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 Table of Contents  
Year : 2017  |  Volume : 5  |  Issue : 1  |  Page : 89-91

Accelerated hypertension: Treatable yet underdiagnosed

Department of Medicine, Maulana Azad Medical College, New Delhi, India

Date of Web Publication16-Jun-2017

Correspondence Address:
Pranav Ish
B1, 1st Floor, Green Park Extension, New Delhi - 110 016
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/amhs.amhs_95_16

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Patients who present in young age with accelerated hypertension (HTN) should always be evaluated for secondary causes of hypertension. Renal parenchyma and vascular diseases constitute the majority of the etiology. Other causes include endocrine diseases such as pheochromocytoma, pregnancy-related HTN, and sleep apnea. We report a 23-year-old female who presented with palpitations and headache under treatment for anxiety from a tertiary care hospital. She was found to have accelerated HTN and was thoroughly worked up for etiology and treatment.

Keywords: Etiology, hypertension, magnetic resonance angiography

How to cite this article:
Ish P, Singh H, Anuradha S, Dewan R. Accelerated hypertension: Treatable yet underdiagnosed. Arch Med Health Sci 2017;5:89-91

How to cite this URL:
Ish P, Singh H, Anuradha S, Dewan R. Accelerated hypertension: Treatable yet underdiagnosed. Arch Med Health Sci [serial online] 2017 [cited 2022 Nov 30];5:89-91. Available from: https://www.amhsjournal.org/text.asp?2017/5/1/89/208212

  Introduction Top

Secondary causes of accelerated hypertension (HTN) include renal parenchymal causes such as chronic glomerulonephritis, renal vascular causes such as renal artery stenosis (RAS), endocrine causes such as hyperthyroidism and pheochromocytoma, and pregnancy-related causes such as preeclampsia and eclampsia. Renal causes are the most common and should be sought for all cases of suspected secondary HTN. Ultrasonography (USG) provides details of kidney architecture and size. Unequal size of kidneys can be associated with RAS which is generally confirmed by Doppler studies or angiography. We present the case of secondary HTN in a 23-year-old female who was diagnosed to have bilateral RAS and review the literature.

  Case Report Top

A 23-year-old female resident of Delhi presented to the Medicine Emergency with complaints of episodic headache and palpitations for 2 months which was worsened for 4 days.

Patient was following up in a tertiary care hospital as a case of anxiety disorder not relieved on medications. Patient complained of having episodes of palpitations and headache lasting from 30 min to 2–3 h. It was not associated with any blurring of vision, nausea, vomiting, or flashes of light. There was no history of loss of consciousness or exertional dyspnea; no complaints of chest pain, syncope, and no sensory or motor deficit. There was no history of lower extremity weakness or claudication. Patient had no history of any substance abuse.

On examination, the patient was conscious and oriented to time, place, and person with Glasgow Coma Scale score of 15. She was thin built, dehydrated, and afebrile. Her pulse rate was – 98/min regular, blood pressure (BP) was – 210/118 mmHg in all four limbs, and her respiratory rate was 16 breaths/min. Pallor was present, and there was no cyanosis, icterus, or clubbing, her jugular venous pressure was not raised, and there were no dilated veins in the neck.

Central nervous system examination was essentially normal with fundus examination suggestive of hypertensive retinopathy. Rest of the physical examination was unremarkable. The investigations of the patient are summarized in [Table 1].
Table 1: Emergency room investigations

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The patient was started on injection furosemide 60 mg and tablet amlodipine 10 mg. However, she was subsequently started on nitroglycerin infusion for HTN control. A strict watch on hydration status, BP, and urine output was done. The patient improved symptomatically and was admitted as a case of accelerated HTN to be evaluated for etiology. Patient electrocardiogram showed left axis deviation and two-dimensional echo revealed moderate concentric left ventricular hypertrophy with ejection fraction of 50% and mild left ventricular dysfunction. Urine for active sediments was showing inactive sediment and no evidence of hematuria. USG abdomen revealed right kidney – 8.2 cm × 2.4 cm and left kidney – 8.2 cm × 3.3 cm with a bilateral increase in echogenicity and no suprarenal abnormality seen. Serum thyroid-stimulating hormone was 0.545 min/ml and 24 h urinary metanephrines was normal. Doppler USG bilateral renal artery was reported normal.

