. In that case, most filtered albumin would be catabolized, and thus urinary albumin would represent only a small fraction of the filtered load. In confirmation of this notion, tubule albumin reabsorptive rates increase in nephrotic rats, though variably.[75] Additional support for the concept comes from evidence of a dual transport system for albumin uptake in the isolated perfused rabbit proximal tubule. This model exhibits both a low-capacity system that becomes saturated once the protein load exceeds physiologic levels and a high-capacity, low-affinity system that permits tubule albumin reabsorptive rates to rise as the filtered load increases.[76] Thus, an increase in the fractional catabolic rate may occur in the nephrotic syndrome. Regardless of whether fractional catabolism is normal or increased, total body albumin stores are markedly decreased. The net result is that absolute catabolic rates are normal or decreased.[66] Nutritional considerations affect this process. In nephrotic rats, absolute catabolic rates are decreased in rats fed adequate dietary protein but increased in rats receiving a low-protein diet.[77] Although decreased catabolism may serve to preserve total albumin stores, it is obviously insufficient to maintain albumin homeostasis.

Albumin Distribution.
In nephrotic syndrome, the extravascular albumin pool is even more depleted than the intravascular pool.[78] Mobilization of extravascular albumin represents an early response to acute albumin loss, but this compensatory mechanism is clearly inadequate in the setting of continuing albumin loss, as in nephrotic syndrome.

延伸閱讀：

腎病綜合征水腫機(jī)制新進(jìn)展

JASN：腎病綜合征新進(jìn)展綜述