An atypical clinical presentation of renovascular hypertension

1. IntroductionRenovascular hypertension is one of the most common forms ofsecondary hypertension, and its prevalence is estimated between 1and 5% in the general hypertensive population [1]. Amongst theseconditions, renal artery stenosis (RAS), defined as N50% stenosis of therenalarterylumen,representsoneoftheleadingcausesofrenovascularhypertension.Itisfrequentlyrelatedtothepresenceofrenalatheroscle-rosis (predominantly in elderly individuals), fibro-muscular dysplasia(FMD) and arteritis (more often in young women). Compared to otherclinical conditions, FMD shows different aetiology, as well as differentclinical presentation, prognosis and therapeutic options [2].We describe here an atypical clinical presentation of RAS due toFMD occurred in a young otherwise healthy woman, then analysingthe diagnostic and therapeutic work-out.2. Clinical case reportA 46-year-old woman had an acute hospital admission for 3-dayworsening dyspnoea on mild efforts (New York Health Association[NYHA] classes II–III) and dry cough by 3 weeks. In her medical historysmokinghabit,familyhistoryforcoronaryarterydiseaseandoccasionalepisodes of severe and pulsing headache, resolved with non-steroidalanti-inflammatory drug assumption (indomethacin), were reported.AttheadmissiontoEmergencyDepartment,thephysicalexaminationshowed a normal female phenotype with gallop rhythm, no detectableheart or vascular (including abdominal) bruits, and pulsating peripheralarteries. Slight swelling jugular and ankle oedema with decreasedbreath sounds at the bilateral lung bases were also described. Clinicblood pressure (BP) levels were 185/100 mm Hg, and heart rate was92bpm.The12-leadelectrocardiogramshowedasinusrhythm,biatrialenlargement signs and left ventricular hypertrophy, according toCornellvoltagecriteria(Fig.1).ThechestX-rayshowedbilateralpleuraleffusions and partial atelectasis of the lower lobes. Echocardiographicexamination confirmed the presence of concentric left ventricle hyper-trophy (left ventricular mass indexed for height^2.7 80.98 g/m^2.7,relative wall thickness 0.54), biatrial enlargement, mild reduction ofleft ventricular ejection fraction reduction (45%), and restrictive fillingat transvalvular Doppler assessment (E/A ratio 2.07). Moderate mitraland mild tricuspid regurgitations with slight increase of pulmonaryarterypressure,mildpericardialeffusionandanenlargementofinferiorvena cava, that was partially collapsible during inspiration, were alsodescribed.Haematological tests reported a slight hypokalaemia (2.9 mmol/l)with creatinine value of 1.5 mg/dl and estimated (Cockroft–Gaultformula) glomerular filtration rate (GFR) of 40 ml/min, slight anaemia(12.1 g/dl of haemoglobin) and increased levels of pro-BNP levels(11,886 pg/ml). The urine collection analysis revealed a slight protein-uria (266 mg/24 h). Also, thyroid hormonal profile and autoimmunityscreening with anti-double strand DNA, Anti Nuclear (ANA), andExtractable Nuclear Antigens (ENA) antibodies dosages did not showabnormal values.The patient was initially treated with intravenous infusion ofcentrally-acting alpha2-adrenergic agonist (clonidine) and potassiumsupplement with progressive BP reductions. In addition, antihyperten-sive treatment with angiotensin-converting enzyme inhibitors (ACEIs),beta-blockers (BBs), calcium channel blockers (CCBs), loop diureticsand spironolactone was started and titrated, with further BP reductionswithout achieving effective BP control [3].After admission to the Cardiology Division, sudden worsening ofrenal function (creatinine value of 2.2 mg/dl and estimated GFR of25 ml/min) was observed, paralleled by increased serum potassiumlevels (5.7 mmol/l) and worsened control of clinic BP levels, despiteoptimal antihypertensive therapy. In view of the clinical suspicion ofrenovascular hypertension, antihypertensive therapy was modified, by