Brain-kidney crosstalk

Abstract

Encephalopathy and altered higher mental functions are common clinical complications of acute kidney injury. Although sepsis is a major triggering factor, acute kidney injury predisposes to confusion by causing generalised inflammation, leading to increased permeability of the blood-brain barrier, exacerbated by hyperosmolarity and metabolic acidosis due to the retention of products of nitrogen metabolism potentially resulting in increased brain water content. Downregulation of cell membrane transporters predisposes to alterations in neurotransmitter secretion and uptake, coupled with drug accumulation increasing the risk of encephalopathy. On the other hand, acute brain injury can induce a variety of changes in renal function ranging from altered function and electrolyte imbalances to inflammatory changes in brain death kidney donors.

Figure 1

Schematic diagram depicting the effect of acute kidney injury on integrity of the blood–brain barrier. IS, indoxyl sulphate; OAT, organic anion transporter; OCT, organic cation transporter; PAH, para-aminohippuric acid; ROS, reactive oxygen species; VEGF, vascular endothelial growth factor.

Figure 2

Schematic cartoon showing potential pathways of brain and kidney crosstalk. OAT, organic anion transporter; RVI, regulatory volume increase.