RENAL ANOXIA SYNDROME: A REVIEW AND REPORT OF 22 CASES

Abstract

Extra-renal azotemias may be classified pathogenetically as being due to shock, dehydration, psychogenic or neurogenic stimulation, hemoglobinurias, allergies, excess protein breakdown, toxic nephrosis and local renal circulatory disturbances (as in heart failure). The common denominator seems to be renal anoxia. In most cases more than one mechanism is involved. In shock, hypotension and increased blood viscosity may diminish renal blood flow while circulating nephrotoxins may damage renal epithelium. Vascular shunts from cortical to juxtamedullary glomeruli may further decrease effective renal flow. In dehydration, electrolyte shifts, blood viscosity changes and increased protein catabolism are involved. Neurogenic and psychogenic mechanisms are demonstrated in postoperative anurias and in the anuria of hysteria. Hemoglobin and its degradation products have been shown to be intensely renal vasoconstrictive. Sulfonamides may combine with renal cell proteins to produce renal allergens. These factors may be superadded to primary renal disease to augment the degree of azotemia. The pathologic lesions vary from none to severe degeneration of renal tubular epithelium not localized to any segment of the nephron. 22 cases were studied. Of these, 12 died. 7 cases with autopsy findings are extensively reported. The true lower nephron nephrosis is most often associated with shock or hemorrhage while other mechanisms causing the renal anoxia syndrome will not show a characteristic histologic pattern.