Renal Anoxia Syndrome: A Review and Report of 22 Cases

AZOTEMIA from nonrenal disease states has received much attention in the literature in recent years. Such azotemia has been described in a multi-tude of conditions — medical, surgical, obstetrical, physical and allergic. A variety of names has been given to this syndrome of renal insufficiency, among them acute Bright's disease, acute tubular nephritis, prerenal azo-temia, lower nephron syndrome, traumatic kidney, shock kidney and crush syndrome. Since the pathogenesis and the pathologic lesions are equivocal and the only discernible common factor seems to be renal anoxia, we con-sider the best description to be renal anoxia syndrome, as suggested by Maegraith et al.1 It is improbable that azotemias produced by such diverse clinical entities are identical in etiology and pathogenesis. Moreover, descriptions of the lesions of the renal anoxia vary considerably. The pathogenesis also has been diversely ascribed to renal vasospasm from hormonal, toxic or neuro-genic mechanisms, to nephrotoxins, to a reduction of renal blood flow by shunting mechanisms, and to nephron nephrosis. It is the purpose of this paper to review the various clinical, pathogenetic and pathologic aspects of this interesting syndrome and to add our experience from our study of 22 cases obtained from the medical and surgical wards of