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Objective: To determine the safety of ceftriaxone in paediatric patients and systematically evaluate the categories and incidences of adverse drug reactions (ADRs) of ceftriaxone in paediatric patients., Methods: We performed a systematic search in Medline, PubMed, Cochrane Central Register of Controlled Trials, EMBASE, CINAHL, International Pharmaceutical Abstracts and bibliographies of relevant articles up to December 2018 for all types of studies that assessed the safety of ceftriaxone in paediatric patients aged ≤18 years., Results: 112 studies met the inclusion criteria involving 5717 paediatric patients who received ceftriaxone and reported 1136 ADRs. The most frequent ADRs reported in prospective studies were gastrointestinal (GI) disorders (37.4 %, 292/780), followed by hepatobiliary disorders (24.6%, 192/780). Serious ADRs leading to withdrawal or discontinuation of ceftriaxone were reported in 86 paediatric patients. Immune haemolytic anaemia (34.9%, 30/86) and biliary pseudolithiasis (26.7%, 23/86) were the two major causes. Haemolytic anaemia following intravenous ceftriaxone led to death in 11 children whose primary disease was sickle cell disease. Almost all biliary pseudolithiasis are reversible. However, the incidence was high affecting one in five paediatric patients (20.7%)., Conclusions: GI ADRs are the most common toxicity of ceftriaxone in paediatric patients. Immune haemolytic anaemia and biliary pseudolithiasis are the most serious ADRs and the major reasons for discontinuation of ceftriaxone. Immune haemolytic anaemia is more likely in children with sickle cell disease and may cause death. Ceftriaxone should be used with caution in children with sickle cell disease., Trial Registration Number: CRD42017055428., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

The outpatient forensic aftercare department of the Charité Berlin treated 32 paraphilic sex offenders with GnRH analogues within the past 5 years. Out of those patients, three men suffered from urolithiasis and were in need of treatment. All 3 patients had previously developed osteopenia/osteoporosis while on antiandrogen treatment.This article describes these 3 cases and suggests an intense consideration of the possible occurrence of urolithiasis in sex offenders on antiandrogen treatment., (© Georg Thieme Verlag KG Stuttgart · New York.)

High dose of vitamin C intake could increase urine oxalate excretion and hence the risk of calcium stone formation. We report a case of left ureteral stone in a 9-year-old boy with an extremely high urine oxalate excretion. Besides, he had a habit of taking high-dose supplementation of vitamin C since the age of 3 years. After vitamin C intake prohibited without other therapy and change of dietary intake, the urine oxalate excretion was decreased to normal level and no recurrence of urolithiasis was present during the 3-year follow-up. Thus, high-dose supplementation with vitamin C for years in a child could induce the urinary stones., (Copyright © 2014 Elsevier Inc. All rights reserved.)

A 64-year-old man with HIV on antiretroviral therapy (including atazanavir, a protease inhibitor) presented with left flank pain, nausea and vomiting. A kidney stone was suspected, and a CT scan demonstrated left hydronephrosis but failed to demonstrate nephrolithiasis or extrinsic compression. The patient had a ureteral stent placed which relieved his symptoms. A few months later, he underwent left ureteroscopy and a large ureteral calculus was found. The stone was removed and analysis showed 43% atazanavir and 57% calcium oxalate. Several months later, the patient developed flank pain on the opposite side. A renal ultrasound suggested right-sided nephrolithiasis and he subsequently underwent ureteroscopy with laser lithotripsy of two stones. Stone analysis showed that they were composed of 100% atazanavir. This case highlights the fact that patients treated with protease inhibitors remain at risk for developing nephrolithiasis. Ultrasonography can be a useful diagnostic tool in the setting of these radiolucent calculi.

Sulfadiazine-related stones are uncommonly reported, but they could be increasingly encountered owing to the use of sulfadiazine for human immunodeficiency virus-related toxoplasmosis. We report on their unusual imaging characteristics, with 4 such stones having very low attenuation compared with more commonly encountered stones. Because their atypical appearance resulted in delayed treatment for our patient in acute renal failure and because the computed tomography imaging characteristics have not been previously defined, we report the findings of stone analysis-confirmed sulfadiazine-related urolithiasis.

