As a consequence of acute circulatory failure due to hemorrhagic, traumatic or toxic shock, renal failure develops. After the peripheral signs of shock have disappeared and blood pressure is restored, urine flow declines to such low values that solute excretion is almost completely suppressed. The serum urea level climbs day by day to values which may reach 600 mg.% or more. In patients who recover, a polyuric phase sets in after a week of oliguria. However, the concentrating power of the kidney is by no means regained. Creatinine U/P’s show values as low as 5, and urine tonicity — as revealed by a specific gravity of 1012 — is equal to that of serum. The state of uraemia shows very little change until the concentrating function of the kidney has been restored (Fig. 1).
KeywordsFiltration Mercury Urea Creatinine Renin
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- 1.Boylan, J. W., and E. Asshauer: Unpublished data.Google Scholar
- 2.Deetjen, P., and K. Kramer: Pflügers Arch. Physiol. (G.) (in press).Google Scholar
- 6.Kramer, K., and P. Deetjen: Unpublished data.Google Scholar
- 9.Munck, O.: Renal Circulation in Acute Renal Failure. Oxford 1958.Google Scholar
- 10.Munck, O., N. Lassen, P. Deetjen and K. Kramer: Lancet (G. B.) (in press).Google Scholar
- 11.Oliver, J., M. MacDowell and A. Fracy: J. Clin. Invest. (U. S. A.) 30, 1305 (1951).Google Scholar
- 12.Pappenheimer, J. P., and W. B. Kinter: Amer. J. Physiol. 185, 371 (1956).Google Scholar
- 14.Trueta, J., A. E. Barcley, P. M. Daniel, K. J. Franklin and M. M. L. Prichard: Studies of the Renal Circulation. Oxford 1947.Google Scholar
- 17.Wiggers, C.: Physiology of Shock. New York 1950.Google Scholar