Adult-onset Transient Pseudohypoaldosteronism Secondary to Ureteral Cancer: A Case Report

Abstract Background: Pseudohypoaldosteronism (PHA) is a disorder in which patients show resistance to aldosterone, and exhibit aldosterone deficiency-like symptoms despite excessive secretion of aldosterone hormone from the adrenal gland. Secondary PHA (described here as transient PHA), which is characterized by transient aldosterone resistance secondary to other conditions, is usually an infantile disease. We report a rare case of adult-onset transient PHA (TPHA). Case presentation: A 70-year-old man admitted to our hospital, presented with renal failure of unknown cause with hypotension. Normal anion gap (AG) metabolic acidosis with hyperkalemia, an electrolyte abnormality, was also observed. A computed tomography (CT) scan showed bilateral ureteral dilatation and hydronephrosis. Blood renin level was found to be 70.5 ng/mL/h (normal: 2.5–21.4 ng/mL/h) and aldosterone level was 678.2 pg/mL (normal: 36–240 pg/mL). Abnormally high levels of aldosterone suggested aldosterone resistance. Based on the above history, a diagnosis of TPHA was made. Bilateral stenting was performed to improve the hydronephrosis, and the symptoms associated with TPHA resolved immediately after the obstruction was released. Bilateral ureteral carcinoma was found to be the cause of hydronephrosis. Conclusions: Though TPHA is predominantly a pediatric disease, our study shows TPHA can also occur in adults if there is a decrease in the filtration rate in the ureter with concomitant chronic inflammation. Aldosterone resistance and electrolyte abnormalities were quickly resolved as soon as the obstruction was released in the present case. This is the first report to show the changes in the hormone (renin and aldosterone) levels before and after lifting the aldosterone resistance through the release of ureteral obstruction. Thus, in cases of normal AG metabolic acidosis with hyperkalemia, pseudohypoaldosteronism should be considered during differential diagnosis, in addition, to type Ⅳ renal tubular acidosis.