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Morning blood pressure surge in early autosomal dominant polycystic kidney disease and its relation with left ventricular hypertrophy

Authors
  • Yildiz, Abdülmecit1
  • Sag, Saim2
  • Gul, Cuma Bulent3
  • Güllülü, Sümeyye2
  • Can, Fatma Ezgi4
  • Bedir, Ömer2
  • Aydin, Mehmet Fethullah1
  • Oruç, Ayşegül1
  • Demirel, Sadettin5
  • Akgür, Suat1
  • Güllülü, Mustafa1
  • Ersoy, Alparslan1
  • 1 Department of Nephrology, Bursa Uludag University Faculty of Medicine, Turkey , (Turkey)
  • 2 Department of Cardiology, Bursa Uludag University Faculty of Medicine, Turkey , (Turkey)
  • 3 Department of Nephrology, Bursa Yuksek Ihtisas Training and Research Hospital, Turkey , (Turkey)
  • 4 Department of Biostatistics, Bursa Uludag University Faculty of Medicine, Turkey , (Turkey)
  • 5 Department of Physiology, Bursa Uludag University Faculty of Medicine, Turkey , (Turkey)
Type
Published Article
Journal
Renal Failure
Publisher
Informa UK (Taylor & Francis)
Publication Date
Jan 21, 2021
Volume
43
Issue
1
Pages
223–230
Identifiers
DOI: 10.1080/0886022X.2020.1864403
PMID: 33478355
PMCID: PMC7833015
Source
PubMed Central
Keywords
License
Green

Abstract

Introduction The activation of the sympathetic nervous system, which usually leads to a swift surge in blood pressure in the morning hours (MBPS) may be the cause of left ventricular hypertrophy (LVH) and endothelial dysfunction (ED) in early autosomal dominant polycystic kidney disease (ADPKD) patients. We studied the association between MBPS and LVH in ADPKD patients with preserved renal functions. Methods Patients with ADPKD with preserved renal functions were enrolled. Prewaking MBPS was calculated using ambulatory blood pressure monitoring. The patients were categorized as MBPS (≥median) and non-MBPS (<median). Left ventricular mass index (LVMI), endothelial-dependent dilatation (FMD, %), and carotid intima-media thickness (CIMT) evaluated. Results Fifty-six patients (30 females and 26 males) were enrolled. Gender distribution was similar-among-the-groups. The mean age was higher in the MBPS group (50.1 ± 13 vs 37.3 ± 10.3). Urinary albumin (49.5 vs 16 mg/g creatinine, p < 0.001), hs-CRP (0.59 vs 0.37 mg/dl, p = 0.045) LVMI (124 ± 27.7 vs 95.2 ± 19.7 g/m2, p < 0.001) and mean awake SBP surge was higher (42 vs 20 mmHg, p < 0.001) and FMD (%) was lower (14.4 ± 6.6 vs 18.9 ± 5.7, p = 0.009) in MBPS group. In the binary logistic regression analysis, the presence of MBPS in model 1 (OR: 6.625, 95% CI [1.048–41.882] p = 0.044), and age in model 2 (OR: 1.160, 95% CI [1.065–1.263] p = 0.001) were the only independent determinant of LVH. Conclusions MBPS seems to be an important and independent determinant of LVH in ADPKD patients with preserved renal functions. It may be worth assessing the effect of reduction in MBPS as a new therapeutic target to prevent LVH in-patients-with-ADPKD.

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