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Cited by 183Renal and Vascular PathologiesRenin-Angiotensin System StudiesTakotsubo Cardiomyopathy and Associated Phenomena

Flash pulmonary oedema and bilateral renal artery stenosis: the Pickering Syndrome

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Messerli, F. H., Bangalore, S., Makani, H., Rimoldi, S. F., Allemann, Y., White, C. J., Textor, S., Sleight, P.·2011·European Heart Journal
DOI 10.1093/eurheartj/ehr056
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Abstract

In 1988 Pickering et al. reported in the Lancet a series of 11 hypertensive patients with bilateral atheromatous renovascular disease who presented with a history of multiple episodes of pulmonary oedema.1 Seven of these patients had stenosis of both renal arteries and in a subsequent series of 90 patients, pulmonary oedema was significantly more common in patients with bilateral than in those with unilateral renal artery stenosis (RAS).2 Successful revascularization of one or both renal arteries eliminated pulmonary oedema in 77% of patients with bilateral RAS.2 The authors concluded that ‘bilateral RAS may be a specific and treatable predisposing factor to pulmonary oedema in azotemic hypertensive patients'.1 Since the initial observation of this clinical entity 29 case reports,3–31 9 case series,1,32–39 and 10 clinical studies1–2,40–47 of flash pulmonary oedema (FPO) and RAS (both unilateral and bilateral) have been published of which 16 case reports, 2 case series, and 7 clinical studies comprising a total of 87 patients relate to bilateral RAS and FPO. The underlying pathophysiological mechanisms responsible for triggering FPO in patients with bilateral RAS have been delineated in several clinical and experimental studies. Since FPO and bilateral RAS seem to be a unique entity with distinct pathophysiological, clinical, and therapeutic features, we propose to name it Pickering Syndrome. In the following, we review incidence, pathophysiology, clinical findings, and treatment of the Pickering Syndrome. Flash pulmonary oedema is a general term used to describe a particularly dramatic form of acute decompensated heart failure. Regardless of its aetiology, an acute increase of left ventricular (LV) end diastolic pressure is the conditio sine qua non for the development of FPO and remains the common denominator of all clinical situations associated with it. However, what distinguishes FPO from other forms of decompensated heart failure is that because of unique underlying pathophysiological mechanisms, flooding of the alveolar space can occur within minutes resulting in an acute life-threatening emergency.48 Atherosclerotic renal artery disease is increasingly diagnosed and strongly associated with atherosclerotic disease in other vascular beds such as the coronary, carotid, and iliofemoral circulation.49 Renovascular hypertension is the most common secondary cause of hypertension. In 26 studies comprising a total patient population of 30 092 undergoing diagnostic coronary angiography for suspected coronary artery disease the prevalence of RAS >50% averaged 8.0% with a range from 3.1 to 22.9% (Table 1).43,50–74 Of all patients with atherosclerotic RAS, 20.3% had significant bilateral RAS. The prevalence of FPO varies a great deal and seems to depend on the pressure load as well as on the degree of renal impairment. In a series of 56 patients with bilateral RAS, Bloch et al.2 reported a history of FPO before revascularization in 23 (41%) patients. Messina et al.35 reported 17 patients with RAS treated at the University of Michigan Hospital, 16 of who had bilateral disease. Mean blood pressure was 207/110 mmHg and serum creatinine was 3.5 mg/dL. Two-thirds of these patients had FPO despite evidence of normal ventricular function. Overall the weighted prevalence of FPO in patients with RAS was 15.3%. In patients with bilateral RAS the weighted prevalence of FPO was 14.3% compared with 3.5% in those with unilateral RAS. Prevalence of RAS >50% in patients undergoing cardiac catheterization aPrevalence of bilateral RAS as % of all RAS patients. RAS, renal artery stenosis. Prevalence of RAS >50% in patients undergoing cardiac catheterization aPrevalence of bilateral RAS as % of all RAS patients. RAS, renal artery stenosis. Bilateral RAS predisposes patients to develop FPO by three main pathophysiological mechanisms: (i) defective natriuresis; (ii) increased haemodynamic burden and exacerbation of diastolic dysfunction;75 and (iii) failure of the pulmonary capillary blood–gas barrier (Figure 1). The Pickering Syndrome. Three main pathophysiological mechanisms contribute to the development of flash pulmonary oedema: defective pressure natriuresis with sodium and fluid retention, increased left ventricular end-diastolic pressure associated with left ventricular hypertrophy and stiffening, and failure of the pulmonary capillary blood–gas barrier. RAAS, renin–angiotensin–aldosterone system; SNS, sympathetic nervous system; Na+, sodium; AII, angiotensin II; ET-1, endothelin-1; NO, nitric oxide. Experimental studies allow us to clearly delineate differences in pathophysiology between unilateral and bilateral RAS. In patients with unilateral RAS corresponding to the 2-kidney-1-clip hypertension model, stenosis of one renal artery decrease ipsilateral renal perfusion thereby activating the renin–angiotensin–aldosterone cascade and causing sodium and fluid retention.76 Concomitantly, stimulation of the sympathetic nervous sy

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Authors
Messerli, F. H., Bangalore, S., Makani, H., Rimoldi, S. F., Allemann, Y., White, C. J., Textor, S., & Sleight, P.
Affiliations
  • St. Luke's-Roosevelt Hospital Center (US)
  • New York University (US)
  • University Hospital of Bern (CH)
  • Ochsner Medical Center (US)
  • Mayo Clinic (US)
  • John Radcliffe Hospital (GB)
Corresponding author
Messerli, F. H.
ORCID
Venue
European Heart Journal
Publisher
Oxford University Press (OUP)
Published
2011-03-15
Volume
32
Issue
18
Pages
2231-2235
ISSN
  • 0195-668X (ISSN-L)
  • 1522-9645
DOI
10.1093/eurheartj/ehr056
OpenAlex
W2103404937
Cited by
183
References
106
Citations by year
2026: 8 · 2025: 9 · 2024: 8 · 2023: 14 · 2022: 14 · 2021: 10 · 2020: 12 · 2019: 17 · 2018: 7 · 2017: 15 · 2016: 14 · 2015: 12 · 2014: 19 · 2013: 17 · 2012: 6
FWCI
11.70
Type
journal article
Language
en
Open access
Licence
other-oa
Locations
  • European Heart Journal (publishedVersion)
  • PubMed (publishedVersion)
  • BORIS (University Library Bern) (submittedVersion, other-oa)
  • Open Access CRIS of the University of Bern
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Renal and Vascular Pathologies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Takotsubo Cardiomyopathy and Associated Phenomena
Keywords
bilateral renal artery stenosis, renovascular hypertension, acute decompensated heart failure, left ventricular end-diastolic pressure, renal artery revascularization, atherosclerotic renovascular disease, hypertension pathophysiology, renal artery stenosis treatment, renal artery stenting, renal artery angioplasty
MeSH terms
Acute Disease, Diagnosis, Differential, Emergency Treatment, Female, Humans, Male, Middle Aged, Pulmonary Edema, Renal Artery Obstruction, Reperfusion, Hypertrophy, Left Ventricular, Atherosclerosis, Vascular Stiffness, Cardio-Renal Syndrome

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