title: Increased Hepato-Splanchnic Vasoconstriction in Diabetics during Regular Hemodialysis.
abstract: OBJECTIVE
  Ultrafiltration (UF) of excess fluid activates numerous compensatory mechanisms during hemodialysis (HD). The increase of both total peripheral and splanchnic vascular resistance is considered essential in maintaining hemodynamic stability. The aim of this study was to evaluate the extent of UF-induced changes in hepato-splanchnic blood flow and resistance in a group of maintenance HD patients during regular dialysis.
  
  
  METHODS
  Hepato-splanchnic flow resistance index (RI) and hepato-splanchnic perfusion index (QI) were measured in 12 chronic HD patients using a modified, non-invasive Indocyaningreen (ICG) dilution method. During a midweek dialysis session we determined RI, QI, ICG disappearance rate (kICG), plasma volume (Vp), hematocrit (Hct), mean arterial blood pressure (MAP) and heart rate (HR) at four times in hourly intervals (t1 to t4). Dialysis settings were standardized and all patient studies were done in duplicate.
  
  
  RESULTS
  In the whole study group mean UF volume was 1.86 ± 0.46 L, Vp dropped from 3.65 ± 0.77L at t1 to 3.40 ± 0.78L at t4, and all patients remained hemodynamically stable. In all patients RI significantly increased from 12.40 ± 4.21 mmHg∙s∙m2/mL at t1 to 14.94 ± 6.36 mmHg∙s∙m2/mL at t4 while QI significantly decreased from 0.61 ± 0.22 at t1 to 0.52 ± 0.20 L/min/m2 at t4, indicating active vasoconstriction. In diabetic subjects, however, RI was significantly larger than in non-diabetics at all time points. QI was lower in diabetic subjects.
  
  
  CONCLUSIONS
  In chronic HD-patients hepato-splanchnic blood flow substantially decreases during moderate UF as a result of an active splanchnic vasoconstriction. Our data indicate that diabetic HD-patients are particularly prone to splanchnic ischemia and might therefore have an increased risk for bacterial translocation, endotoxemia and systemic inflammation.
authors.affiliation: Department of Internal Medicine, Clinical Division of Nephrology, Medical University of Graz, Graz, Austria.
authors.forename: Werner
authors.initials: W
authors.lastname: Ribitsch
authors.affiliation: Institute of Physiology, Medical University of Graz, Graz, Austria.
authors.forename: Daniel
authors.initials: D
authors.lastname: Schneditz
authors.affiliation: Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, Groningen, The Netherlands.
authors.forename: Casper F M
authors.initials: CF
authors.lastname: Franssen
authors.affiliation: Department of Internal Medicine, Clinical Division of Nephrology, Medical University of Graz, Graz, Austria.
authors.forename: Gernot
authors.initials: G
authors.lastname: Schilcher
authors.affiliation: Department of Internal Medicine, Clinical Division of Gastroenterology and Hepatology, Medical University of Graz, Graz, Austria.
authors.forename: Vanessa
authors.initials: V
authors.lastname: Stadlbauer
authors.affiliation: Department of Internal Medicine, Clinical Division of Nephrology, Medical University of Graz, Graz, Austria.
authors.forename: Jörg H
authors.initials: JH
authors.lastname: Horina
authors.affiliation: Department of Internal Medicine, Clinical Division of Nephrology, Medical University of Graz, Graz, Austria.
authors.forename: Alexander R
authors.initials: AR
authors.lastname: Rosenkranz
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001775:Blood Circulation; D048909:Diabetes Complications / Q000503:physiopathology* / Q000628:therapy*; D005260:Female; D017583:Hemodiafiltration / Q000009:adverse effects*; D006439:Hemodynamics; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000009:adverse effects*; D014661:Vasoconstriction