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Technetium‐99m‐dimercaptosuccinic acid studies and urinary tract infection in childhood

New imaging modalities developing in nuclear medicine and ultrasonography are proving invaluable in studying the pathophysiology of many disorders of the infant’s and child’s urinary tract. They have generated an extensive literature (1, 2) and a number of experimental studies (3, 4). Each has its strengths and weaknesses. While experience is gained and technical and interpretative expertise increases, the clinician encounters various uncertainties. The technetium-99m-labelled dimercaptosuccinic acid (Tc-DMSA) study provides a renal image based on DMSA uptake. This in turn is dependent on glomerular filtration, proximal tubule membrane transport and intrarenal blood flow distribution. By using oblique views or tomographic studies the site and extent of any defect of isotope uptake can be clarified without any increase in radiation, which depends on the dose injected. The TcDMSA study also provides an estimate of the percentage of total function contributed by each kidney. Defects of isotope uptake, often diffuse, may be seen when there is acute inflammation of the parenchyma, appearances which can be reversible. Alternatively, more discrete changes may be seen, usually with a broken contour, due to permanent, established pathology (including renal scars). Ultrasonography is recognized as being unreliable in detecting either inflammation or renal scarring or vesicoureteric reflux (VUR) (5, 6). The intravenous urogram (IVU), which demonstrates the structural changes of renal scarring, cysts or hydronephrosis, is also subject to technical and interpretative disadvantages if used only infrequently (7). Problems that arise from total reliance on DMSA studies include: (i) the non-specific nature of a functional image, (iii) differentiation between acute and permanent changes, and (iii) the difficulty in deciding whether the kidney is normal when there are equivocal minor changes (8, 9). Furthermore, the quality of the image, which can vary for technical reasons, will affect interpretation. Interobserver variation has been studied, with differing results (10–12). Resolution of some of these problems has been helped by comparative studies between IVU and DMSA (12–14) experimental studies of UTI in refluxing piglets (3, 4) and rats (15) and by the classification of abnormal DMSA images and their relation to divided function (8, 16). The dilemmas facing the clinician are the timing of the DMSA study, the significance of abnormal images and the radiation dose. The choice oftiming is between an early or a delayed study. DMSA imaging within 5–10 d of the onset of infection will demonstrate parenchymal involvement (whether acute or previously present) and indicate those patients needing intensive treatment, follow-up and further investigation. A disadvantage of this approach is the need for later renal imaging to ensure that treatment has been successful or to confirm permanent change. (It has been suggested, however, that if the study is normal, further imaging is unnecessary unless UTI recurs, more experience is needed before such a policy can be adopted with confidence.) A delayed DMSA study should identify changes that are permanent. This depends on how long reversible changes can persist, an issue which Jakobsson and Svensson have attempted to address (17). On the basis of their findings they recommend postponing the DMSA study until at least 5 months after the UTI. Of the 185 children with symptomatic UTI in their study (100 of them under 1 y old) 85% had an abnormal DMSA; 4–12 months later 58% had abnormal results; but only 41% of the 158 children scanned between 1.5 and 3.9 y after infection had an abnormal DMSA. However, the time at which the images became normal, the type of image that persisted and its relation to recurrent infections remain unclear. Stokland et al. (9) found abnormal DMSA results in 42% of 175 children (75% under 1 y old) with their first known UTI and in 38% of 157 children 1 y after their initial infection (18). All those over 2 y old had VUR. The delayed approach can only be justified by managing all infants and children with UTI as if they had acute renal involvement. This is not always easily achieved. Many parents may wish to have a reason for continuing prophylactic antibiotics. They may also be reluctant to return for invasive investigation of an apparently well child, months after the presenting infection. The significance of DMSA abnormalities in some instances can only be assessed by longer follow-up than is yet available. This applies particularly to abnormal images seen under the age of 1 y without demonstrable VUR. What is known, for example, of the infant’s renal vascular response to febrile infections other than those of the urinary tract and any consequential DMSA changes? Comparison of IVU or DMSA images in patients with radiological renal scarring has generally shown good but Acta Pædiatr 87: 132–3. 1998