Hypertension Journal

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Secondary Causes of Hypertension: Illustrative Cases
  JOHTN
SECONDARY HYPERTENSION
Secondary Causes of Hypertension: Illustrative Cases
Sreenivas K Arramraju
Chief
Department of Cardiology, Citizens Hospital, HyderabadTelangana, India
Correspondence Author: Sreenivas K Arramraju, ChiefDepartment of Cardiology, Citizens Hospital, HyderabadTelangana, India
Phone: +919848046785
e-mail: arramraj@yahoo.com
 
ABSTRACT
Secondary hypertension is defined as increased systemic bloodpressure due to an identifiable cause. The incidence of secondaryhypertension varies from 5 to 10%. The most commonetiology of secondary hypertension is due to renovascularcauses. In this article, we briefly discuss as to when and howto suspect this pathology and give two illustrative real-worldcase examples with follow-up.
Keywords: Renal artery stenosis, Renovascular hypertension,Secondary hypertension.
How to cite this article: Arramraju SK. Secondary Causes ofHypertension: Illustrative Cases. Hypertens J 2017;3(1):20-22.
Source of support: Nil
Conflict of interest: None
 
 

INTRODUCTION

The most common cause of secondary hypertension isrenovascular hypertension.1 We briefly present to youwhen and how to suspect this pathology and give twoillustrative real-world case examples with follow-up.This we feel will help us to understand the importanceof proper evaluation, management of the condition, andalso highlight the role of interventional management inpreventing the progression of disease and onset of endstagerenal disease (ESRD) in young patients.

The commonest causes of renovascular hypertensionare:
Etiology:
  • Nonspecific aortoarteritis
  • Atherosclerosis
  • Fibromuscular dysplasia
  • Other - aortic/renal dissection, Thrombotic/cholesterolemboli, neurofibromatosis, posttransplantstenosis, postradiation stenosis.Renovascular hypertension should be suspected bythe following history and examination signs:History:
  • Onset of hypertension age < 30 years or >55 years

 
  • Sudden-onset uncontrolled hypertension in previouslywell-controlled patient
  • Accelerated/malignant hypertension
  • Intermittent pulmonary edema with normal left ventricular(LV) function.Physical examination/lab investigation:
  • Epigastric bruit, particularly systolic/diastolic
  • Azotemia induced by angiotensin-converting enzymeinhibitors (ACEI).
  • Unilateral small kidney.
Renovascular hypertension - Clinical
  • History
  • Onset hypertension age < 30 or >55 years
  • Sudden-onset uncontrolled hypertension in previouslywell-controlled patient
  • Accelerated/malignant hypertension
  • Intermittent pulmonary edema with normal LVfunction
Physical examination/lab investigation
  • Epigastric bruit, particular systolic/diastolic
  • Azotemia induced by ACEI
  • Unilateral small kidney
The two most common pathologies which are mostcommon are:
Atherosclerotic renal artery stenosis (RAS)
  • 75 to 90% of RAS
  • Usually men, age >55 years, other atheroscleroticdisease
  • Progression of stenosis is 51% at 5 years, 3 to 16% toocclusion, with renal atrophy noted in 21% of RASlesions >60%
  • End-stage renal disease in 11% (higher risk if >60%baseline renal insufficiency, systemic blood pressure(SBP) > 160)
Treatment
  • Percutaneous transluminal renal angioplasty (PTRA)success 60 to 80% with restenosis 10 to 47%
  • Stent success 94 to 100% with restenosis 11 to 23%(1 year)
  • "Cure" of renovascular hypertension < 30 %
Fibromuscular Dysplasia
  • 10 to 25% of all RAS
  • Young female, aged 15 to 40 years
  • 90% is medial disease often involves distal renalarteries
  • 30% progressively worsen but total occlusion is rare

 
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Secondary Causes of Hypertension: Illustrative Cases

Treatment - Percutaneous Transluminal
Renal Angioplasty
  • Successful in 82 to 100% of patients
  • Restenosis in 5 to 11%
  • "Cure" of hypertension in 60%

