Chronic Hypokalemia Secondary to Distal Renal Tubular Acidosis Induced by Sodium Valproate

Introduction: Sodium Valproate is a commonly prescribed medication for the treatment of various conditions, including mood disorders and epilepsy. However, it can lead to rare adverse effects, such as valproate-induced distal renal tubular acidosis (dRTA), which results in a non-anion-gap metabolic acidosis with associated hypokalemia. We report a case of dRTA in a patient with a history of chronic hypokalemia attributed to long-term sodium valproic acid therapy. Case Description: A 61 y.o. female with a past medical history of hypertension, anxiety, depression, and tobacco dependence with half a pack per day, was admitted to the hospital for concern of bilateral lower extremity muscle pain and weakness for the last 5 days which worsened to numbness and led to difficulty ambulating. She mentioned that she has been told on multiple outpatient visits that she had low potassium for the last 1-2 years and no workup was done in the past. She does not recall any family history of hypokalemia. Her home medications include sodium valproate, lisinopril, olanzapine, and ondansetron. On arrival at ED the patient was found to have a Potassium level of 1.8 was a significant drop from her previous labs. On further evaluations, the patient had non-anion gap metabolic acidosis in the blood. Urine studies showed an alkalotic pH of 7.0, potassium of 44, sodium of 93 and chloride of 116 concerning of urine anion gap of 21 suggesting renal tubular acidosis. Other labs like thyroid function tests and renin aldosterone studies were within normal limits. Discussion: Valproate-induced dRTA is a rare and idiosyncratic side effect of long-term valproic acid therapy. DRTA is characterized by impaired acid secretion in the distal renal tubules, leading to metabolic acidosis and hypokalemia. In this case, the patient's chronic hypokalemia was likely exacerbated by valproate use, which prompted the development of dRTA. This case emphasizes the importance of recognizing valproate-induced distal renal tubular acidosis as a rare but potentially serious complication of long-term valproic acid therapy. Prompt diagnosis and appropriate management are vital for the patient's well-being.

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Journal of the American Society of Nephrology
Published
2024-10-01
DOI
https://doi.org/10.1681/asn.2024pkgrtwye
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1
Primary Topic
Pharmacological Effects and Toxicity Studies
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article
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1.11
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article

Chronic Hypokalemia Secondary to Distal Renal Tubular Acidosis Induced by Sodium Valproate

Neeharika Muddana, ABHI LOHANA, Usman Akbar
1 citations
Journal of the American Society of Nephrology
Pharmacological Effects and Toxicity Studies
1.11
article

Chronic Hypokalemia Secondary to Distal Renal Tubular Acidosis Induced by Sodium Valproate

Neeharika Muddana, ABHI LOHANA, Usman Akbar
article en
1 citations

Abstract

Introduction: Sodium Valproate is a commonly prescribed medication for the treatment of various conditions, including mood disorders and epilepsy. However, it can lead to rare adverse effects, such as valproate-induced distal renal tubular acidosis (dRTA), which results in a non-anion-gap metabolic acidosis with associated hypokalemia. We report a case of dRTA in a patient with a history of chronic hypokalemia attributed to long-term sodium valproic acid therapy. Case Description: A 61 y.o. female with a past medical history of hypertension, anxiety, depression, and tobacco dependence with half a pack per day, was admitted to the hospital for concern of bilateral lower extremity muscle pain and weakness for the last 5 days which worsened to numbness and led to difficulty ambulating. She mentioned that she has been told on multiple outpatient visits that she had low potassium for the last 1-2 years and no workup was done in the past. She does not recall any family history of hypokalemia. Her home medications include sodium valproate, lisinopril, olanzapine, and ondansetron. On arrival at ED the patient was found to have a Potassium level of 1.8 was a significant drop from her previous labs. On further evaluations, the patient had non-anion gap metabolic acidosis in the blood. Urine studies showed an alkalotic pH of 7.0, potassium of 44, sodium of 93 and chloride of 116 concerning of urine anion gap of 21 suggesting renal tubular acidosis. Other labs like thyroid function tests and renin aldosterone studies were within normal limits. Discussion: Valproate-induced dRTA is a rare and idiosyncratic side effect of long-term valproic acid therapy. DRTA is characterized by impaired acid secretion in the distal renal tubules, leading to metabolic acidosis and hypokalemia. In this case, the patient's chronic hypokalemia was likely exacerbated by valproate use, which prompted the development of dRTA. This case emphasizes the importance of recognizing valproate-induced distal renal tubular acidosis as a rare but potentially serious complication of long-term valproic acid therapy. Prompt diagnosis and appropriate management are vital for the patient's well-being.

Journal of the American Society of NephrologyVol. 35(10S)
Ark Medical Center (US)
Openalex Percentile: Top 17%
Pharmacological Effects and Toxicity Studies
1.11
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