Introduction: T he prevalence of secondary arterial hypertension represents only 5-10% out of the hypertensive population. Therefore, these situations are frequently overlooked, even though the identification of the hypertensions etiology might help delivering a curative treatment.
Objective: To illustrate the necessity of the etiological diagnosis of secondary hypertension, by exemplifying a clinical case from our clinic.
Case presentation: We report the case of a patient, with a diagnosis of arterial hypertension for 20 years, with high blood pressure values at home (SBP 160-260 mmHg), presenting with headache, vertigo, polydipsia, nocturne polyuria, palpitations and 3 syncopes. Clini-cally the patient presented a systolic murmur II/VI in 2^nd right ICS, BP 260/150 mmHg. ECG: sinus rhythm, intermediate axis, LVH with ventricular strain pattern. The echocardiography showed concentric LVH (IVS 23 mm, PWT 19 mm), EF 55%, late relaxation diastolic dysfunction pattern. Blood tests revealed severe hypo-kalemia 1,8 mmol/L and metabolic alkalosis AR 39.7 mmol/L. ABPM revealed a non-Dipper profile; mean SBP 148 mmHg, mean DBP 79,5 mmHg. Taking into consideration the anamnesis, the clinical and paracli-nical status of the patient, we considered the presence of a secondary hypertension. The CT scan revealed the presence of a nodular lesion, 20/14mm, on the medial branch of the right adrenal gland, characteristic for an adenoma. Hormone and metabolites testing showed an aldosterone to renin ration of 27,8, normal cortizol and metanephrine levels, confirming the diagnosis of Conn adenoma. The patient received double antialdosteronic blockade, beta-blockers, calcium blockers, thiazidic diuretic and central antiadrenergic drugs, managing to control the BP values and the serum K levels. Af-ter equilibration of the hydro electrolytic and acid base homeostasis, a right laparoscopic suprarenalectomy. However, the patient retained the high BP values, requiring continuous antihypertensive treatment.
Conclusions: In this case, the identification of the arterial hypertension etiology, was made late, therefore the curative surgical treatment permitted only the control of the hydro electrolytic and acid base balance, with little influence on the control of the BP. The persistence of high BP values, for 20 years, affected the vascular bed, with a persistence of the hypertensive pathology, of the non-Dipper profile, of the LVH and the associa-ted cardio-vascular risks.