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Abstract: TH-PO386

Nonsteroidal Anti-Inflammatory Drug-Induced Type I (Distal) Renal Tubular Acidosis

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

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


  • Ragunanthan, Branavan Vivek, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
  • Block, Clay A., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
  • Remillard, Brian D., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
  • Hopley, Charles W., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States

Acute kidney injury (AKI) is the most recognized kidney toxicity of non-steroidal anti-inflammatory drugs (NSAID), but NSAIDs have also been linked to the development of acid-base disorders. Here, we present a patient with a history of frequent ibuprofen consumption resulting in the manifestation of a type I renal tubular acidosis (RTA).

Case Description

A 38-year-old man with a history of C6-C7 spinal injury due to a snow-boarding accident causing spastic paraplegia presented to an emergency department with new-onset agitation and confusion. His medications included ibuprofen 800mg every 6-8 hours and oxycodone. Brain imaging and blood and urine cultures were unremarkable. Urine toxicology was positive for his prescribed agent. Laboratory investigations were notable for an ammonia of 74 mcmol/L (normal range: 16 – 60), albumin of 4.4 g/dL (3.2 - 5.2), potassium of 2.8 mmol/L (3.5 – 5.0), venous pH of 7.22 (7.32 – 7.42), venous pCO2 of 36 mmHg (41 – 51), serum bicarbonate of 15 mmol/L (22 – 31), anion gap (AG) of 16, creatinine of 0.97 mg/dL (0.80 – 1.50) correlating to eGFR or 102 mL/min/1.73m2 via CKD-EPI, and glucose of 58 mg/dL (65 – 199). He was administered Dextrose 10% @100 mL/h and lactulose enema with improvement in encephalopathy. Post treatment labs demonstrated a venous pH of 7.26, venous pCO2 of 30 mmHg, serum bicarbonate of 13 mmol/L, AG of 12, urine pH of 7.5, and a urine anion gap at 29 (Urine Na(97mmol/L) + Urine K(32mmol/L) - Urine Cl(100mmol/L)). Acetaminophen, salicylate, ethanol, creatinine-kinase and lactate were all normal/negative. Ibuprofen was discontinued and sodium citrate-citric acid 30mL twice daily was provided. At outpatient follow up, his acid-base disorder had resolved and his mentation normalized.


This case adds to several reports illustrating the association of ibuprofen with type I RTA in setting of preserved renal function. Ibuprofen is postulated to inhibit carbonic anhydrase (CA) II yielding impaired urinary acidification and luminal retention of bicarbonate. Hypokalemia is associated with type I RTA and are potent stimulators of ammoniagenesis. Although impairment of CA is usually associated with proximal (type 2) RTA, impairment of CAII can cause a distal RTA.