Problems of Chronic Pyelonephritis*

The small contracted kidney of chronic pyelonephritis remains one of the enigmas of medicine. Ever since it was fully reviewed in the classical paper by Soma Weiss and Parker in 1939, chronic pyelonephritis has become an increasingly popular diagnosis. As a pathological process its progress is often slow and insidious, and, while it frequently presents clinically as a recurrent or refractory urinary infection, patients are often first seen because of hypertension or proteinuria, or because of one of the many manifestations of renal failure. It is now recognized as the commonest cause of the syndrome of renal failure with hypertension. Despite the intensive clinical studies of the past fifty years and much experimental work in animals, many problems still remain unsolved. How does chronic pyelonephritis arise ? Is it always the end-result of an acute bacterial infection ? What part does obstruction in the urinary tract play in its production, and why does the condition so often appear to be relentlessly progressive ? It is not possible in the course of a single lecture to present a complete survey, but I hope to review some of these problems in the light of recent advances in our knowledge. Chronic pyelonephritis has been defined as the endresult of bacterial inflammation in the kidney (Kleeman et al., 1960)-inflammation usually associated with the Gram-negative coliform bacilli. Until recently it has been essentially a pathological diagnosis, a diagnosis made with confidence only when the kidney could be viewed macroscopically and studied microscopically. The pathologist still has the final word; but modern radiology has provided a means of establishing the diagnosis during life, and now allows the clinician to follow the progress of the disease over years. Unlike other forms of nephritis, chronic pyelonephritis is usually a focal disease, affecting discrete areas of one or both kidneys. The characteristic lesion is the localized pyelonephritic scar, an area of fibrotic renal substance with a sunken cortical scar, interstitial cellular infiltration, dilated tubules, and glomeruli either involved in cellular change or surrounded by periglomerular fibrosis. A diffuse form of chronic pyelonephritis does occasionally occur with typical histology but no local scars. In such cases the possibility of some generalized tubular damage must always be considered ; for the renal changes in gout, in hyperparathyroidism, and in chronic phenacetin poisoning may closely resemble those of chronic pyelonephritis. Whether tubular obstruction alone forms the link between these conditions or whether such obstruction predisposes the kidneys to superadded infection remains uncertain. In chronic phenacetin poisoning renal papillary necrosis is common, and Bengtsson (1962) has shown that, while there is no clear-cut pathological picture by which this form of nephritis can be