Skip to main content

Table 1 Experimental studies on brain-kidney cross-talk

From: Acute kidney injury in neurocritical care

Study

Model

Method

Findings

Arieff et al. [55]

Dog

Bilateral urethral ligation; analyses 72 h later

Increased calcium content in the gray and white matter of the brain after AKI, which was prevented by TPTX; administration of parathyroid extract to normal and post-TPTX dogs associated with an increase in brain calcium; hemodialysis significantly reduced brain calcium content but values remained significantly above normal

Jeppsson et al. [56]

Rat

AKI model: unilateral nephrectomy and renal artery occlusion of the remaining kidney for 70 min; CKD model: unilateral nephrectomy and 70–80% devascularization of the remaining kidney; analyses 2 weeks later

Reduced plasma valine and threonine and increased brain phenylalanine, tyrosine, and histidine

Trachtman et al. [57]

Rat

Bilateral urethral ligation; analyses 8 h and 48 h later

Decreased brain water at 8 h and increased organic osmolyte in the brain at 48 h

Silver et al. [58]

Rat

Bilateral urethral ligation; analyses 42 h later

Increased brain water content in dialyzed over non-dialyzed AKI rats; no significant change in brain organic osmolytes

Adachi et al. [55]

Rat

Bilateral renal artery occlusion vs. sham-operation; analyses 48 h later

Decreased dopamine turnover in striatum, mesencephalon, and hypothalamus, which correlated with impaired motor activity; unchanged cerebral norepinephrine and serotonin turnover and brain water content

Liu et al. [59]

Mouse

Bilateral renal IRI for 60 min vs. sham-operation; analyses 24 h later

In mice with AKI: disrupted blood–brain barrier, increased neuronal pyknosis and microgliosis, increased keratinocyte-derived chemoattractant and G-CSF in the cerebral cortex and hippocampus, and elevated expression of glial fibrillary acidic protein in astrocytes in the cortex and corpus callosum

Palkovits et al. [60]

Rat

Bilateral renal IRI, bilateral urethral ligation, and drug-induced AKI vs. sham; analyses 24 h later

Moderate increase in neuronal activation in the biogenic amine expressing cell group

Salama et al. [61]

Rat

Bilateral renal IRI

Increased TLR-4 expression within the hippocampus and striatum

Chou et al. [62]

Mouse

Bilateral renal IRI for 60 min vs. sham-operation; analyses 2 h and 24 h later

In mice with AKI: higher serum and brain levels of KS, G-CSF, and MCP-1, increased brain vascular permeability, and altered genes expression in the hippocampus 2 h after reperfusion before changes in SCr

Arieff et al. [55]

Dog

Bilateral urethral ligation; analyses 72 h later

Increased calcium content in the gray and white matter of the brain after AKI, which was prevented by TPTX; administration of parathyroid extract to normal and post-TPTX dogs associated with an increase in brain calcium; hemodialysis significantly reduced brain calcium content but values remained significantly above normal

Jeppsson et al. [56]

Rat

AKI model: unilateral nephrectomy and renal artery occlusion of the remaining kidney for 70 min; CKD model: unilateral nephrectomy and 70%–80% devascularization of the remaining kidney; analyses 2 weeks later

Reduced plasma valine and threonine and increased brain phenylalanine, tyrosine, and histidine

Trachtman et al. [57]

Rat

Bilateral urethral ligation; analyses 8 h and 48 h later

Decreased brain water at 8 h and increased organic osmolyte in the brain at 48 h

Silver et al. [58]

Rat

Bilateral urethral ligation; analyses 42 h later

Increased brain water content in dialyzed over non-dialyzed AKI rats; no significant change in brain organic osmolytes

Adachi et al. [55]

Rat

Bilateral renal artery occlusion vs. sham-operation; analyses 48 h later

Decreased dopamine turnover in striatum, mesencephalon, and hypothalamus, which correlated with impaired motor activity; unchanged cerebral norepinephrine and serotonin turnover and brain water content

Liu et al. [59]

Mouse

Bilateral renal IRI for 60 min vs. sham-operation; analyses 24 h later

In mice with AKI: disrupted blood–brain barrier, increased neuronal pyknosis and microgliosis, increased keratinocyte-derived chemoattractant and G-CSF in the cerebral cortex and hippocampus, and elevated expression of glial fibrillary acidic protein in astrocytes in the cortex and corpus callosum

Palkovits et al. [60]

Rat

Bilateral renal IRI, bilateral urethral ligation, and drug-induced AKI vs. sham; analyses 24 h later

Moderate increase in neuronal activation in the biogenic amine expressing cell group

Salama et al. [61]

Rat

Bilateral renal IRI

Increased TLR-4 expression within the hippocampus and striatum

Chou et al. [62]

Mouse

Bilateral renal IRI for 60 min vs. sham-operation; analyses 2 h and 24 h later

In mice with AKI: higher serum and brain levels of KS, G-CSF, and MCP-1, increased brain vascular permeability, and altered genes expression in the hippocampus 2 h after reperfusion before changes in SCr

  1. AKI acute kidney injury, CKD chronic kidney disease, G-CSF granulocyte-colony stimulating factor, IRI ischemia–reperfusion injury, KS keratinocyte-derived chemokine, MCP-1 monocyte chemoattractant protein-1, SCr serum creatinine, TLR-4 toll-like receptor-4, TPTX thyroparathyroidectomy