A brief review of the literature on traumatic anuria (acute tubular necrosis, lower nephron nephrosis) has been presented, including a complete bibliography. Special attention was paid to the pathology and pathogenesis of the syndrome and it was concluded that Oliver's recent work (271) probably comes closest to presenting the true picture. He describes tubular necrotic lesions for which the chemical toxins (mercuric chloride, carbon tetrachloride) were responsible, and tubulorhectic lesions which were characteristic of the shock kidney. These lesions could appear at any level in the renal tubule and were characterized by destruction of the basement membrane. Pigment casts were apparent if intravascular pigment release was associated with the illness. The work of Phillips, Van Slyke and associates (291, 292, 355, 356), of Oliver (271) and of Block et al (41) lead one to conclude that renal ischemia is the chief pathogenetic mechanism, though it is obvious that specific extrinsic renal toxins play a major role in specific cases. The role of hemoglobin appears to be chiefly in the production of obstructive casts later in the course of the disease; these pigments are precipitated in the lower nephron where urine is concentrated; and acidified, and dehydration and oliguria contribute to their formation.
Three hundred rats were studied in eighteen experiments concerning crush syndrome. It was concluded that the most important single factor tending to aggravate the renal effects of crushing injury is the antecedent state of dehydration. Myoglobin is not an essential factor in the development of renal damage but tends to aggravate the existing uremia. Acute renal failure was seen to be a late effect of shock; animals developed acute tubular necrosis only if initial shock was severe, but not severe enough to produce death from circulatory failure. Development of this delicate balance of factors was aided by reduction of renal reserve by unilateral nephrectomy. A seldom described but distinct and consistent phenomenon was observed in the development of marked, immediate and persistent diuresis in response to the trauma of limb ligation. This polyuria was of a dilute urine and was taken as an indication of initial increased glomerular filtration followed by decreased reabsorption of water because of tubular damage. It was not an indication of a recovery phase as is recorded in the clinical syndrome.
Testosterone propionate, desoxycorticosterone acetate, cortisone acetate and Compound F did not appear to be promising as therapeutic agents, although in one experiment Compound F showed some promise. Neither did combined therapy with testosterone and cortisone reduce the mortality rate or decrease uremia.
Although there was no doubt that the syndrome of acute renal failure due to acute tubular necrosis could be produced in large numbers of these relatively inexpensive laboratory animals by dehydration and limb ligation, production could not altogether be standardized and the syndrome ran such a short course that serial observations were difficult to obtain and separation of shock deaths was occasionally impossible. It is felt that future work might well make use of some other laboratory animal, perhaps the dog or cat, and that an initial stress of controlled hypotension or renal artery occlusion could be used. It is also our opinion that further investigation into the value of Compound F as a therapeutic agent in this syndrome is justified. / Medicine, Faculty of / Graduate
| Identifer | oai:union.ndltd.org:UBC/oai:circle.library.ubc.ca:2429/40841 |
| Date | January 1953 |
| Creators | Morton, Kenneth Sherriffs |
| Publisher | University of British Columbia |
| Source Sets | University of British Columbia |
| Language | English |
| Detected Language | English |
| Type | Text, Thesis/Dissertation |
| Rights | For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use. |
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