title: Mechanisms and Treatment of Intradialytic Hypertension.
abstract: BACKGROUND
  Intradialytic hypertension is a condition where there is an increase in blood pressure (BP) from pre- to post-hemodialysis; this condition has been recently identified as an independent mortality risk factor in hypertensive hemodialysis patients. The mechanisms and management of intradialytic hypertension have been explored in numerous research studies over the past few years.
  
  
  CONCLUSIONS
  Patients with intradialytic hypertension have been found to be more chronically volume overloaded compared to other hemodialysis patients, although no causal role has been established. Patients with intradialytic hypertension have intradialytic vascular resistance surges that likely explain the BP increase during dialysis. Acute intradialytic changes in endothelial cell function have been proposed as etiologies for the increase in vascular resistance, although it is unclear if endothelin-1 or some other vasoconstrictive peptide is responsible. There is an association between dialysate to serum sodium gradients and BP increase during dialysis in patients with intradialytic hypertension, although it is unclear if this is related to endothelial cell activity or acute osmolar changes. In addition to probing the dry weight of patients with intradialytic hypertension, other management strategies include lowering dialysate sodium and changing antihypertensives to include carvedilol or other poorly dialyzed antihypertensives.
  
  
  CONCLUSIONS
  Hemodialysis patients with intradialytic hypertension have an increased mortality risk compared to patients with modest decreases in BP during dialysis. Intradialytic hypertension is associated with extracellular volume overload in addition to acute increases in vascular resistance during dialysis. Management strategies should include reevaluation of dry weight and modification of both the dialysate prescription and medication prescription.
authors.affiliation: University of Texas Southwestern Medical Center, Department of Internal Medicine and Division of Nephrology, Dallas, TX, USA.
authors.forename: Peter Noel
authors.initials: PN
authors.lastname: Van Buren
authors.forename: Jula K
authors.initials: JK
authors.lastname: Inrig
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight; D002227:Carbazoles / Q000627:therapeutic use*; D000077261:Carvedilol; D015314:Dialysis Solutions / Q000737:chemistry / Q000627:therapeutic use; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005440:Fluid Therapy / Q000009:adverse effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000209:etiology / Q000401:mortality / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D011412:Propanolamines / Q000627:therapeutic use*; D006435:Renal Dialysis / Q000009:adverse effects*; D012307:Risk Factors; D012964:Sodium / Q000009:adverse effects; D016019:Survival Analysis; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents; D002227:Carbazoles; D015314:Dialysis Solutions; D011412:Propanolamines; D000077261:Carvedilol; D012964:Sodium