It is now universally obvious that any discussion on chronic pyelonephritis necessitates exact definition. There has been so much loose talk on the subject that some doubt arises as to whether there really is any such entity. Let us take for our definition “those changes in the kidney which result directly from bacterial infection” and confine ourselves to what appear to be acceptable facts. Of these the first in importance from a radiological point of view is that the condition must be focal. This is a basic concept. Generalized changes resulting from bacterial action have simply not yet been described unless they follow the confluence of focal lesions, and conditions in the kidney which are not focal in character are therefore not of direct bacterial origin. The second fact of importance is that the late infective process, which usually commences in the medulla, is a localized area of fibrosis or scar, usually large and affecting the whole of the thickness of the renal substance. The outer surface is dragged inward, and the renal papilla outward with secondary distortion of the calyx (Fig. 1). The surface depression is irregular, with well defined edges, and may vary in diameter from a few millimeters to several centimeters. The surrounding renal tissue is completely normal or hypertrophied. Indeed, one of the dramatic features of the coarse scar is the sudden change from gross abnormality to normality at its edges. In this it resembles an infarct. These large scars are the hallmark of the renal condition known as primary atrophic pyelonephritis. Their size is a peculiar feature of the disease and requires stressing (Fig. 1). Small scars from infection inevitably occur, but it is not proved that they have any more significance than small scars elsewhere in the body. Certainly, the presence of a few small scars scattered throughout a kidney, even if proved to be of bacterial origin, can scarcely justify an overall diagnosis of chronic pyelonephritis. The stem of the affected calyx may not be dilated unless the scar is very large. With associated obstruction or severe vesicoureteral reflux some dilatation is to be expected, but neither gross reflux nor obstruction are necessarily a part of the primary picture. The cup of the calyx is no longer a cup, the papilla no longer projects into it. From being, as it were, just the porcelain of the cup the calyx now becomes both porcelain and the space within it and presents a clubbed appearance with a smooth margin quite unlike the ragged cavity found in active tuberculosis or in extensive papillary necrosis. The renal substance between the clubbed calyx and the surface may be only slightly reduced in thickness in an early stage but becomes progressively narrower as contraction advances until only a few millimeters of scar tissue remain of the normal 2.5 cm of renal substance.
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