Unilateral renal artery stenosis causing hypertensive flash pulmonary oedema

Abstract

Flash pulmonary oedema can occur as a result of multiple triggers that may act independently or in concert. One such precipitating factor is bilateral renal artery stenosis which can be treated either with revascularisation or with medical therapy. Unilateral renal artery stenosis, however, is a rare cause of flash pulmonary oedema, especially when the contralateral kidney is still functional. We describe a case of an elderly woman with a history of heart failure with preserved ejection fraction and multiple hospitalisations for hypertensive crisis and flash pulmonary oedema who was found to have right, ostial renal artery stenosis that was treated with stent placement.

Background

Flash pulmonary oedema is a dramatic form of acute decompensated heart failure that involves rapid retention of fluid following accelerated elevations in left ventricular diastolic filling pressures, leading to respiratory distress.¹ Aetiologies for flash pulmonary oedema include valvular heart disease, myocardial ischaemia, malignant hypertension, cardiomyopathy and renal artery stenosis. In the case of renal artery stenosis, low renal artery perfusion pressure can be a precipitant for flash pulmonary oedema through blood pressure elevation and sodium retention.^{1 2} This process has mostly been described in bilateral rather than unilateral renal artery stenosis. We present a case of a 69-year-old woman with diastolic and renal dysfunction who developed multiple episodes of malignant hypertension and flash pulmonary oedema as a result of right, ostial renal artery stenosis. She was deemed an appropriate candidate for revascularisation and a renal artery stent was placed to prevent further recurrences of flash pulmonary oedema.

Case presentation

A 69-year-old woman with a medical history significant for coronary artery disease with three drug-eluting stents to the right coronary artery, heart failure with preserved ejection fraction, moderate mitral regurgitation, stage IV chronic kidney disease, hypertension and hyperlipidaemia presented to the emergency department with suddenly worsening dyspnoea despite extra doses of her home diuretic. It was associated with orthopnoea, paroxysmal nocturnal dyspnoea and bilateral lower extremity swelling.

On arrival, she had a blood pressure of 195/80 mm Hg, a heart rate of 90 beats/min, a respiratory rate of 26 breaths/min and an oxygen saturation of 98% on bilevel positive airway pressure ventilation. Physical examination demonstrated accessory respiratory muscle use, internal jugular venous distention, coarse crackles in the lung bases bilaterally and pitting oedema in both lower extremities up to the anterior shins. An ECG showed normal sinus rhythm and left ventricular hypertrophy (figure 1). Her labs demonstrated a brain natriuretic peptide of 1280 pg/mL, a troponin of 0.05 ng/mL, a blood urea nitrogen of 10.71 mmol/L and a creatinine of 171 μmol/L which was near her baseline. A chest X-ray showed bilateral pleural effusions with interstitial oedema (figure 2). She was given intravenous bumetanide and admitted to the coronary care unit for acute decompensated heart failure and flash pulmonary oedema in the setting of hypertensive emergency.

Figure 1.

ECG on the day of admission showing normal sinus rhythm and left ventricular hypertrophy.

Figure 2.

Anterior-posterior chest X-ray demonstrating blunting of costophrenic angles, prominent interstitial markings and cephalisation.

Of note, the patient had three previous hospitalisations over the last month with similar presentations. Each time, she was found to be in acute respiratory distress secondary to flash pulmonary oedema due to malignant hypertension. During each admission, she received aggressive diuresis and was discharged on multiple anti-hypertensive agents including dihydropyridine calcium channel blockers, thiazide diuretics and beta-blockers. On this fourth hospitalisation, a right heart catheterisation was performed revealing left and right heart failure with mean right atrial pressure of 14 mm Hg, right ventricular pressure of 52/15 mm Hg, mean pulmonary artery pressure of 37 mm Hg, mean pulmonary capillary wedge pressure of 26 mm Hg and a cardiac index of 3.4 L/min/m². She was treated with a continuous infusion of intravenous nitroglycerin which improved her blood pressure and pulmonary congestion. Euvolemia was achieved using push doses of intravenous bumetanide. The patient’s renal function did progressively worsen and her creatinine went as high as 227 μmol/L with an estimated glomerular filtration rate (eGFR) of 19 mL/min/1.73 m².

Attention was then directed towards identifying the cause of her repeat presentations, as she seemed to be failing her multiagent anti-hypertensive regimen despite ostensibly good medication compliance. A transthoracic echocardiogram demonstrated a left ventricular ejection fraction of approximately 55%, dilated left atrium, mild-to-moderate mitral regurgitation and Doppler findings consistent with a diastolic dysfunction. Given her significant known coronary disease, there was a high degree of suspicion for disease in other vascular beds. A duplex renal ultrasound was then obtained to evaluate for secondary causes of hypertension and flash pulmonary oedema. The left renal artery was patent with no haemodynamically significant stenosis. The right renal artery showed significantly elevated spectral Doppler flow velocities consistent with >60% stenosis of the vessel. Rather than subject the patient to multiple contrast loads with CT angiogram followed by renal angiography, the decision was made to go directly to renal angiography. Access was obtained via the left brachial artery to better facilitate an angle of approach enabling catheter engagement in the right renal artery. An 80% focal, calcific stenosis of the right ostium was visualised and successfully treated with an express SD renal stent (videos 1 and 2).

