Epstein Murray, Lifschitz Meyer D
Division of Nephrology and Hypertension, University of Miami, Miller School of Medicine, South Florida Veterans Affairs Foundation for Research and Education (SFVAFRE), Miami, Florida, USA.
Adult Nephrology Unit, Shaare Zedek Medical Center, Jerusalem, Israel.
Kidney Int Rep. 2016 Apr 8;1(1):43-56. doi: 10.1016/j.ekir.2016.03.001. eCollection 2016 May.
In addition to the classic and well-established "feedback control" of potassium balance, increasing investigative attention has focused on a novel and not widely recognized complementary regulatory paradigm for maintaining potassium homeostasis-the "feed-forward control" of potassium balance. This regulatory mechanism, initially defined in rumen, has recently been validated in normal human subjects. Studies are being conducted to determine the location for this putative potassium sensor and to evaluate potential signals, which might increase renal potassium excretion. Awareness of this more updated integrative control mechanism for potassium homeostasis is ever more relevant today, when the medical community is increasingly focused on the challenges of managing the hyperkalemia provoked by renin-angiotensin-aldosterone system inhibitors (RAASis). Recent studies have demonstrated a wide gap between RAASi prescribing guidelines and real-world experience and have highlighted that this gap is thought to be attributable in great part to hyperkalemia. Consequently we require a greater knowledge of the complexities of the regulatory mechanisms subserving potassium homeostasis. Sodium polystyrene sulfonate has long been the mainstay for treating hyperkalemia, but its administration is fraught with challenges related to patient discomfort and colonic necrosis. The current and imminent availability of newer potassium binders with better tolerability and more predictive dose-response potassium removal should enhance the management of hyperkalemia. Consequently it is essential to better understand the intricacies of mammalian colonic K handling. We discuss colonic transport of K and review evidence for potassium (BK) channels being responsible for increased stool K in patients with diseases such as ulcerative colitis.
除了经典且已确立的钾平衡“反馈控制”外，越来越多的研究关注集中在一种新颖且尚未得到广泛认可的维持钾稳态的补充调节模式——钾平衡的“前馈控制”。这种调节机制最初是在瘤胃中定义的，最近已在正常人类受试者中得到验证。目前正在进行研究以确定这种假定的钾传感器的位置，并评估可能增加肾钾排泄的潜在信号。当医学界越来越关注管理由肾素 - 血管紧张素 - 醛固酮系统抑制剂（RAASi）引发的高钾血症的挑战时，了解这种更新的钾稳态综合控制机制在当今变得更加重要。最近的研究表明，RAASi处方指南与实际临床经验之间存在很大差距，并强调这种差距在很大程度上被认为是由高钾血症导致的。因此，我们需要更深入地了解维持钾稳态的调节机制的复杂性。聚苯乙烯磺酸钠长期以来一直是治疗高钾血症的主要药物，但其给药存在与患者不适和结肠坏死相关的诸多挑战。具有更好耐受性和更可预测的剂量 - 反应性钾清除效果的新型钾结合剂的当前及即将上市，应能改善高钾血症的管理。因此，更好地理解哺乳动物结肠钾处理的复杂性至关重要。我们讨论了结肠对钾的转运，并综述了钾通道（BK通道）导致溃疡性结肠炎等疾病患者粪便钾增加的证据。
