Mitch W E, Walker W G
Lancet. 1977 Aug 13;2(8033):328-30. doi: 10.1016/s0140-6736(77)91487-8.
The role of raised plasma renin and angiotensin-II concentrations in the development of acute renal failure in man was examined in patients in shock from various causes and in patients in whom hypotension was used to promote haemostasis. Ten of the thirteen patients in shock had raised angiotensin-II concentrations in peripheral blood and acute renal failure manifested by oliguria, increasing serum-creatinine, a urine osmolality of less than 400 mos-mol/kg and a urine/plasma osmolality ratio of less than 1-5. Although patients who were hypotensive for periods of 1 h 45 min to 4 h to promote haemostasis during surgery had similarly raised plasma-renin activity and angiotensin-II concentrations in peripheral venous blood, they did not have acute renal failure. It is concluded that high plasma-angiotensin-II concentrations do not explain the pathogenesis of acute renal failure in patients in shock.