Verification study on the NORIP LDH reference intervals with a proposed new upper reference limit.

We verified the lactate dehydrogenase (LDH) reference interval (RI) provided by the Nordic Reference Interval Project (NORIP). The serum LDH concentration was analysed on the Dimension Vista 1500 system with an IFCC method with a bias of +2.1 % and +2.7 % against NFKK Reference Serum X and ERM-AD453/IFCC, respectively, showing verification of transference of the NORIP RI. Selective data mining in clinical laboratory information systems for retrospective serum LDH test results was used to calculate an indirect RI. For the adult age group (18 to <70 years) the limits of the interval was 127 U/L (90 % CI: 123-132 U/L) and 240 U/L (90 % CI: 234-243 U/L). However, the NORIP upper limit for the adult age group is 205 U/L (90 % CI: 198-210 U/L). Accordingly, 25.1 % of LDH test results were above the NORIPs upper limit of 205 U/L. If LDH analysis was requested by the hospital's medical departments, outpatient clinics or general practitioners 29.2 %, 26.2 % and 20.9 %, respectively, were above the 205 U/L limit. Differences in transport time before centrifugation of blood, and different transport principles could not explain the relative high percent of test results above the NORIP 205 U/L limit. The indirect finding of an upper limit of 240 U/L (90 % CI: 234-243 U/L), and the relative high number of test result >205 U/L, suggests that the NORIP upper limit should be adjusted.

Urinary excretion of alpha1-microglobulin and albumin in acute myocardial infarction. Correlation with plasma concentrations of troponin I and C-reactive protein.

OBJECTIVES: Microalbuminuria associated with myocardial infarction (MI) is normally ascribed to glomerular factors, but could just as well involve pathophysiological processes located in other parts of the nephron, e.g. proximal tubules where plasma albumin normally filtered through the glomerulus is almost completely reabsorbed. The aims of this study were to establish whether impaired tubular reabsorption of filtered albumin contributes to microalbuminuria during MI, and whether the urinary excretion of protein relates to plasma levels of C-reactive protein (CRP) and troponin I. MATERIAL AND METHODS: We monitored plasma CRP and troponin I as well as the urinary excretion of albumin and alpha1-microglobulin, a low-molecular-weight plasma protein and marker of tubular proteinuria, in 18 patients with MI. RESULTS AND CONCLUSIONS: The urinary excretion of alpha1-microglobulin and albumin was significantly elevated in nine patients, and the urinary excretion of the two proteins correlated significantly. A decrease in tubular reabsorption of albumin may thus be at least one of the causative factors underlying microalbuminuria during MI. The plasma levels of CRP and troponin I were also significantly higher in this group of nine patients, and correlated with urinary protein excretion, suggesting an interrelationship between inflammatory response and tubular dysfunction. Extrarenal inflammatory processes seem to affect renal tubular function, thereby contributing to microalbuminuria during MI.