Melamine (Tripolycyanamide) and its derivatives have recently become a public concern on food safety. To better understand melamine and its major derivative cyanuric acid.literature on their chemical properties, metabolism, biological effects, relevant toxicology studies, and the detection methods is reviewed. Studies indicate that the acute toxicity of melamine and cyanuric acid is low. In mammalian, these compounds are hardly metabolized in vivo and are rapidly eliminated in the urine. When used in large dosage,these compounds demonstrate marked renal toxicity,as well as toxic effect towards heart. The renal toxicity is exemplified by the calculi formation, acute renal failure, and subsequently induced carcinomas of the urinary bladder. Among the tested species, male cats and rats are more prone to be affected by the compounds. The HPLC/MS/MS is becoming the mainstay of the detection methods. Despite of the achieved knowledge on melamine and cyanuric acid, further research is warranted to unveil the mechanism of underlying susceptibility of kidney, to develop better analytic methods,and to explore possible biomarkers for better clinical diagnosis.

We report on the first case of acute renal failure related to obstructive urinary tract lithiasis involving sulfadiazine crystals in a kidney transplant recipient. This patient had disseminated toxoplasmosis which was treated by sulfadiazine (4 g/day) and pyrimethamine (50 mg/day). In the fourth week of anti-toxoplasmosis therapy, he presented with obstructive acute renal failure: the plasma creatinine level increased from 220 micromol/l to 547 micromol/l. Apercutaneous pyelography was conducted showing the presence of a lithiasis located at the junction between the graft ureter and the bladder. Six days later, he underwent surgery to retrieve an orange-colored, friable stone. Its spectrophotometric analysis confirmed that the stone consisted of N-acetyl sulfadiazine crystals.

Formation of calculi in efferent urinary passages is always due to supersaturation of urinary calculi substances and associated increased crystallization. Apart from the typical calculi, consisting of calcium oxalate, inorganic phosphates, uric acid or cystine, there are occasional signs of rare substance classes. Although more than 50 silicate stones have already been reported internationally, this stone entity remains relatively unknown. In particular, the occurrence of silicate stones in the absence of magnesium trisilicate abuse is extremely rare. A medium-sized left-sided ureterolith was removed from a 54-year-old male patient using a ureteroscope. X-ray diffraction showed it to be a compound stone consisting of 40% silicate. The patient, who in 1986 was living close to the nuclear reactor accident in Chernobyl, showed no signs of a constant uptake of magnesium trisilicate. However, he had undergone partial (2/3) gastrectomy 4 months before for a drug-refractory gastric ulcer, which had been diagnosed at the end of the 1980s and treated with excessive dosages of a magnesium trisilicate antacid preparation until the time of the operation. The patient had also been suffering from unstable angina pectoris since 1986 and treated with Pentalong (pentaerythrityltetranitrate) for 17 years. We were also able to detect silicium dioxide in components of this drug using X-ray diffraction. Silicate uroliths are extremely rare but they can be clearly identified by X-ray diffraction or infrared spectroscopy and distinguished from artifacts or quartz pebbles. Formation of calculi can be prevented by increasing diuresis as well as switching to a different drug and reducing the dosage.

We report a case of ammonium acid urate stone due to laxative abuse. A 27-year-old female complained of left flank pain. Computed tomography revealed bilateral ureter stones (right 16.5 x 9.0 mm; left 4 mm), while left ureter stone was radiolucent on the plain X ray film. Bilateral hydronephrosis was seen, but no therapy was performed for the right stone, because 99mTc-MAG3 scintigraphy revealed that right kidney had no function. The left stone was successfully removed by transurethral approach. The stone was revealed to be an ammonium acid urate by infrared spectrophotometry. She had been taking many laxatives (bisacodyl, sennoside, aloe extract) for 12 years to control her body weight. Ammonium acid urate stones are rarely seen in developed countries. We have reviewed 9 cases in Japan, describing ammonium acid urate stones due to laxative abuse. Among these patients, 24-hour urine volume and excretion in urinary sodium were decreased, and serum aldosterone was increased. The involvement of laxative abuse should be considered when ammonium acid urate is formed in a woman with a low body mass index.

