Influence of standard haemodialysis treatment on transcription of human serum- and glucocorticoid-inducible kinase SGK1 and taurine transporter TAUT in blood leukocytes.

BACKGROUND: Standard haemodialysis (HD) rapidly alters osmolality and composition of extracellular fluid and, thus, challenges cell volume constancy. Cell volume-sensitive genes upregulated by osmotic cell shrinkage include those encoding for taurine transporter TAUT as well as for serum- and glucocorticoid-inducible kinase SGK1. METHODS: Six HD patients were haemodialysed for 4 h with high-flux dialysers. Blood was drawn from the arterial section of the fistula immediately prior to start of HD and subsequently after 60, 120 and 240 min of HD treatment and, in addition, 120 min after HD treatment. Taurine plasma concentrations ([taurine]p) and erythrocytic taurine content ([taurine]e) were determined by high-performance liquid chromatography. SGK1 and TAUT transcript levels in leukocytes were quantified by real-time polymerase chain reaction. RESULTS: The [taurine]p was significantly higher in HD patients before HD treatment when compared with healthy controls and it decreased significantly during 4 h of HD. The ratio of SGK1/GAPDH and of TAUT/GAPDH transcript levels increased significantly by 50% or 27%, respectively, during HD. CONCLUSIONS: Standard HD treatment decreases plasma taurine concentration and upregulates leukocyte SGK1 and TAUT transcription. As SGK1 is a potent regulator of ion channels and transporters in nervous system, heart muscle and epithelial cells, the deranged regulation of SGK1 may contribute to acute side effects of HD treatment.

Improved acidosis correction and recovery of mesothelial cell mass with neutral-pH bicarbonate dialysis solution among children undergoing automated peritoneal dialysis.

Acid-base balance and peritoneal membrane longevity are of utmost relevance for pediatric patients undergoing peritoneal dialysis (PD). PD fluids with neutral pH and reduced glucose degradation product contents are considered more biocompatible, because they preserve peritoneal cell functions in vitro. To investigate the clinical effects of a novel PD fluid buffered with 34 mM pure bicarbonate at neutral pH, a randomized, prospective, crossover comparison with conventional, acidic, 35 mM lactate PD fluid was performed for two consecutive 12-wk periods with 28 children (age, 6 mo to 15 yr) undergoing automated PD (APD). Blood bicarbonate levels and arterial pH were significantly higher after 3 mo of bicarbonate PD (24.6 +/- 2.3 mM and 7.43 +/- 0.06, respectively), compared with lactate PD (22.8 +/- 3.9 mM and 7.38 +/- 0.05, respectively; P < 0.05). This effect was reversible among patients who returned from bicarbonate to lactate fluid. Low initial pH and young patient age independently predicted increased blood pH during bicarbonate APD. Peritoneal equilibration tests revealed subtle changes in solute transport, with a less steep creatinine equilibration curve during bicarbonate dialysis, suggesting reduced peritoneal vasodilation. The peritoneal release of carcinogen antigen-125 increased twofold during bicarbonate APD (29 +/- 15 versus 15 +/- 8 U/ml per 4 h, P < 0.01), which is consistent with recovery of the mesothelial cell layer. This effect was fully reversed when the patients returned to lactate fluid. Effluent carcinogen antigen-125 levels were inversely correlated with peritoneal glucose exposure during lactate but not bicarbonate APD, indicating improved in vivo mesothelial cell tolerance of high-dose glucose with the neutral-pH PD fluid with reduced glucose degradation product content. Among children undergoing APD, neutral-pH, bicarbonate-buffered PD fluid provides more effective correction of metabolic acidosis and better preservation of peritoneal cell mass than do conventional, acidic, lactate-based fluids.