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Necrosis of the papilla and chronic interstitial nephritis of the renal cortex are the two renal 1esions most commonly. described in cases of analgesic nephropathy. Some authors believed that the necrosis of the papilla was secondary to the cortical changes by which fibrosis of the cortex produced ischemia of papilla and necrosis. However, other authors have suggested that the pathogenesis is, in fact, the reverse and that the cortical changes in analgesic nephropathy are caused by the medullary necrosis. An experimental study was therefore undertaken to clarify this problem and also to determine the influence of increased intrapelvic pressure on the postpapillectomy renal alterations. Followings are the results: 1. In `the group having renal papillectomy, marked tubular dilatation and interstitial edema of the medulla are prominent changes upto two weeks after removal of the papilla. Tubules are usu. ally filled with various casts. After three weeks, there starts the tubular atrophy and interstitial fibrosis with mil infiltration of inflammatory cells. The tubular atrophy and renal scarring become much severe and diffuse six weeks after papillectomy. but glomeruli remain relatively intact. 2. The degree of tubular changes and parenchymal scarring are assumed influential to the size of removed papilla. The tubular atrophy is prominent in distal convoluted tubules and collecting tubules, and the interstitial changes extend from the medulla to the cortex in the late stage. 3. Focal or scattered depositions of amorphous calcium or calcium oxalate are found in about one fourth of cases. 4. In the group having partial ureteral ligation a week after renal papillectomy, the tubular and interstitial changes appear earlier and are more remarkable than those of papillectomy alone. The inflammatory reaction is also more prominent, and conglomeration of glomerulus is noted in some instances of the later stage. The form of the renal scarring found in this experimental study closely resembles that seen in analgesic nephropathy in man. This findings support the view that the cortical lesions in analgesic nephropathy develop as a direct consequence of papillary necrosis and additional ureteral ligation enhances interstitial nephritic process. It is possible that the tubular atrophy and interstitial edema that develop shortly after removal of the papilla may produce cortical changes.
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