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Background: Distinguishing between a reset osmostat and SIADH in a hyponatremic patient can prove to be challenging in certain circumstances. Reset osmostat is an uncommon and under recognized cause of hyponatremia. Thus, it is important to recognize it as it does not require any treatment. Clinical Case: A 48 year old male with history of chronic hyponatremia of unknown cause, fatty liver, hypertension, was in the hospital post operatively after resection of a meningioma along dura. Endocrine was consulted for management of his chronic hyponatremia. Had chronic hyponatremia for over 20 years and was always asymptomatic. Normally drank 6-7 L of water at home, mostly at night. Also found to have a spinal compression fracture of unknown cause. Both his father and brother had chronic hyponatremia of unknown cause as well, suggesting possible familial component. His baseline sodium levels were 129-133 mmol/L. In the hospital, serum sodium levels decreased to the 120s. TSH was 0.307mcunit/mL (0.27-4.2). Was also placed on 1.5 L fluid restriction. Urine osmolality was 900 mOsm/kg (500-800) with sodium of 123 mmol/L (136-145), consistent with SIADH. A rare inherited disorder, nephrogenic SIADH (NSIADH), was considered. However, it has an X-linked inheritance pattern. Fluid restriction was removed, then did fluid load with 2L of water and obtained urine sodium, serum sodium, urine osmolality, serum osmolality, Copeptin (pro-AVP) before fluid load and 1 hour after fluid load. Serum sodium level went from 127mmol/L before to 125 mmol/L after. Urine osmolality improved from 984 mOsm/kg prior to 575 mOsm/kg after. Urine sodium went from 183 mmol/L prior to 91 mmol/L after. Serum osmolality went from 278 mOsm/kg (270-310) to 268 mOsm/kg after. His co-peptin pro-AVP levels were 16.4 pmol/L (ref. &amp;lt;13.1). They are found to be low in NSIADH. It was decided that his chronic hyponatremia was likely due to reset osmostat. After discharge and follow up, his serum sodium was rechecked and was 128 mmol/L. It would have been challenging, but useful, to try a vaptan for diagnostic purposes and possibly to increase serum sodium. However, there are complications from overcorrection. Since patient had long standing asymptomatic chronic hyponatremia with family history, it was decided not to pursue aggressive measures just to “normalize” serum sodium. Otherwise, it would have been an example of treating the numbers and not the patient. Conclusions: Case demonstrates the importance of keeping the patient, their symptoms, and clinical picture in mind, and to not just follow numbers, as difficult as it may be, especially when managing conditions in which diagnosis may be uncertain or unclear. Sometimes no intervention is needed at all, however tempting it may be to do one, it is important to keep the former option in mind. An asymptomatic patient with longstanding chronic hyponatremia due to reset osmostat is an example of that.

Challenges of Managing and Diagnosing Reset Osmostat vs SIADH in a Patient With Personal and Family History of Chronic Hyponatremia