Introduction: Hepatitis B virus infection (HBV) is a major public health problem worldwide, affecting about 400 million people around the world. About 20% of patients with HBV infection have a wide range of extrahepatic damages that include systemic, renal, cardiovascular, cutaneous, cerebral, hematological, immunological abnormalities, etc.

Objective: Highlighting problems in estimating the ca-use of hypertension in a patient with reactivated occult viral hepatitis B, with multiorgan impairment: cardiac, renal, cerebral.

Methods: The clinical case of a 1-year-old patient dia-gnosed with malignant renoparenchymal hypertension possibly induced by reactivated occult viral hepatitis B, with high viremia and extrahepatic impairment (cardiovascular, renal and cerebral) is presented. The patient is hospitalized with clinical manifestati-ons of toxic and infectious syndrome, intestinal transit disorders, abdominal colic, blood pressure (BP) values up to 200/120 mm Hg. In the past, the patient was diagnosed with mixed tubulointerstitial nephritis, but with preserved renal function, hypertensive syndrome and acute myocarditis manifested with impaired pump function of the left ventricular myocardium. Following the investigations, it was estimated that the patient had iron deficiency anemia grade II, leukocytosis with neu-trophilia, thrombocytosis, increased acute phase reac-tants, hypoproteinemia, hypoalbuminemia, hypocalcemia, slightly elevated transaminases. In urine – leuko-cyturia, cylindruria, erythrocyte, proteinuria, hypocal-ciuria, hyponatriuria. Echocardiographic examination revealed conclusive signs of cardiac remodeling on an idemn heart – slightly dilated left ventricular (LV) ca-vity, hypokinesia and mild hypertrophy of the interventricular septum, low LV myocardial pump function. The selective aortography excluded the renovascular cause of hypertension. The magnetic resonance ima-ging reveals suspicious imaging signs for inflammatory changes in the bilateral renal parenchyma, more pro-nounced on the right and diffuse abdominal lymphadenopathy. The laboratory examination shows marked hepatocytolysis syndrome and high viremia expressed by quantitative HBV DNA with extremely high values. In evolution, against the background of antihypertensive, nephro- and hepatoprotective treatment, the BP values and renal function are normalized, the hepato-cytolysis syndrome and HBV viremia persist.

Conclusions: The clinical case presented highlights the complexity and severity of cardiac and renal lesions of-ten uncorrelated with the symptoms at the time of hospitalization. The multidisciplinary approach allowed the identification of the possible cause of hypertension and inflammatory changes in the bilateral renal parenchyma, premise for starting antiviral therapy.