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Abstract: SA-PO985

Ibuprofen Induced Renal Tubular Acidosis

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports


  • Jan, Muhammad Yahya, Indiana University School of Medicine, Indianapolis, Indiana, United States
  • Baig, Mirza Mukarram, Indiana University, Indianapolis, Indiana, United States
  • El-Achkar, Tarek M., Indiana University , Indianapolis, Indiana, United States

Ibuprofen is a widely available over the counter analgesic. We report a rare but potentially fatal case of renal tubular acidosis (RTA) from ibuprofen overuse.


A 58 year old African American male with no past medical history presented to the emergency department with complaints of generalized upper and lower extremity weakness 2 weeks after undergoing dental extraction. This was associated with poor oral intake. He reported taking up to 60 pills of 200mg Ibuprofen daily for 10 days (up to 12 grams/day) for pain. He denied diarrhea or vomiting. Physical exam showed normal vital signs and generalized weakness in all extremities, with preserved reflexes and sensation. History was negative for autoimmune diseases and any other medication use.

Lab results showed serum potassium of 1.8mmol/l (3.5-5.5), creatinine of 2.79mg/dl (0.6-1.1), bicarbonate of 10mmol/l (21-32), chloride of 110mmol/l (98-106), blood urea nitrogen of 69 mg/dl (7-18), phosphorus of 2.3mg/dl (2.5-4.9 mg/dl) and normal sodium level. Venous blood gas showed a pH of 7.10 (7.35-7.45) and pCO2 of 33 mm Hg (35-48). Urine pH was 6.0(5-8) with a positive urine anion gap. Serum alcohol, acetone, isopropyl alcohol, methanol, salicylate, acetaminophen levels and urine drug screen was negative. Thyroid stimulating hormone level and kidney ultrasound were normal. Given the severe non anion gap metabolic acidosis, he was diagnosed with distal renal tubular acidosis due to ibuprofen overuse, in the absence of other identifiable etiology.

He was admitted to the intensive care unit for monitoring due to severe acidosis and wide QRS interval on electrocardiogram. He was managed with intravenous fluids and potassium repletion, followed by sodium bicarbonate infusion and oral citrate. His motor strength gradually improved over 4 days and he was discharged home, after correction of the metabolic acidosis and normalization of kidney function.


Ibuprofen is known to inhibit carbonic anhydrase enzyme in the renal proximal tubule as well as the collecting ducts and can cause proximal as well as distal RTA. Timely repletion of potassium prior to correction of acidosis is vital in preventing fatal arrhythmias. Ibuprofen toxicity should be considered in the differential diagnosis of patients who present with severe hypokalemia and metabolic acidosis.