ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: FR-PO219

Severe Hypothyroidism May Contribute to AKI but Not Hyponatremia: A Case Report

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Carbajal, Nicholas Julius, Ochsner Health, New Orleans, Louisiana, United States
  • Kanduri, Swetha Rani, Ochsner Health, New Orleans, Louisiana, United States

Hypothyroidism is commonly encountered in patients with chronic kidney disease but rarely contributes to acute kidney injury. Majority of the published cases of acute kidney injury (AKI) have associated rhabdomyolysis secondary to severe hypothyroidism. In addition, hypothyroidism work up is typically included as a standard practice in the etiology of hyponatremia. Herein, we report a severe case of hypothyroidism resulting in AKI without associated rhabdomyolysis or hyponatremia.

Case Description

An 89-year-old woman presented to emergency department with a chief complaint of left-sided hip pain following mechanical fall. Review of systems positive for fatigue and constipation. Medical history was pertinent for CKD IIIb, hypothyroidism and hypertension. Physical examination revealed persistent bradycardia (HR;30-50 bpm) and 2+ bilateral lower extremity edema. Telemetry additionally demonstrated intermittent sinuses pauses. Laboratory data at the time of admission revealed serum creatinine (Scr) of 1.8 mg/dL (baseline 1.3 mg/dL), thyroid stimulating hormone (TSH) of 298 uIU/mL, free T4 < 0.40 ng/dL and total T3 < 40 ng/dL, creatinine phosphokinase (CPK) was 404 U/L and serum sodium was 136 mmol/L. Urine analysis consistent with 1+protein, no blood and urine sediment notable for waxy and granular casts. Urine protein: creatinine ratio (UPCR) was 0.28 mg/dL and a kidney ultrasound was negative. Other serologies including AST, ALT, cortisol resulted negative. Upon further inquiry patient mentioned of missing several doses of levothyroxine as she ran out of several medications. Patient was started on intravenous (IV) fluid supplementation and high doses of IV levothyroxine. Meanwhile, with persistent bradycardia, a pacemaker was implanted. She had gradual resolution of her symptoms and thyroid function tests with thyroid hormone supplementation. Her Scr returned closed to baseline and she was eventually discharge on levothyroxine dose of 88 mcg daily with close follow up.


Severe hypothyroidism can cause AKI secondary to associated cardiac conduction abnormalities and hemodynamic alteration, even in the absence of rhabdomyolysis. In addition, the traditional teaching of hypothyroidism as a cause of hyponatremia is a very rare entity.