SAT-466 Hashimoto’s Glomerulonephritis: A Reality or Just a Coincidence?

Background: Glomerulonephritis is a common health problem surrounding nephrologists, mainly characterized by nephrotic range proteinuria, low serum albumin level and edema. There are several causes such as infections, cancer or autoinmune disorders, like Hashimoto’s thyroiditis. This is a chronic inflammation of the thyroid gland caused by high serum thyroid autoantibodies leading to hypothyroidsm. In the last years, many authors worldwide have found an uncommon association between Hashimoto’s disease and nephrotic syndrome. This may be attributed to cross-reacting antigens, such as thyroglublin, that become deposited in the glomeruli. Clinical Case: A 40‐year women was admitted to our hospital with typical symptoms of nephrotic syndrome. The patient has a history of hypothyroidsm two years ago, treated with levothyroxine 200 mcg. Initial tests were congruent with glomerular impairment: low serum albumin 2.8 g/dl (NR > 3.5 g/l), hypercholesterolemia 300 mg/dl, (NR <200 mg/dl) and nephrotic-range proteinuria (9g/24h). Viral infections such as HIV, hepatitis B and C, herpes virus and rubella were discarded. Moreover, autoantibodies such as ANA, ANCAc and ANCAp were studied with no contributory results. Tumor markers were also tested and a complete body CT scan was performed looking for some occult cancer, but nothing contributory was found. Thyroid hormones levels were out of range (TSH: 20.04 mIU/l, NR: 0.27-4.20 mIU/l; FT4: 5 pmol/L, NR: 12-22 pmol/L). ATPO and ATG were performed, which were positive and in several fold higher levels than expected. (ATPO: >600 U/ml, N<34 U/ml; ATG: 195 U/ml, N <115 U/ml) During hospitalization a kidney biopsy was performed. The anatomic pathology report was compatible to membranous glomerulonephritis. Since there was no clear etiology of the nephrotic syndrome, we assumed that Hashimoto’s disease had an important role in this particular case, having already discarded the most common causes. We decided to optimized levothyroxine dose (from 200 mcg qd to 250 mcg qd) and ACE inhibitors (losartan 50 mg qd) were added to the therapeutic plan. During the follow up (one year later), we observed an improvement in thyroid hormone levels (TSH: 0.94 mIU/l, FT4: 14.17 pmol/L) and a decreased in proteinuria (3g/24h); however, ATPO and ATG levels persisted high (ATPO: >600. ATG: 170.6). No immunosuppressive therapy was used at all. Conclusion: This is the first case in our hospital demonstrating the possible association between Hashimoto’s disease and membranous glomerulonephritis. Santoro et al. strongly believe that there is a trully relationship connecting both entities, suggesting that similar imnunological abnormalities ought to be the key point in the pathogenesis of the two conditions. Reference: (1) Santoro, D., Vadalà, C., Siligato, R., Buemi, M., & Benvenga, S. Autoimmune thyroiditis and glomerulopathies. Frontiers in endocrinology, 8, 119. (2017)