Efficiency of different strategies to detect autoantibodies to extractable nuclear antigens.

Autoantibodies to extractable nuclear antigens (anti-ENA) are identified mainly in samples positive for antinuclear antibodies (ANA). Although the method of choice for ANA screening is indirect immunofluorescence (IIF), several techniques are available to detect anti-ENA. The aim of this study was to compare the efficiency of five different strategies to determine anti-ENA. During a 2-year period we screened ANA in 30375 samples with IIF, and the 4475 samples ANA positive were tested for anti-ENA by double immune diffusion screening or fluoroenzymeimmunoassay (Screening FI); anti-ENA specificities were then determined by line immunoassay (LIA) or fluoroenzymeimmunoassay (FI). We compared five strategies that involved FI or LIA identification of anti-ENA with or without prior screening, or an algorithm that combined fluorescence pattern, number of anti-ENA specificities requested by the clinician and ANA dilution titer. One cost unit (CU) was defined as the cost of 1 test of ANA determination. We detected 553 anti-ENA positive samples. The most efficient strategy was the algorithm, at a cost of 3.3 CU per sample processed, the second most efficient strategy was screening plus FI identification (cost=3.8 CU), and the third most efficient strategy was screening plus LIA identification (cost=3.9 CU). The fourth most efficient strategy was FI identification without prior screening (13.3 CU per sample) and the least efficient was LIA identification without prior screening (13.6 CU per sample). In conclusion, an algorithm that combined techniques for detection, ANA titer, fluorescence pattern and number of specificities requested was the most efficient strategy for determining anti-ENA.

Determination of Clara cell protein urinary elimination as a marker of tubular dysfunction.

Clara cell 16-kDa protein (CC16) is a protein expressed primarily by the bronchial cells. It is rapidly eliminated by glomerular filtration, reabsorbed almost entirely, and catabolized in proximal tubule cells. To date, normal values for urinary CC16 in healthy children have not been determined. We have studied 63 pediatric patients (mean age 8.17 +/- 3.91 years) and 31 healthy children (control group; mean age 8.83 +/- 3.65 years). In the control group, the CC16/creatinine ratio was 1.22 +/- 1.52 microg/g. In 16 out of 31 control children, the value of the ratio was zero. Fourteen patients (22.2%) showed a high CC16/creatinine ratio; in contrast, among these same patients, the ratio N-acetyl-beta-D: -glucosaminidase (NAG)/creatinine was elevated in seven cases (11.1%) and the ratio beta2-microglobulin/creatinine was elevated in seven cases (11.1%). The three parameters were in agreement in 51 patients (80.9%). Among the patients, the CC16/creatinine ratio was correlated with both the beta2-microglobulin/creatinina ratio (r = 0.76, P < 0.001) and the NAG/creatinine ratio (r = 0.6, P < 0.001). Our findings indicate that CC16 is a good marker of proximal tubular function in childhood. The highest observed values were in children with proximal tubulopathies, in children with chronic renal failure, and in those treated with cyclosporine.