1P-S6-4

NEW APPROACHES TO URINARY TRACT INFECTIONS IN CHILDHOOD

Prof. Dr. Enver Hasanoglu

Gazi University Faculty of Medicine

Department of Pediatric Nephrology

Ankara, TURKEY

Although over the past decade we have gained many new insight into the etiology and pathophysiology of urinary tract infections (UTIs), this issue remains a common problem in childhood. Experimental studies combined with clinical observations have clearly demonstrated the critical role of infections in irreversible/progressive renal scarring and subsequent renal failure, which is the most severe long-term sequelae of childhood UTIs. Remarkable success rate of nonsurgical management of vesicoureteral reflux and nonobstructive hydronephrosis, the recognition of the importance of bladder and bowel dysfunction in the cause of recurrent UTIs has led improved management of these children and has prevented them from unnecessary surgical procedures. The imaging modalities and their timing have also changed. New evidence shows that the radiologic studies may be performed during a brief hospital admission or as soon as practical on an outpatient clinic, eliminating the previously recommended 4- to 6-week waiting period during which many children were lost to follow-up. Today intravenous pyelography is completely replaced by ultrasonography and renal cortical scintigraphy for the evaluation and follow-up of UTIs. Sonography is a non-invasive and radiation-free technique that shows structural abnormalities of the urinary tract. Technetium 99m-labeled dimerkaptosuccinic acid (DMSA) renal scan allows for identification of acute pyelonephritis and the ability to document the extent and progression of renal parenchimal damage. Indirect voiding scintigraphy with Technetium 99m-labeled mercaptoacetyltriglycine (MAG3) is an invasive and alternative investigation method for vesicouretreral reflux diagnosis and follow up.

More recently, some inflammatory mediators i.e. cytokines, chemokines have begun to be studied for clarifying the exact mechanism of renal scarring during the courses of pyelonephritic attacks. Increased urinary excretion of interleukin-6 (IL) and IL-8 levels were highlighted in some clinical-based studies, IL-1 beta, IL-4, IL-6, IL-10, IL-12, transforming growth factor beta and tumor necrosis alpha mRNA expression in the kidney tissue were also demonstrated in experimental acute pyelonephritic mice models. These cytokines are accused for mediating the inflammatory process and producing further damage in kidney tissues. Since developing kidneys are highly susceptible for these factors in infancy, prompt antimicrobial therapy and an additional appropriate hydration for the mechanical dilution of leukocytes and cytokins in the urine are of particular importance. Although speculative, considering that there is a close link between angiotensin II and type I receptor-mediated renal scarring, angiotensin II type I receptors blokers have been suggested as a complementary therapy for preventing possible deleterious effects of acute pyelonephritis on young kidneys. The goal of the therapy is to prevent renal scarring and progress to renal failure and for this approach prompt and agressive antimicrobial therapy is essential especially during the infancy.