Introduction: The etiology of arterial hypertension (AH) is only found in 5-10% of patients, the renovascular cause being the most common, with a prevalence of 1-5% of the total of hypertensives. Renovascular AH (RVAH) is due to renal hypoperfusion, usually by renal artery stenosis (RAS) and activation of the renin-angiotensin system. The most common cause of RAS is atherosclerosis, and at younger age, predominantly under 40 years and females, another etiology is fibromuscular dysplasia. The optimal therapeutic management in RVAH is medical because the clinical trials achieved so far have not demonstrated a real benefit of revascularization. Renal revascularization can be considered in patients with anatomically and functionally significat RAS.
Case presentation: We present the case of a 42 years old man, smoker with a history of AH, without chronic treatment, directed to our clinic from a territorial hospital where he addressed for a constrictive chest pain, for the first time in his life, which occured at a normal effort and passed in 30 minutes. ECG was showing left ventricular hypertrophy (LVH) and ST segment elevation up to 4 mm in V1-V3 and TnI=0.081 ng/ml. At the clinic presentation the patient was stable haemodynamic, without pain, TA=190/110 mmHg, symmetrical bilateral pulses. Biological: hypercholesterolemia, hypokalemia (K=2.6 mEq/L), nitrate retention syndrome, moderate proteinuria. ECG: sinus rhythm, 92/ min, intermediate QRS axis, LVH with secondary re-polarization changes. Transthoracic echocardiography showed slightly dilated cardiac cavities, predominantly septal light diffuse hypokinesia, LVH (IVS=14 mm, LVPW=14 mm), EF=45%, diastolic dysfunction type
1.A coronarography was performed that targeted normal epicardial coronary arteries and, because of AH, hypokalemia and nitrate retention syndrome, an angiography of renal artery (RA) was also performed, that showed chronic occlusion of the left RA. Antihypertensive and recovery hypokalemia therapy was initia-ted. After that an 24 –hour ambulatory blood pressure (BP) monitoring was made which showed average BP by day=143/92 mmHg and by night=132/94mmHg, nondipper profile. Abdominal ultrasound revealed normal-size kidneys, adrenal glands without tumor formations, liver steatosis. The nephrologic exam excluded a nephrotic syndrome. With the optimization of treatment, resulted a good control of the BP values and the renal function of the patient remained stationary.
Conclusions: In our patient the antihypertensive medication demonstrated therapeutic efficacy, but given the long-term evolution, SAH by chronic kidney artery occlusion is an interdisciplinary challenge. This is the reason for which, a medical-surgical team has been es-tablishe, who has decided the technical impossibility of the interventional or surgical revascularization. The remaining solution is nephrectomy in case of AH that become resistant on medication or worsening of the renal function.