Renal anoxia and the traumatic uræmia syndrome

Darmady, E. M.

doi:10.1002/bjs.18003413505

Cited by 25 publications

(5 citation statements)

References 35 publications

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“…Postmortem renal histology revealed renal tubular degeneration [5,6] in a similar pattern to that produced by clamping of the renal artery in animal models. From these observations, a paradigm of ischemic ARF secondary to inadequate blood flow was developed [7,8] .…”

Section: Introductionmentioning

confidence: 86%

Renal Blood Flow during Acute Renal Failure in Man

et al. 2009

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Background:In the critically ill, ischemia secondary to decreased renal blood flow (RBF) is believed to be central to the pathogenesis of acute renal failure (ARF); however, the scientific basis for this conclusion has not been systematically evaluated. Methods: Systematic interrogation of the Pubmed database, and screening bibliographies of retrieved reports, for studies of human ARF where RBF was measured. Results: Thirty-two articles published between 1944 and 2008 describing RBF in 373 patients with ARF were identified. Overall, mean RBF during ARF was 387 ml/min. It was 329 ml/min when estimated by clearance-based techniques (15 studies) and 471 ml/min when measured with nonclearance-based techniques (17 studies). Only 46 patients had measurements in the intensive care unit where mean RBF was 306 ml/min. Normal RBF was reported in 14 publications, mean 1,192 ml/min. Conclusions: Limited information is available on RBF during ARF in the critically ill. Measurements in contemporary patients are required to further our understanding of this condition.

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Section: Introductionmentioning

confidence: 86%

Renal Blood Flow during Acute Renal Failure in Man

et al. 2009

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“…Twelve hours after admission his blood pressure fell to 100/70 mm. Hg, without signs of clinical shock, remained low for 24 hours, and then gradually rose to 120/80. SGOT activity 8 hours after the onset of the hypotension had increased to 870 units ( fig.…”

Section: Methodsmentioning

confidence: 95%

High Serum Transaminase Activity in Heart Disease

Killip

Payne

1960

Circulation

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A survey of all patients with very high serum glutamic oxalacetic transaminase activity encountered during a 30-month period at The New York Hospital revealed 17 patients with cardiac disease who had 1 or more serum glutamic oxalacetic transaminase (SGOT) determinations exceeding 500 units. None had clinical evidence of primary liver or gallbladder disease. Eleven were admitted with acute myocardial infarction, 6 with severe heart failure. All 17 developed hypotension or shock and all but 1 right heart failure prior to high SGOT activity. Several patients had abnormalities of liver function when SGOT activity was very high. In 4 there was an excessive increase in prothrombin time following administration of anticoagulants. In the 8 patients who came to autopsy there was histologic evidence of acute hepatic central necrosis. In 4 there was necrosis of both heart and liver, in 4 necrosis of liver alone. Clinical and autopsy data from a control series of patients with heart disease selected without regard for the level of SGOT activity corroborate the association between hypotension, central necrosis of the liver, and increased SGOT activity. Increase in venous pressure in the absence of hypotension was not associated with acute central necrosis or elevated SGOT activity. It is concluded that very high SGOT activity (>500 units) in patients with heart disease is at least in part caused by acute hepatic central necrosis secondary to a drop in cardiac output and reduced hepatic blood flow. Caution is urged in the interpretation of increased blood activity of intracellular enzyme systems as evidence for myocardial necrosis. Acute circulatory changes may result in hepatic necrosis and increased blood enzyme activity without myocardial infarction.

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“…AKI is most commonly associated with systemic diseases, such as septic shock, major surgery and cardiogenic shock [1], but a specific mechanism causing AKI to develop in specific patients can rarely be determined. Since the early description of an "acute uremia syndrome" in crush injury victims during World War II [5,6] and its association with histopathological findings similar to those found in experimental renal artery ligation, ischemia or some form of alteration in renal blood flow has been thought to play a pivotal role in the pathogenesis of AKI. This paradigm that essentially all AKI in critically ill patients is the result of some form or degree of ischemia remains of continuing conceptual dominance to this day [7].…”

Section: Introductionmentioning

confidence: 99%