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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.
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Abstract titles should be brief and reflect the content of the abstract.
Heparin is a well-recognized cause of type 4 renal tubular acidosis (RTA) associated with hyponatremia, hyperkalemia, and metabolic acidosis. Heparin suppresses aldosterone synthesis by inhibiting the adrenal zona glomerulosa and impairing angiotensin II signaling, typically resulting in mild-moderate electrolyte derangements. Here, we present a case of heparin induced type 4 RTA that led to severe and fatal hyponatremia and hyperkalemia.
We report a 70-year-old man with hypertension who presented with acute cord compression due to metastatic prostate cancer and underwent thoracic laminectomy. He subsequently received unfractionated heparin for thromboprophylaxis and dexamethasone for cord compression. Nine days later, he became altered and hypotensive, requiring vasopressor support and ICU level care. Labs revealed Na 106 mmol/L, serum osmolarity 235, K 7.3 mmol/L, and CO₂ 21 mmol/L. Urinary studies were consistent with salt losing nephropathy (urine osmolarity 642 mOSm/L, urine Na 47 mEq/L) and inappropriate potassium excretion in setting of hyperkalemia (urine K 29.3 mEq/L, urine creatinine 24.7 mg/dL, and fractional excretion of potassium 12.5 %). Aldosterone was inappropriately low relative to renin (Aldosterone 23 ng/dL and renin 61.64 ng/mL/h). Normal cortisol level and unremarkable CT imaging of the adrenal glands excluded primary adrenal insufficiency. Given the constellation of hypovolemic hyponatremia, hyperkalemia, and metabolic acidosis, severe type IV RTA from heparin use was suspected. Hypertonic saline, sodium zirconium cyclosilicate, and fludrocortisone were administered, and heparin, lisinopril, and hydrochlorothiazide were discontinued, resulting in rapid normalization of serum sodium, potassium, bicarbonate, and blood pressure.
Although heparin associated Type 4 RTA is a well-known pharmacologic effect, its clinical impact is often underestimated. Most patients develop only mild-moderate hyponatremia and hyperkalemia, but in this case, heparin precipitated life-threatening hyperkalemia and profound hyponatremia despite preserved renal function. This case highlights that even routine heparin prophylaxis can cause severe aldosterone deficiency. Prompt recognition and discontinuation of heparin, along with temporary mineralocorticoid replacement, can be lifesaving.