Patient was kept on amlodipine 10 mg and enalapril 5 mg in ward. However, during the course of hospital stay, patient's kidney function tests worsened while being on angiotensin-converting enzyme (ACE) inhibitors and patient developed hypotension when she was given diuretics [Laboratory reports in [Table 2]. Patient's BP fluctuated from 90 systolic to 200 despite multiple dose adjustments and with different drug combinations.
Table 2: Follow-up investigations

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On the basis of strong clinical suspicion (young age, deterioration of kidney function tests (KFT) on ACE inhibitors, and other investigations being normal), magnetic resonance angiography (MRA) of the renal arteries (RAs) was done which confirmed the diagnosis of bilateral RAS [Figure 1],[Figure 2],[Figure 3]. The bilateral RAs were visualized only in the proximal part with attenuation of mid and distal segments, and USG correlation revealed right kidney – 7.2 cm × 3.8 cm and left kidney measured 7.4 cm × 3.6 cm with increased cortical echogenicity.
Figure 1: Magnetic resonance angiography of aorta showing attenuation of bilateral renal arteries with normal other branches of abdominal aorta

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Figure 2: Magnetic resonance angiography of aorta showing normal branches with attenuation of mid and distal part of renal arteries

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Figure 3: Magnetic resonance angiography of aorta showing bilateral renal artery stenosis

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Thus, a final diagnosis of bilateral RAS with accelerated HTN with nephropathy was made with etiology being fibromuscular dysplasia (FMD); perimedial fibroplasia as the ostia of the RAs were not visible in the magnetic resonance imaging (MRI) angiography.

  Discussion Top

RAS is a disease of the large extra-renal arterial vessels, most commonly caused by atherosclerotic obstructions. Arterial HTN, progressive renal failure, flash pulmonary edema, and multivessel coronary disease are clinical manifestations of RAS requiring intervention and treatment. In the past, RAS was underrecognized, underdiagnosed, and undertreated. With improved noninvasive imaging techniques such as MRI angiography, computed tomography (CT) angiography, and high-resolution renal duplex sonography, the diagnosis is currently more frequently established.[1]

While captopril renography was used in the past, Doppler ultrasound (US) of the RAs, angio-CT, or MRA has replaced other modalities, and they are now considered the screening tests of choice. An arteriogram is rarely needed for diagnostic purposes only. Color-Doppler US (CDUS) is a noninvasive, repeatable, inexpensive diagnostic procedure which can accurately screen for renovascular diseases but needs to be performed by an expert. However, when a discrepancy exists between clinical data and the results of Doppler US, additional tests are mandatory, like MRA, which is as safe though slightly more expensive test.[2]

Contrast-enhanced US has recently added new possibilities to CDUS in the detection or RAS as it improves visualization of the main RAs and accessory vessels and reduces the number of equivocal examinations. Main indications include cases where Doppler trace is difficult to obtain because of the overlying tissues, calcifications, or weakness of the signal. Missouris et al.[3] showed that renal duplex scanning using contrast enhancement produces more reproducible spectral waveforms, improves accuracy, and reduces the time needed for the examination. However, MRA remains the gold standard and is especially useful for the final word and in diagnostic dilemmas.

Atherosclerosis accounts for approximately 90% of cases with RAS and most commonly involves the origin and the proximal third of the main renal artery. Other causes include FMD which constitutes nearly 10% and rarer causes such as aortorenal dissection, vasculitis involving the renal artery (i.e., polyarteritis nodosa), arteriovenous malformations involving the renal artery, irradiation of the renal artery, and scleroderma.

FMD was first described in 1938 by Leadbetter and Burkland, and it was later classified pathologically by Harrison and MacKormack in 1971 into:

  • Medial fibroplasia (90%) which has classic “string of beads” appearance involving middle-to-distal portion of the artery
  • Perimedial fibroplasia (5%–10%) which has focal stenoses–ostium/trunk or bifurcation of RAs
  • Intimal/medial fibroplasia (10%) which has a focal, concentric stenosis or long tubular lesion.[4]

FMD has a strong predilection for young women, being 8 times more common in females, is frequently bilateral, nonatherosclerotic, noninflammatory involving the renal, carotid, and vertebral arteries and may have a genetic predisposition. In contrast with the management of patients with atherosclerotic RAS, the treatment of renal FMD is far more certain with percutaneous transluminal renal angioplasty (PTRA) being the intervention of choice.

Thus, in our patient, a diagnosis of FMD-related RAS causing accelerated HTN was made, and the patient underwent successful PTRA.

This case highlights the importance of the following facts:

  • Any young patient or any older patient with sudden loss of control of BP should be evaluated for secondary causes of HTN
  • Even if Doppler studies are normal and if strong clinical suspicion is present, then further imaging evaluation of the patient should be done
  • FMD–PTRA is effective, has a low recurrence, should be picked early to prevent cardiac and renal complications, and hence the treatment of choice.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Simon JF. Stenting atherosclerotic renal arteries: Time to be less aggressive. Cleve Clin J Med 2010;77:178-89.  Back to cited text no. 1
Granata A, Fiorini F, Andrulli S, Logias F, Gallieni M, Romano G, et al. Doppler ultrasound and renal artery stenosis: An overview. J Ultrasound 2009;12:133-43.  Back to cited text no. 2
Missouris CG, Allen CM, Balen FG, Buckenham T, Lees WR, MacGregor GA. Non-invasive screening for renal artery stenosis with ultrasound contrast enhancement. J Hypertens 1996;14:519-24.  Back to cited text no. 3
Chrysant SG, Chrysant GS. Treatment of hypertension in patients with renal artery stenosis due to fibromuscular dysplasia of the renal arteries. Cardiovasc Diagn Ther 2014;4:36-43.  Back to cited text no. 4


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2]


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