2017
DOI: 10.1007/s11255-017-1656-1
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Position-related renal perfusion disturbances as a possible underestimated mechanism in patients with resistant hypertension: a case vignette

Abstract: Position-dependent renal perfusion should be considered in patients with large blood pressure fluctuations and extreme dipping. If morphological imaging shows no abnormalities, functional imaging provides additional information. Further investigation is needed, foremost if nephropexy could improve blood pressure control in some of these patients.

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Cited by 4 publications
(6 citation statements)
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“…Orthostatic hypertension may develop in cases of reduced renal blood flow during standing. This particular condition has been observed in patients with nephroptosis, a clinical entity characterized by increased mobility of the kidneys and defined as significant descend of the kidney (by at least 5 cm or two vertebral bodies on intravenous urography) when standing . Descend of the kidney can cause stretching and torsion of the renal artery, reduction of renal blood flow and, consequently, OHT .…”
Section: Pathophysiologymentioning
confidence: 97%
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“…Orthostatic hypertension may develop in cases of reduced renal blood flow during standing. This particular condition has been observed in patients with nephroptosis, a clinical entity characterized by increased mobility of the kidneys and defined as significant descend of the kidney (by at least 5 cm or two vertebral bodies on intravenous urography) when standing . Descend of the kidney can cause stretching and torsion of the renal artery, reduction of renal blood flow and, consequently, OHT .…”
Section: Pathophysiologymentioning
confidence: 97%
“…This particular condition has been observed in patients with nephroptosis, a clinical entity characterized by increased mobility of the kidneys and defined as significant descend of the kidney (by at least 5 cm or two vertebral bodies on intravenous urography) when standing . Descend of the kidney can cause stretching and torsion of the renal artery, reduction of renal blood flow and, consequently, OHT . Lastly, other, relatively rare, OHT causes that should be suspected in cases of extreme orthostatic BP increase are pheochromocytoma, mast cell activation, and norepinephrine transporter deficiency …”
Section: Pathophysiologymentioning
confidence: 99%
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“…Структурні та/або функціональні порушення ниркової судинної системи, як і при АГ, також можуть зумовлювати патогенетичні механізми ОАГ. Зниження ниркового кровотоку активує РААС, викликаючи вазоконстрикцію, затримку води і солі та підвищення АТ (реноваскулярна АГ, нефроптоз) [7,8,32,34].…”
Section: патогенетичні механізми оагunclassified
“…Наявні дані, що торакальна симпатектомія усунула ОАГ у п'яти пацієнтів, але за рахунок виникнення ОГ після операції [49]. Реваскуляризація нирки може бути терапевтичним варіантом лікування ОАГ у разі супутнього значного стенозу ниркових артерії [50].…”
Section: лікуванняunclassified