SUN-067 Severe acute hyponatraemia in a patient with Sjogren's syndrome

Abstract

Sjogren's syndrome is an auto-immune rheumatological condition associated with joint pains, dry eyes and mouth. It has previously been associated with syndrome of inappropriate anti-diuretic hormone (SIADH) (de Villiers, Willem & Klemp, P., 1991) and with hyporeninaemic hypoaldosteronism (Onozaki, Akira et al.) as potential causes of hyponatraemia, however the literature is sparse. Sjogren's syndrome is associated with other renal diseases diagnosed on biopsy such as renal tubular acidosis, glomerulonephritis and interstitial nephritis. This case explores a patient with a more severe episode of hyponatraemia in the context of background renal salt wasting and strong immunological and clinical evidence of Sjogren's syndrome. The information from this case report was gathered retrospectively from the patient's case notes and test results with their explicit consent. The patient was admitted under the medical team generally unwell with acute confusion in July of 2018. They were normally completely well, only taking lansoprazole (a proton pump inhibitor) and ramipril (an angiotensin converting enzyme inhibitor (ACE-I)) for hypertension. They were found to have a serum sodium of 109mmol/l and were given 2.7% sodium chloride intravenously. Renal function, measured with creatinine, was stable at the patient's baseline throughout the admission. The patient was then taken to an intensive care setting and further tests showed a urinary sodium of 64 mmol/l, a urinary osmolality of 476 and serum osmolality of 237 mosm/kg H20. This was felt to be due to renal salt wasting or potentially SIADH. There were no suspicious lung lesions on x-ray imaging despite the patient being an active smoker. The patient improved clinically and biochemically with fluid restriction to 1.5L daily and sodium rose to 131mmol/l over 6 days of this management. Cortisol was in the normal range and urinary sodium fell to 24mmol/l. The patient had been complaining of joint pains and dry mouth and eyes from before admission and further outpatient tests showed positive anti-CCP antibodies, strong positive to anti-Ro and anti-La antibodies and increased IgG. They were seen by rheumatology in the next 9 months who diagnosed Sjogren's syndrome with palindromic rheumatism of the hand joints. Tests in October 2019 show a persistently low serum sodium at 129mmol/l and a urinary sodium of 71mmol/l. Serum osmolality is now normal at 278 mosm/kg H20 and osmolality of urine is 553 mmol/kg. Renin and aldosterone levels are now normal. The patient is now clinically well with no symptoms of hyponatraemia and is not on any specific treatment for Sjogren's syndrome. The onset of symptoms associated with Sjogren's syndrome coincided with the acute severely hyponatraemic episode described above. Tests are consistent with renal salt wasting or SIADH which is not commonly described in existing literature. An association between hyponatraemia and Sjogren's may help to shed light into the effects of Sjogren's on the kidney. Whilst it has been associated with intersitial nephritis, renal tubular acidosis or glomerulonephritis (Goules et al. 2019) the association with acute, severe hyponatraemia has been less described. In this patient there is suspicion for ongoing hyponatraemia caused by Sjogren's syndrome given recent test results, the definite mechanism of which is unclear.