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Neoplasms arising in the kidney cortex may not cause hematuria until they break into the renal pelvis; they are not apt to produce pain until they invade the capsule; patients seldom notice the kidney mass themselves, and as a result the tumor has, in most instances, grown to large proportions before recognition. These so-called “nephromata” tend to erode venous channels and thus metastasize widely. By the time the lesion is recognized the tumor is large, it has often metastasized, and as a result the prognosis is most unfavorable. Classification According to Boyd (1a), “there is no more perplexing chapter in the whole of pathology than that which deals with tumors of the kidney.” The influence of Orawitz (2) is still felt, in that all cortical tumors except the embryoma are apt to be roughly construed as hypernephroma. On the other hand, there are those who deny the existence of a true hypernephroma, i.e., a tumor arising from misplaced islands of adrenal tissue, as Carson (3), Judd and Hand (4). These writers state that hypernephroma should be considered as a true renal carcinoma. Arguments against the adrenal origm of this tumor have been listed as follows: (a) No epinephrin has been synthesized from these growths.—Greer and Wells (5), Brooks (6). (b) Double-refracting fat present in hypernephroma is present, also, in the protoplasm of renal epithelium and carcinoma.—Löhlein (7). (c) Tumors of the adrenal may produce abnormalities of the sexual organs, as virilism. Such changes have never been noted with hypernephroma.—Tuffier (8), Ewing (9a), Boyd (1b). (d) The hypernephroma is composed of lipoid-filled cells which have the usual vacuolated appearance following routine preparation in alcohol and xylol. According to the Grawitzian school, these cells closely simulate those in the adrenal cortex, but identical cells are found in adenomata of the kidney. Furthermore, the hypernephromata may take on tubular formation, which is never present in the adrenal.—Boyd (1b). Portmann (10), on the other hand, definitely assumes the presence of hypernephroma. He states: “It originates from an inclusion of suprarenal cortical tissue. It is often confused with carcinoma because it is inclined to deviate very considerably in its histologic structure; however, these two groups have nothing in common from a clinical standpoint.” He (Portmann) continues with the statement that the hypernephroma remains encapsulated for a long period of time and its growth is usually slow, while adenocarcinoma has a tendency to early infiltration and therefore more rapid extension. Furthermore, hypernephromata tend to erode veins and metastasize widely, while adenocarcinomata spread by lymphatic extension. Ewing (9b) takes a more middle ground in that he agrees to the occurrence of adrenal inclusions in the kidney and to the fact that tumors may arise within these rests.
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William E. Howes (1944) studied this question.
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