UROLOGY • January 2015 EMJ EUROPEAN MEDICAL JOURNAL 68 KIDNEY STONES AND CEFTRIAXONE Murat Dursun, 1 *Alper Otunctemur, 2 Emin Ozbek 2 1. Department of Urology, Bahcelievler State Hospital, Istanbul, Turkey 2. Department of Urology, Okmeydani Training and Research Hospital, Istanbul, Turkey *Correspondence to alperotunctemur@yahoo.com Disclosure: No potential conflict of interest. Received: 20.10.14 Accepted: 01.12.14 Citation: EMJ Urol. 2015;3[1]:68-74. ABSTRACT Metabolic causes such as hypercalciuria, urinary tract infection, and obstruction are the most common aetiologies of urolithiasis, and drugs, although important in this regard, are rarely the cause of urolithiasis. Administration of one of these drugs, ceftriaxone (CTX), has been associated with biliary pseudolithiasis in adult and paediatric patients, and rarely may cause urolithiasis. Several factors, including drug concentration and incubation time, are very important for determining the degree of CTX/calcium (Ca) crystallisation in the urine. According to this data, CTX crystallisation was a dose and time-dependent reaction. It is particularly important to monitor patients on high-dose long-term CTX treatment with the urinary Ca to creatinine ratios, ultrasound sonography, and renal function testing, as these individuals may be at greater risk of large stones and renal damage. This type of screening may help prevent permanent complications in the future. This underlying review will help to educate readers on the pathophysiology and interaction between CTX and urolithiasis. Keywords: Ceftriaxone, urolithiasis. INTRODUCTION The prevalence of urolithiasis requiring medical or surgical treatment is 5-10% and increasing worldwide. 1 Calcium (Ca) oxalate is the most prevalent type of kidney stone disease in the United States and has been shown to occur in 70-80% of the kidney stone population. 2 The prevalence of recurrent Ca oxalate stones has progressively increased in untreated subjects, approaching a 50% recurrence rate over 10 years. 3 The lifetime risk for kidney stone disease currently exceeds 6-12% in the general population. 4 In the inal quarter of the twentieth century, the prevalence of kidney stone disease increased in both males and females, and all ethnicities. 4 Metabolic causes such as hypercalciuria, urinary tract infection (UTI), and obstruction are the most common aetiologies of urolithiasis, and drugs, although important in this regard, are rarely the cause of urolithiasis. Drugs may be responsible for 1–2% of all renal calculi. 5 This drug adverse event most often afects patients who have received high-dose and/or long-term treatment of some drugs with lithogenic potential. 5 According to mechanisms of calculi formation, lithogenic drugs can be classiied into two groups. 5 The irst group consists of drugs that induce metabolic abnormalities (e.g. hypercalciuria, 6,7 hypocitraturia, 8,9 hyperuricosuria, 10 and alteration of urine acidity 8,9 ) which subsequently provoke formation of metabolic calculi; e.g. Ca-containing stones and uric acid (UA) nephrolithiasis. 5 The second group consists of drugs that can be crystallised directly in the urine due to their high excretory levels and poor solubility. 11-14 The most important drugs are silica- containing anti-acids, furosemide, acetazolamide, ciproloxacin, sulfonamides, aminophylline, corticosteroids, triamterene, phenytoin, probenecid, lithium, indinavir, and ceftriaxone (CTX). 15 Administration of one of these drugs, CTX, has been associated with biliary pseudolithiasis in adult and paediatric patients, and rarely may cause urolithiasis. 16,17 Although only limited information exists in the literature regarding the incidence of urolithiasis following CTX therapy, the present review is aimed to demonstrate interaction between CTX and urolithiasis.