Nephrolithiasis is a known complication of the use of sulfadiazine in the treatment of cerebral toxoplasmosis. Radiographic diagnosis of this complication has historically been challenging. Between March 1999 and June 2002, 11 patients were treated for cerebral toxoplasmosis with sulfadiazine-containing therapy. Four of these patients (36.4%) developed nephrolithiasis during this period. Case patients had received sulfadiazine for a median of 35.5 days prior to nephrolithiasis. All cases were diagnosed by spiral CT scans. Although studies are needed to evaluate the sensitivity and specificity of this modality, spiral CT may aid in the diagnosis of sulfadiazine-induced nephrolithiasis.

We report on a patient with bilateral ureteral calculi composed of guaifenesin metabolite as determined by infrared spectroscopy. These stones may be associated with excessive guaifenesin intake related to the current popularity of ephedrine preparations.

The incidence of drug-induced stone disease is 0.44%. A 57-year-old woman with ulcerative colitis presented with obstructive nephropathy and pyelonephritis. She underwent cystoscopy, bilateral retrograde pyelography, and bilateral ureteral stent placement. A 6-cm bladder calculus and two 3-mm right distal ureteral calculi were discovered. Later, cystolithotomy was performed. The stone analysis demonstrated sulfapyridine, a sulfasalazine metabolite. Patients with inflammatory bowel disease can develop urolithiasis owing to acidic urine and low-volume urine production. Patients receiving aminosalicylates are at an increased risk of urolithiasis and may benefit from oral hydration and urinary alkalization.

We report a 27 years old male, treated with Indinavir as a prophylactic anti-HIV agent, who consulted for left ureteral pain. Intravenous and retrograde pyelograms disclosed a radioluscent stone, that was removed surgically. The physical-chemical study of the stone, demonstrated indinavir sulphate crystals.

Objective: Evaluation of the treatment of complicated ureteric stones in patients treated with indinavir., Patients and Methods: From March 1997 to May 1998, 10 patients (7 males, 3 females, aged 30 to 56 years), treated by triple combination therapy for HIV infection, were drained for stones attributed to indinavir (CRIXIVAN), which had become obstructive and complicated. The duration of treatment with indinavir ranged from 14 days to 2 years. No patient had a history of urological disease. One patient presented with bilateral stones. All patients presented complicated clinical features: fever in 3 cases; severe pain in 8 cases, with delayed excretion more than 4 hours on IVU in 6 cases. All stones were radiolucent except for one slightly radioopaque stone. The stone was situated in the lumbar ureter in 3 cases, iliac ureter in 1 case and pelvic ureter in 8 cases., Results: In 10 out of 11 cases, a double J stent was inserted, preceded by drainage by simple ureteric catheter (infected urine) in 1 case and by percutaneous nephrostomy (PCN) with antegrade insertion of the stent (failure of the retrograde route) in 1 case. No complementary stone fragmentation or extraction treatment was necessary after this procedure. Stents were left in place for 3 to 7 weeks. In one case, a stone of the lumbar ureter required PCN followed by extracorporeal lithotripsy., Conclusion: In the case of complications requiring a urological procedure, insertion of a double J stent allows curative treatment of very friable indinavir stones, which are fragmented by passage of the stent.

Objective: We describe the unique CT features of ureteric calculi in six HIV-infected patients receiving indinavir, the most commonly used HIV protease inhibitor, which is associated with an increased incidence of urolithiasis., Conclusion: Ureteric obstruction caused by precipitated indinavir crystals may be difficult to diagnose with unenhanced CT. The calculi are not opaque, and secondary signs of obstruction may be absent or minimal and should be sought carefully. Images may need to be obtained using i.v. contrast material to enable diagnosis of ureteric stones or obstruction in patients with HIV infection who receive indinavir therapy.

Indinavir sulfate is a protease inhibitor used in the treatment of the human immunodeficiency virus (HIV). This case report describes the radiographic and urologic manifestations of indinavir urolithiasis in two pediatric patients with acquired immunodeficiency syndrome (AIDS). Management involves aggressive hydration and surgical intervention when indicated.

