Abstract: SA-PO0589
Enoxaparin-Induced Renal Tubular Acidosis Type 4
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Ramos, Brianna Eillen, Creighton University School of Medicine - Phoenix Health Sciences Campus, Phoenix, Arizona, United States
- Reynolds, Austin, Creighton University School of Medicine - Phoenix Health Sciences Campus, Phoenix, Arizona, United States
- Wagoner, Mark, Creighton University School of Medicine - Phoenix Health Sciences Campus, Phoenix, Arizona, United States
- Boddupalli, Saisridhar, Dignity Health Arizona, Phoenix, Arizona, United States
- Bhalla, Sarabjit S., Southwest Kidney Institute PLC, Tempe, Arizona, United States
Introduction
Renal tubular acidosis (RTA) type IV is characterized by aldosterone deficiency or resistance, leading to hyperkalemia and a nonanion gap metabolic acidosis [1]. It most commonly occurs in patients with chronic kidney disease and diabetes mellitus, but may also arise from medication-induced hypoaldosteronism [1,2]. Enoxaparin, a low molecular weight heparin, has a rare but underrecognized association with hyperkalemia and RTA type IV. We describe a case of a 61-year-old woman who developed enoxaparin-induced RTA type IV during hospitalization.
Case Description
A 61-year-old female with a history of CKD, DMII, COPD, CAD, PVD status post right above-knee and left below-knee amputation, and PE on apixaban, presented with chest pain and dyspnea. She was admitted after CT chest angiogram showed an empyema without evidence of pulmonary embolism. She was started on empiric antibiotics, underwent chest tube placement, and was started on enoxaparin for DVT/PE at treatment dosing.
On admission, potassium was 3.9 mmol/L. By hospital day two, labs showed hyperkalemia, hyponatremia, and nonanion gap acidosis. Evaluation for adrenal insufficiency was negative with an appropriate ACTH response, and RTA type IV was suspected. She was started on sodium bicarbonate and Lokelma with partial improvement. However, her potassium level rose to 6.3 mmol/L.
Nephrology was consulted and identified enoxaparin as a possible cause. She was subsequently switched to apixaban from enoxaparin as no more procedures were planned. After discontinuing enoxaparin, the patient’s hyperkalemia and NAGMA resolved, and she was deemed medically stable for discharge.
Discussion
Heparin-induced hypoaldosteronism is a rare cause of RTA type IV, with unfractionated heparin producing ~33% greater aldosterone suppression than LMWH [3,4]. Standard LMWH prophylaxis seldom meets the threshold for clinically significant aldosterone suppression, contributing to the rarity of this complication. A dose-dependent relationship with aldosterone inhibition has been described, most prominent at higher doses.
Prior studies suggest prophylactic LMWH dosing does not significantly affect aldosterone levels in diabetic nephropathy [5]. However, this patient’s concurrent CKD and DMII likely increased her susceptibility. This case demonstrates how enoxaparin-induced RTA type IV, though rare, is a preventable cause of electrolyte derangements in at-risk patients and should be considered after the exclusion of more common etiologies.
Acknowledgment
1. Bello et al. J Bras Nefrol. 2017;39:481-5.
2. Baleguli et al. Cureus. 2021;13:e20312.
3. Hottelart et al. Artif Organs. 1998;22:614-7.
4. Siebels et al. Thromb Res. 1992;66:467-73.
5. Benck et al. Clin J Am Soc Nephrol. 2007;2:58-67.