title: Excessive fall of blood pressure during maintenance hemodialysis in patients with chronic renal failure is induced by vascular malfunction and imbalance of autonomic nervous activity.
abstract: Acute hypotension during maintenance hemodialysis (HD) is not only a critical complication, but also an independent risk factor for mortality in patients with chronic renal failure (CRF). This study was designed to clarify the mechanisms underlying excessive fall of blood pressure during HD. Fifty-six CRF patients with HD thrice a week were divided into two groups according to the intradialytic hypotension episodes after 4 weeks of the observation period; the hypotension group, showing four or more episodes of intradialytic hypotension, and the non-hypotension group, showing three episodes of intradialytic hypotension or less. The intradialytic hypotension was defined as a fall of ≥30 mm Hg in the systolic blood pressure during HD. The brachial-ankle pulse wave velocity (ba-PWV), serum high-sensitivity (hs)-CRP, reactive oxygen species (ROS) generation, and serum malondialdehyde-modified LDL (MDA-LDL) were measured before HD. The high- frequency (HF) and low-frequency components (LF) of the heart rate variability and entropy were analyzed by the maximal entropy method. The ba-PWV, hs-CRP, ROS generation, and MDA-LDL were significantly higher in the hypotension group than in the non-hypotension group. HF, LF/HF, and entropy during HD increased significantly in the non-hypotension group, while entropy during HD decreased significantly in the hypotension group as compared with the baseline. LF/HF and entropy during HD were significantly lower in the hypotension group than in the non-hypotension group. These findings suggest that the major factors causing excessive fall of blood pressure during HD in patients with CRF might be vascular malfunction and imbalance of autonomic nervous activity.
authors.affiliation: Department of Angiology and Cardiology, Kitasato University Graduate School of Medical Sciences, Kanagawa, Japan.
authors.forename: Kazuya
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Kobayashi
authors.forename: Toshiki
authors.initials: T
authors.lastname: Kutsuna
authors.forename: Akira
authors.initials: A
authors.lastname: Ishii
authors.forename: Takuya
authors.initials: T
authors.lastname: Matsumoto
authors.forename: Miyako
authors.initials: M
authors.lastname: Hara
authors.forename: Naoko
authors.initials: N
authors.lastname: Aiba
authors.forename: Minoru
authors.initials: M
authors.lastname: Tabata
authors.forename: Naonobu
authors.initials: N
authors.lastname: Takahira
authors.forename: Takashi
authors.initials: T
authors.lastname: Masuda
mesh_terms: D000704:Analysis of Variance; D001341:Autonomic Nervous System / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006017:Glycolipids / Q000378:metabolism; D006801:Humans; D007022:Hypotension / Q000209:etiology* / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy*; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D009043:Motor Activity; D018384:Oxidative Stress; D006435:Renal Dialysis / Q000009:adverse effects*; D059289:Vascular Stiffness; D014882:Water-Electrolyte Balance
chemical_list: D015415:Biomarkers; D006017:Glycolipids