Case Example 1 - Case of Fibromuscular Dysplasia

A 19-year-old female presented with a history of headacheand giddiness of 2 weeks duration. She had a bloodpressure (BP) of 180/120 mm Hg without any significantdifference in all four limbs. Her pulse rate was 85/minute.Systemic examination was normal but for an abdominalbruit. Ultrasound abdomen revealed contracted kidneyon right with suspicion of left RAS. Her baseline creatininewas 1.5 gm/dL. Her angiogram revealed small contractednonright kidney with tight RAS in distal portionof her left renal artery (Fig. 1). She was planned for leftPTRA and stenting. A 6 × 18 mm Palmaz Stuart stent wasdeployed (Fig. 2). She had a 20% residual stenosis in spiteof high-pressure postdilatation. Her renal parameters improved - serum creatinine (S. creatinine) decreasedto 0.9 mg/dL and her BP was 120/80 mm Hg only with2.5 mg Nebivolol. She was also given dual antiplateletdrugs (aspirin 150 mg once daily and clopidogrel 75 mgtwice daily initially for 6 weeks which was later decreasedto once daily) along with atorvastatin 40 mg per day.

Secondary Causes of Hypertension: Illustrative Cases
Fig. 1: Renal angiogram of left renal artery showing criticalstenosis

Secondary Causes of Hypertension: Illustrative Cases
Fig. 3: Renal angiogram showing restenosis of left renal arterystent (2016)

 
She was doing well till September 2016, when sheagain started developing higher BP with worsening of S.creatinine to 1.5 mg/dL. She was suspected to have developedrestenosis in the stent and was taken up for repeatrenal angiography which revealed a tight stenosis againwithin the stent at the site of original lesion (Fig. 3). Thistime (October 2016) she was stented with drug-elutingstent - Promus Element 4 × 15 mm stent was postdilatedwith 5 mm NC balloon (Fig. 4). Her S. creatinine againimproved and BP control is better with two drugs.

Case Example 2 - Atherosclerotic RAS

A 65-year-old man was admitted with complaints ofsudden-onset chest pain, breathlessness, and sweating of 1 day duration. He also had recent history of bilateralleg swelling.

Secondary Causes of Hypertension: Illustrative Cases
Fig. 2: Renal angiogram postrenal angioplasty and stenting ofleft renal artery (2013)

Secondary Causes of Hypertension: Illustrative Cases
Fig. 4: Renal angiogram postrenal angioplasty and stenting ofleft renal artery stent restenosis

Hypertension Journal, January-March, Vol 3, 2017 21

Sreenivas K Arramraju

Secondary Causes of Hypertension: Illustrative Cases
Fig. 5: Renal angiogram showing atherosclerotic right renalartery stenosis

He was hypertensive and diabetic. He also had ahistory of coronary artery disease and had undergonepercutaneous coronary intervention in 1999 and 2007 andcoronary artery bypass grafting in 2008. On examination,patient was conscious, alert, and well-oriented afebrile, hehad bilateral pedal edema. His pulse rate was 74/minuteand BP was 200/90 mm Hg. Investigations revealed araised creatinine (1.99 mg/dL). His two-dimensionalechocardiogram revealed moderate LV dysfunction. Hiscath study revealed patent grafts but both renal arterieshad critical stenosis (Fig. 5) with left-sided contracted kidney. He was subjected to right renal artery stentingwith 6 × 18 mm stent. Poststenting, the renal perfusionimproved with no residual stenosis (Fig. 6) and S. creatinineimproved to 1.2 mg/dL after 3 days and BP wasbetter controlled with two drugs.
 
Secondary Causes of Hypertension: Illustrative Cases
Fig. 6: Renal angiogram postrenal angioplasty and stenting ofright renal artery

REFERENCE
  1. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A,Bohm M, Christiaens T, Cifkova R, De Backer G, Dominiczak A,et al. 2013 ESH/ESC guidelines for the management of arterialhypertension: the Task Force for the Management of ArterialHypertension of the European Society of Hypertension (ESH)and of the European Society of Cardiology (ESC). Eur HeartJ 2013 Jul;34(28):2159-2219.

 
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