Abstract: TH-PO1105

Low K, Not OK: Distal Renal Tubular Acidosis Associated with Autoimmune Thyroiditis

Session Information

Category: Fluid, Electrolytes, and Acid-Base

  • 704 Fluid, Electrolyte, Acid-Base Disorders


  • Yen, Timothy, Methodist Dallas Medical Center, Dallas, Texas, United States
  • Collazo-Maldonado, Roberto L., Methodist Dallas Medical Center, Dallas, Texas, United States

Profound hypokalemia can present with hypokalemic paralysis. This is a rare but potentially fatal condition. Potassium wasting secondary to renal tubular acidosis (RTA) is a common cause of severe hypokalemia. RTAs are associated with multiple systemic diseases including autoimmune disorders and endocrinopathies.


A 43 year old Hispanic woman with a previous history of calcium phosphate renal stones presented to the ED after she awoke with generalized limb paralysis and inability to rise from bed. She denied having similar symptoms in the past, and review of symptoms was negative. She denied having a history of family illness, or using alcohol, tobacco or drugs. The patient did not take any medications or herbal supplements. Vital signs were normal on admission except for sinus bradycardia of 49 BPM. On examination, she had 3/5 strength in all extremities but normal sensation and reflexes. Her blood and urine investigations were suggestive of a distal RTA. The patient had a normal anion gap metabolic acidosis (pH 7.236, HCO3 15 mmol/L), severe hypokalemia (K 1.8 mmol/L), with normal serum calcium and magnesium levels. Urine studies revealed a urine pH of 7.5 and anion gap of 31 (Cl 90 mmol/L; K 15 mmol/L; Na 106 mmol/L). The patient was given IV and oral potassium replacement before being started on a bicarbonate infusion. By morning, her serum potassium level had risen to 3.6 mmol/L and her weakness had completely resolved. Investigations into the etiology of her RTA were performed. ESR and CRP levels were normal, and screening for ANA and Anti-SSA/SSB was negative. Thyroid function tests ordered to investigate her sinus bradycardia revealed subclinical hypothyroidism (TSH 14.0 uIU/L, free T4 1.10 ng/dL) with an elevated anti-thyroid peroxidase antibody (2729 IU/mL). The patient was discharged in stable condition and placed on a regimen of 1.6 mcg/kg/day of levothyroxine with oral bicarbonate and potassium supplements.


This is a case of a previously healthy middle aged woman who presented with hypokalemic paralysis caused by a distal RTA. The patient lacks any classical risk factors for acquired RTA except for elevated anti-thyroid peroxidase antibody. Internists and nephrologists must be aware of this rare but documented association between autoimmune thyroiditis and distal RTA.