Journal Article

Molecular basis for the dialysis disequilibrium syndrome: altered aquaporin and urea transporter expression in the brain

Marie-Marcelle Trinh-Trang-Tan, Jean-Pierre Cartron and Lise Bankir

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 20, issue 9, pages 1984-1988
Published in print September 2005 | ISSN: 0931-0509
Published online June 2005 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/gfh877
Molecular basis for the dialysis disequilibrium syndrome: altered aquaporin and urea transporter expression in the brain

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Background. Cerebral disorders caused by brain oedema characterize the dialysis disequilibrium syndrome, a complication of rapid haemodialysis. Brain oedema is presumably caused by the ‘reverse urea effect’, i.e. the significant urea gradient between blood and brain after dialysis, with, as a result, an inflow of water into the brain. To assess the molecular basis of this effect, we examined the expression of urea transporter UT-B1 and aquaporin (AQP) 4 and AQP9 in the brain of uraemic rats.

Methods. Brain, kidneys and one testis were collected from four sham-operated (control) and four uraemic rats, 10 weeks after 5/6 nephrectomy (Nx). Protein abundance was measured by semi-quantitave immunoblotting using affinity-purified rabbit anti-rat antibodies applied on tissue crude homogenates.

Results. The results are expressed as means±SE of band density (arbitrary units). In Nx compared with control rats, the brain expression of UT-B1 was reduced by half (32±3 vs 62±8, P<0.01) whereas that of AQ4 was doubled (251±13 vs 135±5, P<0.001), and that of AQP9 increased by 65% (253±22 vs 154±10, P<0.01). UT-B1 expression was also lowered by Nx in kidney medulla (45±21 vs 141±4, P<0.01) but was unchanged in testis.

Conclusions. The conjunction of a reduced expression of UT-B and an increased expression of AQPs in brain cells may bring a new clue to understanding the DDS mechanism. Because of low UT-B abundance, urea exit from astrocytes is most probably delayed during rapid removal of extracellular urea through fast dialysis. This creates an osmotic driving force that promotes water entry into the cells (favoured by abundant AQPs) and subsequent brain swelling.

Keywords: chronic renal failure; kidney; oedema; rat; subtotal nephrectomy; UT-B1

Journal Article.  3135 words.  Illustrated.

Subjects: Nephrology

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