Addendum Regarding “The Unappreciated Role of Extrarenal and Gut Sensors in Modulating Renal Potassium Handling: Implications for Diagnosis of Dyskalemias and Interpreting Clinical Trials” (Kidney Int Rep. 2016;1:43–56)

Shortly after the in press publication of the review “The Unappreciated Role of Extrarenal and Gut Sensors in Modulating Renal Potassium Handling: Implications for Diagnosis of Dyskalemias and Interpreting Clinical Trials”¹, Lise Bankir and associates published a paper² suggesting that glucagon could serve as the mediator for the rapid renal response to an ingestion of potassium. This hypothesis is relevant to and complements our discussion of both (a) the putative location for the GI potassium sensor and, (b) the potential signal(s) that might modulate the increase in renal potassium excretion.