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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Sodium thiosulphate (STS) infusion is used for treatment of calciphylaxis and cyanide poisoning. Calciphylaxis, or calcific uremic arteriolopathy is characterized by vascular calcification in the skin leading to ischemia and necrosis, particularly in ESRD patients. Despite its use the safety profile and frequency of adverse effects of STS is insufficiently documented. We present a rare case of high anion gap metabolic acidosis, encephalopathy, transaminitis and stress cardiomyopathy with STS initiation in End Stage Renal disease (ESRD) patient.
68 yr Old fully functional woman with ESRD on Peritoneal Dialysis (PD) for 2 years, Hypertension and recent biopsy proven calcinosis cutis of painful subcutaneous buttock nodule who was started on STS 12.5 mg with intermittent Hemodialysis (iHD). Patient was transitioned from PD to iHD to facilitate the intravenous administration of STS. Patient received two doses of STS and within 48 hours of second dose she developed shortness of breath, palpitation and was found to be confused. Admission vitals were B.P 158/117, HR 102, RR 25, SaO2 100% on 2L oxygen via NC. Labs enlisted in table. CT head showed no acute abnormality, CXR showed mild pulmonary edema. Viral Hepatitis panel was negative. US abdomen showed right lobe of liver of 19.3 cm, with heterogeneous appearance and prominence of the left lobe. Echo showed new reduced EF 25% and patient was diagnosed with Non-ischemic Cardiomyopathy due to Stress Cardiomyopathy. STS was discontinued and patient underwent iHD thrice/week. Hypoxia resolved in 24 hours post iHD and mental status improved in 3 – 4 days. Within 5 days of admission labs improved significantly (as enlisted in table) and eosinophil increased from normal to 3.2%. Patient was treated empirically with ceftriaxone and doxycycline to cover for possible pneumonia. Blood cultures were negative. Sepsis and autoimmune etiologies were ruled out.
Patient’s presentation was concerning for encephalopathy and Drug induced Liver injury (DILI). Mild eosinophilia during hospitalization also supports DILI. The rapid resolution of lab abnormalities and improvement in mental status with discontinuation of STS further supports a causative link. Congestive hepatopathy was also a contributor for LFT elevation but cannot alone explain the abrupt AST/ALT increase to > 1000. As LFTs started improving within 48 hours of admission, liver biopsy was not done. Hydrogen sulfide is a known metabolite of STS which causes inhibition of mitochondrial ATP production and can cause lactic acidosis. LFT elevation and Stress cardiomyopathy can be seen as indirect effect of metabolic acidosis.
This case elicits potential less known systemic adverse effect of STS like transaminitis and cardiomyopathy in ESRD patients. Given the time course and resolution of symptoms after discontinuation of STS, it is safe to attribute it to STS. More studies are needed to establish full spectrum of direct and indirect STS adverse effects for its safe use in dialysis patients.
