VALSALVA RETINOPATHY AND OPTIC NERVE DRUSEN IN A PATIENT WITH CYSTIC FIBROSIS

urinary sodium excretion and improved hyponatremia substantially. Thereafter, we administered glucocorticoid therapy (prednisolone, 40 mg/d). During glucocorticoid therapy, the plasma rennin activity and plasma aldosterone concentration increased gradually, and fludrocortisone was discontinued (Figure). Treatment with fludrocortisone acetate ameliorated all of our patient’s symptoms, which demonstrated that hyporeninemic hypoaldosteronism was the cause of her renal salt wasting and hyponatremia. We hypothesized that interstitial changes involved in Sjogren’s syndrome inhibited renin release from the kidney. However, a renal biopsy specimen lacked apparent morphological changes. In this regard, it is of interest that humoral factors inhibit aldosterone production and cause hyperreninemic hypoaldosteronism (5). Although no humoral factors that inhibit renin secretion have been identified, an unidentified factor may have inhibited renin excretion, since glucocorticoid administration successfully increased plasma renin activity and suppressed anti–Sjogren’s syndrome A titers. These findings indicate that Sjogren’s syndrome could cause salt-losing nephropathy, and that glucocorticoid therapy is particularly effective for such a pathological condition. Akira Onozaki, MD Tetsuo Katoh, MD Tsuyoshi Watanabe, MD Department of Medicine III Fukushima Medical University School of Medicine Fukushima, Japan