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Abstract: TH-PO389

Distal Renal Tubular Acidosis as the Initial Manifestation of Hashimoto Thyroiditis

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Diniz, Renan Gomes Mendes, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Sousa Pontes, Irma Bandeira de, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • de Menezes, Liudmila G R, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Gonçalves, José Guilherme Rezende Ramos Salles, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Campos, Diogo, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Maia, Tassila Gomes, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Rodovalho Guimaraes, Marilia, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Arantes de Oliveira, Marcia Fernanda, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Smolentzov, Igor, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Vieira Jr., Jose M., Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Seabra, Victor F., Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
  • Andrade, Lucia, Hospital das Clinicas - University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil
Introduction

Distal renal tubular acidosis (dRTA) is a rare disorder, characterized by inadequate proton secretion in the distal tubule and collecting duct in the presence of metabolic acidosis. In adults, the most common cause of dRTA is autoimmune disease, and the association with Hashimoto thyroiditis (HT) has rarely been studied.

Case Description

A 25-year-old female diagnosed with nephrolithiasis 2 years prior presented to the emergency room complaining of weakness, loss of coordination and strength, pain and paresthesias. On examination, her arms showed decreases in speed, range of motion and deep tendon reflexes. Labs revealed severe hypokalemia (2.0 mEq/L), together with increase in CPK (3412 U/L), hyperchloremic metabolic acidosis (anion gap 9) and urinary pH of 8.5. Intravenous potassium and bicarbonate were started in the with gradual symptom improvement. On day 4 she was discharged on oral potassium citrate (40 mEq/d) and sodium bicarbonate (6 g/d). On follow-up, there was complete symptom resolution, normalization of potassium (4.3 mEq/L) and improved bicarbonate (20 mEq/L), but thyroid hormones were altered (TSH = 73.58, T4 < 0.42). We started levothyroxine at 25 µg/d. The patient tested positive for anti-TSH receptor antibody (1.95 IU/L) and anti-thyroid peroxidase antibody (> 900 IU/ml), thus confirming the diagnosis of HT. The levothyroxine dose was increased to 100 µg/d due to persistence of the hormonal alteration (TSH = 51, T4 = 0.48).

Discussion

In this case, the dRTA might have been due to a reduction in the number or function of H+- and H+/K+-ATPases. To our knowledge, this is the sixth reported case of dRTA secondary to HT, which may be underdiagnosed.

VariableNormal rangeAdmissionFollow-up
(01/31/23)(08/02/23)
pH(7.35-7.45)7.247.3
Bicarbonate (mEq/L)(22-28)11.120.0
Base excess(10 ± 2)−14.7−4.2
Anion gap(8-12)96
Sodium (mEq/L)(135-145)141140
Potassium (mEq/L)(3.5-5.0)2.44.3
Chloride (mEq/L)(98-106)121114
Ionized calcium (mmol/L)(4.49-5.29)5.414.68
Magnesium (mg/dl)(1.6-2.6)3.12.5