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.
Highlights
Encephalopathy and altered higher mental functions are common clinical complications of acute kidney injury
These animal studies support the concept that inflammation associated with Acute kidney injury (AKI) with increased circulating cytokines leads to disruption of the blood–brain barrier (BBB), allowing increased access to inflammatory cells, cytokines, complement, amino acids and organic osmolytes
Cerebral dysfunction is a common finding in patients with AKI
Summary
Alteration of essential amino acid concentrations, inflammatory mediators and organic osmolyte in the brain. Models of local inflammation induced by tumour necrosis factor alpha or generalised sepsis cause activation of brain astrocytes, resulting in changes to the BBB, and increased permeability These animal studies support the concept that inflammation associated with AKI with increased circulating cytokines leads to disruption of the BBB, allowing increased access to inflammatory cells, cytokines, complement, amino acids and organic osmolytes. Changes in catecholamine neurotransmitter metabolism have been associated with impaired motor activity [29], which is supported by experimental studies reporting a fall in plasma valine and threonine but increased brain phenylalanine, tyrosine, and histidine [30], so potentially increasing the amount of cerebral monoamine neurotransmitters, with alteration of mental status and motor disability [31] (Table 2). How important these changes in neurotransmitters are in causing the alteration of cerebral function often witnessed in clinical practice is unknown, the increased risk of developing delirium in the intensive care setting associated with the use of gamma aminobutyric acidA agonists and anticholinergic drugs suggests that alterations in these neurotransmitters play a contributory role [32]
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