Kidney Week

Abstract: PUB255

Unveiling the Effects:The Influence of Trimethoprim Sulfamethoxazole (TMP-SMX) on Electrolyte and Acid-Base Disturbances

Session Information

• Publication Only

Category: Fluid, Electrolytes, and Acid-Base Disorders

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

Authors

• Vazquez Morales, Emily, Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Emily Vazquez Morales, MD

• Adams Chahin, Juan J., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Juan J. Adams Chahin, MD

• Gonzalez Rivera, Adriel, Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Adriel Gonzalez Rivera, MD

• Ocasio Melendez, Ileana E., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Ileana E. Ocasio Melendez, MD, FASN

Introduction

Trimethoprim sulfamethoxazole (TMP-SMX) is an antibiotic commonly used as treatment and prophylaxis for infectious processes including Pneumocystis jirovecii pneumonia (PCP) in HIV patients, but it has been associated with various metabolic disturbances including renal tubular acidosis. This case will describe the chronology of a patient’s metabolic derangements after medication was started.

Case Description

A 53-year-old woman with alcohol and drug abuse was brought to the ED due to loss of consciousness requiring intubation upon arrival due to alcohol withdrawal symptoms. On initial laboratory tests, patient tested positive to HIV and days later she developed respiratory distress. Chest CT scan was performed and demonstrated right lower lobe necrotizing pneumonia. HIV viral load was elevated at 5,920 with an associated low CD4 count of 31. Opportunistic infections were high on the differential which included PCP and prophylactic treatment with TMP-SMX was began. Nephrology service was consulted approximately 5 days after initiation of therapy due to increasing trend in serum creatinine levels, hyperkalemia, normal anion gap metabolic acidosis and hyponatremia. Urine spots yielded a urine anion gap of 44.6. Alkali therapy was initiated, and hyperkalemia management was provided, and type 4 renal tubular acidosis was highly suspected due to temporal association with TMP-SMX administration. The offending agent was discontinued after discussion with ID and Pulmonology services. Patient’s serum creatinine, hyponatremia, hyperkalemia, and non-anion gap metabolic acidosis resolved afterwards.

Discussion

Our case represents a patient who developed several metabolic disturbances TMP-SMX may cause. There are no accepted treatments for TMP-SMX induced RTA and literature has demonstrated that patients improve after withdrawal of medication. Although patients often show improvement after discontinuing treatment, it may sometimes be delayed and can increase the patient's morbidity. Therefore, it is crucial to consistently evaluate for hyperkalemia, hyponatremia, metabolic acidosis and increases in serum creatinine levels after initiating medication.