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本周，查房时教授提问：腹透病人一天丢失蛋白多少？
答：太棒了，这个我看过，大概10g，合并感染时增加50%，
再问：既然如此，腹透病人丢失蛋白多于肾综病人（尿中）丢失蛋白，为什么在临床中低蛋白/低白蛋白血症在肾综病人中出现却多于腹透？
答：囧
低白蛋白血症是肾病综合征的四大特点之一，在内科学时我们就牢牢记住了这一点。
往往我们提到低蛋白血症很自然的与「大量蛋白尿」联系在一起，但是遇到这样的问题，就有点困惑了。
试图从生成障碍、代谢增加、体内激素水平等方面解释，均效果不佳；
检索中外文献，试图发现是否人关注过两者比较，无收获。
想找有没有人研究低蛋白血症/营养不良状态的因素，同样无满意收获。
倒是有一些关于腹透病人低蛋白血症的原因的研究：
（1）摄入不足
（2）丢失过多
（3）合并感染、消耗疾病
（4）内分泌紊乱促分解激素增加，促合成的激素减少
回头翻翻教科书，The Kidney 还是不负所托，大致如图
尿中丢失与低白蛋白血症的存在联系，但是关系存在矛盾且不能完全解释。
低白蛋白血症的重要机制。肝脏本身具有强大的储备能力，其最高较正常可上升3倍。
在肾综病人中可以发现白蛋白合成较平时上升，但并不足弥补丢失，且远未达到上限。
肝脏合成白蛋白的速度受肝脏间质中白蛋白浓度决定的胶体渗透压调节，低白蛋白血症时肝脏间质中白蛋白浓度下降--》胶体渗透下降，肝脏胶体渗透压感受器接受到信号后上调其合成速度，但是在肾综病人，间质白蛋白浓度相对变化不大，胶体渗透压的感受器反馈出现障碍，导致肝脏不能合成足够多的白蛋白。
白蛋白代谢每天约6-10%的白蛋白，约10g白蛋白代谢在血管内皮细胞，但是肾病综合征的病人，大量蛋白尿，蛋白尿除了从尿中排，还有很大一部分被肾小球滤过后在小管重吸收后代谢掉了。
如上图，24小时尿蛋白定量可能仅仅反映了蛋白丢失的冰山一角。
存在但不主要地位。
教授提问的问题基本明白了，有所收获，下一步是不是可以尝试，如何通过改善肝脏内渗透压感受器的反馈来纠正低白蛋白血症？似乎是个有意思的问题。
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.
延伸阅读：
肾病综合征水肿机制新进展
JASN：肾病综合征新进展综述
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