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Maria Alejandra Ramos Guifarro, Endocrinology – Chief of Endocrinology, Hospital Escuela Universitario

Daniel Andrés Guifarro Rivera, Medical Student – Medical Student, Universidad Nacional Autónoma de Honduras

Luis Fernando Guifarro Rivera, MD – Medical Doctor, Universidad Nacional Autónoma de Honduras

Carlos Rivera


Objective :

Primary hyperaldosteronism is a renin-independent cause of increase in aldosterone secretion; it is due to an aldosterone-producing adenoma in approximately 30-40% of the cases. Polycystic kidney disease is a multisystemic disorder caused by the formation of cysts in the kidneys, that can lead to renal replacement therapy in up to 50% of patients. The therapeutical approach of patients with coexistence of both disorders is under debate.
We present the case of a 43-year-old male,known for poorly responsive hypertension;treated with irbersartan who developed severe lower limb weakness during a flight from Tegucigalpa to Tokyo,progressing to lower limb paresia and he was unable to walk out of the plane at arrival. He was transferred to a hospital,where he was found to have reduced muscle tone and strength,laboratory tests reported hypokalemia and elevated levels of aldosterone. An abdominal CT described a right adrenal gland mass, that measured 20.7x23.3x25.8mm, with well defined borders,no calcifications and adrenal washout of 56% suggestive of an adenoma.

Methods : n/a

Results : n/a

Discussion :

Probable primary hyperaldosteronism was diagnosed, he was started on amlodipine, eplerenone and oral potassium supplement; and advised to complete follow up back home. He was evaluated in our Endocrinology outpatient clinic; followup reported in urine: renin: 32.9ng/L (2.6-27.7), adrenaline: 1.06ug/L (<120), noradrenaline: 20.4ug/L (<105), metanephrine: 72ug/L (<300), normetanephrine: 181ug/L (<400); and in plasma: aldosterone: 640ng/L (22.1-353), renine: 32.9ng/L (2.6-27.4), aldosterone/renine ratio: 19.48 (<2), metanephrines and normetanephrines were normal. A surgical consult was performed and a right side adrenalectomy was planned; but his pre-operatory CT showed an additional mass in the left adrenal gland, suggestive of an adenoma and severe polycystic kidney disease.Serum creatinine was 2.2mg/dl at the time,GFR:38.95 ml/min/1.73m2. On followup by Endocrinology the patient´s blood pressure was found adequately controlled with no weakness and improved potassium levels; after reviewing available literature on the conservative medical treatment of adrenal tumors in patients with coexistant polycystic kidney disease we decided to keep him on spironolactone 25mg per day. At his serum creatinine is 1.4mg/dl, serum potassium: 5.17meq/L and has normal BP findings. 

Conclusion :

The therapeutical approach of patients with coexistence between polycystic kidney disease and adrenal tumors is debatable with reported cases of deterioration of kidney function after adrenal surgery. Our patient was managed conservatively with medical treatment,and has had an adequate response 6 months after.

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