We report on 4 cases of urinary stone observed in patients treated with the drug Crixivan (Indinavir Sulfate) and review the literature. Comments include stone composition, clinical aspects, treatment and prevention.

The development of HIV protease inhibitors has dramatically improved the treatment prognosis of HIV-infected patients. The treatment, however, is associated with the potential for adverse events that are unique to protease inhibitors. One of them, Indinavir, can lead to the development of urinary stones. Three weeks after starting treatment with Indinavir, Zidovudine and Lamivudine, a 66-year-old patient developed symptomatic hydronephrosis on the right side due to multiple Indinavir stones blocking the ureter. Microhematuria and characteristic crystals were found in the urine. After interruption of treatment and increased fluid intake, the crystallurea was not longer detectable and the patient became asymptomatic within 3 days. Nephrostomy and ureteral stent placement were not necessary. Patients on treatment with Indinavir are required to maintain a fluid intake of at least 1.5-2 l/day to reduce the risk of crystallization and urinary stones. Pharmacologic metaphylaxis to prevent crystallization is not recommended.

Sulfadiazine-nephropathy and -nephrolithiasis were well known complications of high dose sulfadiazine therapy 50 years ago. In the last few years high dose sulfadiazine therapy has been widely used for treatment of toxoplasmic encephalitis in AIDS patients. As a consequence sulfadiazine-nephropathy and -nephrolithiasis have become increasingly common. We describe 2 patients with the typical picture of these complications. Therapy is based on the fact that the solubility of sulfadiazine and its acetylated metabolite are markedly improved at higher urine-pH levels. Urine alkalinization is also effective for prophylaxis during sulfadiazine treatment. We present our guidelines for prophylaxis and treatment of these complications.

We describe 3 cases of urinary calculi that developed during the course of long-term solvent abuse. The patients regularly sniffed a lacquer thinner (major component toluene) or a cement (xylene and cyclohexane) for 2 to 6 years before the development of urolithiasis. The occurrence of proteinuria and hematuria was closely related to solvent sniffing in 2 of the 3 patients. Regular, long-term solvent abuse must be included in the causes of urolithiasis, particularly in juveniles and young adults.

As calcium oxalate stones are the most important component in urolithiasis, an experimental model has to be designed to clarify the pathogenesis and aid in their prevention. Hyperoxaluria as well as hypercalciuria were produced in rats by administering ethylene glycol (0.5%, in drinking water administered ad libitum) and 1-alpha (OH) D3 (0.5 micrograms/rat given every other day), respectively, for three to four weeks. Neither drug alone produced stones efficiently as did the combination regimen of these two compounds. The occurrence of stones was 77.3%, and with only a moderate degree of renal functional impairment. Biochemical and histological data were obtained using this model.

The first case of an obstructing stone composed of a pure metabolite of the sulfamethoxazole-trimethoprim combination is reported. Its coincident occurrence with an obstructing calcium oxalate stone, producing oligura and acute azotemia, is noteworthy.

A young man who presented initially with a ureteral stone was found to have toluene-induced renal tubular acidosis. Persistent toluene sniffing resulted in recurrent calculi and life-threatening hypokalemic paralysis. The pathophysiology, classification and treatment of renal tubular acidosis are discussed.

A possible association between treatment with methyldopa and the occurrence of renal stones was sought by retrospectively comparing 54 hypertensive patients with calculi detected by X-ray examination with a control group matched for age and sex. Treatment with methyldopa was equally frequent in both groups. There was a significant excess of methyldopa use in a subgroup of 16 patients with bilateral calculi, but the drug could be the primary cause of stone formation in, at most, four of these patients. If methyldopa does cause renal stones, it is probably an uncommon event, but precipitation of the drug from the urine may worsen a tendency to stone formation, which will lead to a higher incidence of bilateral calculi.

A 68-year-old white man with Paget's disease and open-angle glaucoma was treated with methazolamide, 50 to 100 mg three times daily. Ten months after the medication was initiated he developed ureteral colic and a calcium oxalate stone was surgically removed. Three months after the drug was reinstituted the patient passed three calcium phosphate stones. This suggested a casual relationship between methazolamide and stone formation, although renal calculi also complicate Paget's disease and acetazolamide had been administered briefly.