%0 Journal Article
%T Ibuprofen-Induced Hypokalemia and Distal Renal Tubular Acidosis: A Patient¡¯s Perceptions of Over-the-Counter Medications and Their Adverse Effects
%A Mark D. Salter
%J Case Reports in Critical Care
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/875857
%X We highlight a case of distal renal tubular acidosis secondary to ibuprofen and codeine use. Of particular interest in this case are the patient¡¯s perception of over-the-counter (OTC) medication use, her own OTC use prior to admission, and her knowledge of adverse reactions or side effects of these medications prior to taking them. 1. Introduction Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) which is available over-the-counter (OTC) as a nonprescription drug. It is used widely as an antipyretic and analgesic. Our patient had hypokalemia secondary to type one, distal renal tubular acidosis (dRTA), after long-term ibuprofen and codeine use. The combination of biochemical abnormalities including hypokalemia, hyperchloremic metabolic acidosis, hypophosphatemia, and urine pH >5.5 was consistent with those found in our patient [1¨C3]. The mechanism behind ibuprofen-induced renal tubular acidosis is not well understood and is believed to involve the inhibition or deficiency of carbonic anhydrase activity, especially carbonic anhydrase type two, which is the predominant form in the kidneys. Essentially, the hyperchloremic metabolic acidosis is a result of impairment of renal acidification and the hypokalaemia is due to the acidosis impairing proximal sodium reabsorption, causing increased potassium secretion in the distal tubules [4¨C6]. 2. Case Presentation A 38-year-old patient presents with myalgia, evolving paralysis, and vomiting for 3 weeks on a background of iron deficiency anaemia, migraines, and gastroesophageal reflux disease. Her only medications were esomeprazole 20£¿mg and amitriptyline 50£¿mg. She had been sent in by her GP with moderate hypokalaemia (potassium 2.6£¿mmol/L, range 3¨C5£¿mmol/L) and possible myositis (CK 2500£¿u/L) after blood tests the prior evening. Her examination demonstrated conjunctiva pallor, minor right upper quadrant, and epigastric tenderness. Neurological exam showed generalised upper and lower limbs flaccid weakness (grade 3/5 proximally and 4/5 distally) with normal sensation and cranial nerve examination. Repeat blood tests demonstrated a hyperchloremic metabolic acidosis, hypokalemia (potassium 2.1£¿mmol/L), a mild transaminitis, an inflammatory response (WCC 27.1 ¡Á 109/L and procalcitonin 108£¿ug/L with normal CRP), and a creatinine kinase 26,100£¿u/L. This was in the context of normal renal function (urea 5.4£¿mmol/L and creatinine 85£¿umol/L). Urinary myoglobin was 266,900£¿ug/L, pH 9, and spot urinary potassium 22£¿mmol/L (overall >20£¿mmol over a 24-hour period). ECG showed mild ST depression without U waves and a
%U http://www.hindawi.com/journals/cricc/2013/875857/