FROM ARTERIAL HYPERTENSION TO CHRONIC PERSISTENT HYPOTENSION: IS THE KIDNEY GUILTY?

Abstract

Objective: AA Amyloidosis is rarely known to cause cardiovascular disturbances, and especially blood pressure involvement. Our case reports a rare hypertensive phenotype as the patient experienced a switch from arterial hypertension, necessitating medical treatment, to chronic hypotension as their AA amyloidosis progressed. Design and method: Case report Results: We report the case of a 60-year-old male with background history of uncontrolled arterial hypertension on Losartan since 2017. He suffered a nephrotic syndrome in 2022, which led to the diagnosis of AA Amyloidosis with ulcerative colitis. He was put on Ramipril and aminosalicylates. Ever since then, he presented with low blood pressure, as the systolic BP never surpassing 100 mmHg, whereas it fluctuated above 130mmHg before and even on hypertension drugs. His physical examination showed no anomalies. Ramipril was discontinued, but hypotension persisted until today with symptoms consisting of lightheadedness. All causes for transient hypotension were explored and excluded: Antihypertension drugs were discontinued, all causes of hypovolemia were excluded (dehydration, low water intake, diarrhea, bleeding, chronic vomiting). Adrenal amyloidosis was also excluded. Further cardiovascular assessment with electrocardiography and transthoracic echocardiography showed no abnormalities. An ambulatory BP monitoring showed a mean BP of 100/65mmHg, with rare occurrences of systolic values of 120mmHg. An autonomic nervous system test, using Ewing tests, showed significant vagal hyperactivity, with no sympathetic nervous dysfunction, as well as no postural hypotension. The decision was to increase volemia (high water & salt intake) but with no results. He was put on Fludrocortisone 0,1 mg daily. On follow-up check-up one month later, blood pressure levels improved slightly, with a systolic BP of 110mmHg and no symptoms. Ramipril was reintroduced for primary nephroprotection, which was tolerated with no symptoms. Conclusions: Cardiovascular autonomic anomalies can rarely be seen in AA amyloidosis, and permanent hypotension has not been described before as far as we know. Exclusion of transient hypotension causes is mandatory, and autonomic nervous system testing should be part of the global assessment and strategy.