One of the most frequent bacterial infections in children are urinary tract infections (UTIs). In recent years, an increasing incidence of UTIs caused by resistant bacterial strains has been observed, especially with extended-spectrum β-lactamase-producing Enterobacteriaceae that represent about 15% of UTIs. A retrospective study was performed comprising 331 pediatric cases with UTI. Our study aimed to detect the resistance of the uropathogens to common drugs used in UTI treatment. High resistance rates have been recorded for ampicillin, amoxicillin, trimethoprim/sulfamethoxazole (TMP/SMX), cefuroxime, and ciprofloxacin, among E. coli and Klebsiella. The multidrug-resistance (MDR) rate was detected in one-third of the uropathogens, among which more than half were isolated in patients with urinary tract abnormalities. Our study highlighted that nitrofurantoin, ceftriaxone, amikacin and carbapenem may be used for the empirical treatment for febrile or complicated UTI in children. This is the first comprehensive study that evaluates antibiotic resistance in UTIs in children, and their association with urinary tract abnormalities in Romania. As a result of this research, the protocol for initial empiric treatment of infants with febrile or complicated UTI should be modified considering a detailed and ongoing monitoring of local sensitivity of uropathogens to antimicrobial agents.
Nephrogenic diabetes insipidus (NDI) is characterized by impaired urinary concentrating ability, despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine vasopressin (AVP). NDI can be inherited or acquired. NDI can result from genetic abnormalities, such as mutations in the vasopressin V2 receptor (AVPR2) or the aquaporin-2 (AQP2) water channel, or acquired causes, such as chronic lithium therapy. Congenital NDI is a rare condition. Mutations in AVPR2 are responsible for approximately 90% of patients with congenital NDI, and they have an X-linked pattern of inheritance. In approximately 10% of patients, congenital NDI has an autosomal recessive or dominant pattern of inheritance with mutations in the AQP2 gene. In 2% of cases, the genetic cause is unknown. The main symptoms at presentation include growth retardation, vomiting or feeding concerns, polyuria plus polydipsia, and dehydration. Without treatment, most patients fail to grow normally, and present with associated constipation, urological complication, megacystis, trabeculated bladder, hydroureter, hydronephrosis, and mental retardation. Treatment of NDI consist of sufficient water intake, low-sodium diet, diuretic thiazide, sometimes in combination with a cyclooxygenase (COX) inhibitor (indomethacin) or nonsteroidal anti-inflammatory drugs (NSAIDs), or hydrochlorothiazide in combination with amiloride. Some authors note a generally favorable long-term outcome and an apparent loss of efficacy of medical treatment during school age.
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