Observation on decreased serum glutamic oxalacetic transaminase (SGOT) activity in azotemic patients
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, Techicon Instruments Corp., Tarrytown, New York) method (SGOT, SMA) and by the Henry-Karmen kinetic assay (SGOT, K). Extremely low SGOT (SMA) activity (less than 10 IU) 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.
Available from: Heng-chih Pan
- "They may be normal even when active hepatic injury occurs in patients with azotemia or ESRD   or be elevated falsely due to injury in other organs. Several studies demonstrated that patients with ESRD had elevated glutamic oxalacetic transaminase after HD, although the mechanism is unknown . When considering hepatic clearing effects, hepatic clearance of sorbitol was similar before and after HD . "
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The galactose single-point (GSP) test assesses functioning liver mass by measuring the galactose concentration in the blood 1 hour after its administration. The purpose of this study was to investigate the impact of hemodialysis (HD) on short-term and long-term liver function by use of GSP test.
Seventy-four patients on maintenance HD (46 males and 28 females, 60.38 ± 11.86 years) with a mean time on HD of 60.77 ± 48.31 months were studied. The GSP values were compared in two groups: (1) before and after single session HD, and (2) after one year of maintenance HD.
Among the 74 HD patient, only the post-HD Cr levels and years on dialysis were significantly correlated with GSP values (r = 0.280, P < 0.05 and r = -0.240, P < 0.05, resp.). 14 of 74 patients were selected for GSP evaluation before and after a single HD session, and the hepatic clearance of galactose was similar (pre-HD 410 ± 254 g/mL, post-HD 439 ± 298 g/mL, P = 0.49). GSP values decreased from 420.20 ± 175.26 g/mL to 383.40 ± 153.97 g/mL after 1 year maintenance HD in other 15 patients (mean difference: 19.00 ± 37.66 g/mL, P < 0.05).
Patients on maintenance HD for several years may experience improvement of their liver function. However, a single HD session does not affect liver function significantly as assessed by the GSP test. Since the metabolism of galactose is dependent on liver blood flow and hepatic functional mass, further studies are needed.
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ABSTRACT: Vitamin B6 deficiency was evaluated in 37 patients with chronic renal failure and in 71 patients undergoing maintenance hemodialysis (HD) or intermittent peritoneal dialysis (PD). Vitamin B6 deficiency was assessed by the in vitro activity of erythrocyte glutamic pyruvic transaminase (EGPT), without (basal) and with (stimulated) the addition of pyridoxal-5-phosphate to the assay, and the EGPT index (stimulated activity ./. basal activity). Basal and stimulated EGPT activities were below normal in the HD patients, and the EGPT index was increased in each group of patients, indicating vitamin B6 deficiency. Supplemental pyridoxine hydrochloride was given to 30 HD patients who received 1.25 to 50 mg/day (37 studies), 6 PD patients who were given 1.25 or 2.5 mg/day (7 studies), and 8 nondialyzed patients with mild to severe renal failure who received 2.5 mg/ day. In all HD patients, 10 or 50 mg/day of pyridoxine hydrochloride rapidly corrected the abnormal EGPT index and maintained normal values; with supplements of 5.0 mg/day or less, the index was often abnormal, particularly in those who were septic or taking pyridoxine antagonists. In PD patients and nondialyzed patients with renal failure, 2.5 mg/day of pyridoxine hydrochloride was inadequate to correct rapidly the abnormal index in all patients. These findings suggest that HD patients should receive 10 mg/day of supplemental pyridoxine hydrochloride (8.2 mg/day pyridoxine). PD patients and patients with chronic renal failure should receive about 5.0 mg/day of supplemental pyridoxine hydrochloride (4.1 mg/day pyridoxine). When sepsis intervenes or vitamin B6 antagonists are taken, 10 mg/day of pyridoxine hydrochloride may be a safer supplement for all patients.
Available from: Robert Rej
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ABSTRACT: Aminotransferases are ubiquitous enzymes of mammalian cells and several are of important diagnostic use. The application of aspartate aminotransferase activity measurements in serum from individuals suffering from myocardial infarction brought about a new dimension in clinical laboratory testing in the 1950s. This review focuses on measurement techniques for aspartate aminotransferase and their application (a subsequent article will review other aminotransferases). Assay techniques measuring enzyme activity are direct spectrophotometric measurements, manometric techniques, assays using dye substances, coupled enzyme techniques, and radiometric procedures. Of these procedures, the one employing malate dehydrogenase and NADH is the most important and is covered in particular detail. The estimation of the mitochondrial isoenzyme of aspartate aminotransferase is also of clinical interest, in particular for estimating severity of disease or in specific applications (e.g., chronic alcoholism). Methods reviewed for estimation of this enzyme are electrophoresis, chromatography, differential kinetic behavior, and immunochemical separation. Determination of the enzyme protein by techniques independent of its catalytic activity are also reviewed.
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