GEORGE A. COHEN, M.D.; JOHN A. GOFFINET, M.D.; RICHARD K. DONABEDIAN, M.D.; HAROLD O. CONN, M.D.
Grant support: in part by a grant from the Stratfield Fund.
▸Requests for reprints should be addressed to Harold O. Conn, M.D., Department of Medicine, Veterans Administration Hospital, West Haven, CN 06516.
COHEN GA, GOFFINET JA, DONABEDIAN RK, CONN HO. Observations on Decreased Serum Glutamic Oxalacetic Transaminase (SGOT) Activity in Azotemic Patients. Ann Intern Med. 1976;84:275-280. doi: 10.7326/0003-4819-84-3-275
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Published: Ann Intern Med. 1976;84(3):275-280.
Serum glutamic oxalacetic transaminase (SGOT) activity may be decreased or even absent in patients with uremia. We correlated urea concentration with SGOT activity by the automated Rush (AutoAnalyzer, Technicon Instruments Corp., Tarrytown, New York) method (SGOT, SMA) and by the Henry-Karmen kinetic assay (SGOT, K). Extremely low SGOT (SMA) activity (< 10 lU) was found in 6% of 5030 consecutive samples, and 71% of them occurred in patients with azotemia. SGOT activity was inversely proportional to urea concentration. A similar but less obvious pattern was observed with the SGOT (K) assay. SGOT activity increased significantly after hemodialysis in a group of 16 patients studied by both methods. It was not inhibited either by urea or uremic serum added in vitro. The explanation for this phenomenon is not known.
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Nephrology, Renal Replacement Therapy.
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