Video 1.

bcr-2021-244402supp001.mp4 ^{(668.9KB, mp4)}

DOI: 10.1136/bcr-2021-244402.video01

Video 2.

bcr-2021-244402supp002.mp4 ^{(668.9KB, mp4)}

DOI: 10.1136/bcr-2021-244402.video02

Outcome and follow-up

On the day of discharge, the patient was asymptomatic, her blood pressure was better controlled with a systolic ranging in the 140s mm Hg and her renal function improved with a creatinine of 147 μmol/L and an eGFR of 30 mL/min/1.73 m². In the 3 months following her last admission, she did not exhibit any further episodes of dypsnoea nor did she have hospitalisations for flash pulmonary oedema.

Discussion

Renal artery stenosis involves the narrowing of the renal arteries and is predominantly caused by either atherosclerosis or fibromuscular dysplasia. Prevalence of renal artery stenosis ranges from 14% to 42% in patients with peripheral vascular disease.³ Progressive occlusion can lead to complications including treatment-resistant hypertension and ischaemic nephropathy.⁴ An association has also been drawn between renal artery stenosis and flash pulmonary oedema.⁵ The original mechanism proposed for this fluid overload requires the presence of either bilateral renal artery stenosis or renal artery stenosis involving a solitary functioning kidney rather than unilateral renal artery stenosis in bilateral functioning kidneys.

When an occlusion is significant enough to decrease renal perfusion, the juxtaglomerular apparatus responds by secreting renin, thereby activating the renin–angiotensin–aldosterone system (RAAS).² Activation of RAAS leads to arteriole vasoconstriction and sodium retention. If both kidneys are functional, the stimulation of RAAS will occur on the kidney affected by renal artery stenosis. Fluid retention will then follow, resulting in an increase in atrial pressure and a release of natriuretic peptides. The kidney that is unaffected by stenosis will then facilitate natriuresis in order to achieve euvolemia.⁶ When renal artery stenosis occurs bilaterally or with a solitary functioning kidney, the aforementioned compensation mechanism is compromised, thereby leading to accelerated fluid retention and flash pulmonary oedema. This entity was first described in 1988 and though its incidence remains unclear, it is most commonly found in bilateral renal artery stenosis.⁵

This case is unique in that it is one of few to report flash pulmonary oedema triggered by unilateral renal artery stenosis in the setting of a contralateral, functional kidney.^{7 8} In addition to RAAS, there are likely a number of other factors that work together to contribute to this presentation. Long-standing hypertension, which is in part due to RAAS, can cause diastolic dysfunction and impaired left ventricular filling. In turn, changes in end diastolic volume can make a patient more vulnerable to slight fluctuations in volume status. A sudden increase in volume from RAAS activation will cause significant hypertension and increased filling of a non-compliant left ventricle, triggering a surge in end diastolic ventricular pressures leading to flash pulmonary oedema.^{8 9} In addition to diastolic dysfunction, the patient presented in this case did suffer from chronic kidney disease at baseline. When eGFR is reduced, sensitivity to natriuretic peptides is decreased and natriuretic efficiency is diminished.¹⁰ Therefore, unilateral renal artery stenosis with suboptimal renal function may behave similarly to bilateral renal artery stenosis with both causing flash pulmonary oedema.²

In terms of treatment, there has been much debate over the years as to whether revascularisation plus medical therapy confers a benefit in reducing hypertension and progression of chronic kidney disease over medical therapy alone. Indeed, a few studies published in the 1990s and early 2000s indicated that percutaneous transluminal renal angioplasty and stent placement may help improve and possibly even normalise blood pressure.^{11 12} Other uncontrolled studies at around the same time also suggested that stenting may halt the progression of renal dysfunction.^{13 14} These series of studies led to a rapid rise in renal artery stenting during this time period.¹⁵ Subsequently, a number of small randomised controlled trials countered the conclusions made by these previous studies, claiming that there is no significant difference between renal artery angioplasty and medical therapy with respect to changes in blood pressure.^16–18 These studies culminated in the Angioplasty and Stenting for Renal Artery Lesions and the Cardiovascular Outcomes in Renal Atherosclerotic Lesions trials which showed that not only did revascularisation not offer a clinically significant benefit in improving blood pressure or renal function when compared with optimal medical therapy alone, it also did not change clinical outcomes overall, including death from renal or cardiovascular causes.^{19 20}

One significant limitation of these recent studies especially when pertaining to our case is that they did not include patients with acute complications from renal artery stenosis such as acute kidney injury and flash pulmonary oedema.¹⁹ Further studies are required for this specific patient population to determine if patients such as the one presented in this case would benefit from revascularisation over medical therapy alone in order to prevent further hospitalisations and improve mortality.

Learning points.

• Patients with hard-to-control hypertension and recurrent flash pulmonary oedema should be evaluated for renal artery stenosis, especially those with significant vascular disease.

• Flash pulmonary oedema can occur in unilateral renal artery stenosis and concomitant chronic renal insufficiency or diastolic dysfunction may predispose patients to this phenomenon.

• Revascularisation of unilateral renal artery stenosis may be beneficial in lowering blood pressure, improving renal function and preventing recurrent flash pulmonary oedema.

Ethics statements

Patient consent for publication

Obtained.