Background: A failure of urine ammonium to increase during acidosis indicates impaired renal acidification, and the urinary ammonium concentration is therefore a useful investigation in determining the cause of a metabolic acidosis. However, urine ammonium measurements are not widely available in routine diagnostic laboratories. This has led to the use of urine anion or osmolar gaps, which are unsatisfactory as surrogates for urine ammonium measurement. Methods: We evaluated the adaptation of two widely available automated plasma ammonium assays for measurement of urinary ammonium. Results: Both assays showed good recovery and linearity in urine samples spiked with ammonium chloride, and acceptable precision. Urine ammonium concentrations estimated from urinary anion and osmolar gaps showed poor agreement with measured urine ammonium concentrations. Conclusions: Direct urine ammonium measurements are easily performed with modern autoanalysers by simple adaptation of routine plasma ammonium assays. The use of urine anion and osmolar gaps should be abandoned where direct measurement is available.
Aim: To investigate and describe cardiac troponins in subjects with acute kidney injury (AKI). Methods: A prospective observational study of troponin in subjects presenting with AKI in a tertiary hospital. Creatine kinase-MB (CKMB), troponin I (Abbott Laboratories), and troponin T (Roche 4th generation) were measured. Patients with conditions known to cause elevated troponin levels were excluded. Results: Nineteen subjects were enrolled in the study. Six subjects had troponin I and T concentrations above the 99th percentile of a reference population. There was high concordance of result between troponin I and troponin T. However, the concordance of elevated troponin levels with CKMB was less marked at 45%. Statistically significant factors associated with elevated troponin levels were age over 60 years, abnormal electrocardiogram, and history of previous ischemic heart disease. Conclusion: This is the first study able to demonstrate impaired renal function occurring acutely, without known confounders, results in elevated troponin levels. This suggests that impaired renal function disease influences plasma troponin levels in AKI as well as in chronic kidney failure.
The challenges associated with diagnosing tuberculous pleural effusion have led to the use of pleural fluid adenosine deaminase (pfADA) as a biomarker for infection. This study retrospectively reviewed the diagnostic performance of pfADA, the pleural fluid lactate dehydrogenase (LD)/ADA ratio, and combinations of these two parameters in 1,637 episodes of pleural effusion in the low-tuberculosis (TB)-incidence setting of Auckland, Aotearoa New Zealand, from between March 2008 and November 2014. The median pfADA in 57 TB pleural effusion episodes (58.1 U/liter) was significantly higher ( < 0.001) than in 1,580 non-TB pleural effusions (11.4 U/liter). The median LD/ADA ratio in TB pleural effusion (8.2) was significantly lower ( < 0.001) than in non-TB pleural effusions (30.5). The pfADA and pleural fluid LD/ADA ratio AUC values (that is, receiver operating characteristic [ROC] curve analysis with determination of the ROC area under the curve) were 0.93 and 0.94, respectively. The pfADA thresholds of ≥15 and ≥30 U/liter demonstrated sensitivities of 100% (95% confidence internal = 93.7 to 100) and 93.0% (83.3 to 97.2), specificities of 62.7% (60.3 to 65.0) and 87.3% (85.6 to 88.9), positive predictive values (PPVs) of 8.8% (6.9 to 11.2) and 20.9% (16.4 to 26.4), and negative predictive values (NPVs) of 100% (99.6 to 100) and 99.7% (99.3 to 99.9), respectively. LD/ADA ratio thresholds of <25 and <15 demonstrated sensitivities of 100% (93.5 to 100) and 89.1% (78.2 to 94.9), specificities of 61.6% (59.1 to 64.0) and 84.8% (82.9 to 86.5), PPVs of 8.5% (6.6 to 10.9) and 17.3% (13.3 to 22.0), and NPVs of 100% (99.6 to 100) and 99.5% (99.0 to 99.8), respectively. A combination of pfADA ≥ 30 U/liter and an LD/ADA ratio < 15 increased the specificity and PPV to 97.8% (96.9 to 98.4) and 57.3% (46.5 to 67.5) but decreased the sensitivity to 85.5% (73.8 to 92.4). The primary value of pfADA in a low-TB-incidence setting, such as Auckland, is in utilization of its high NPV.
Analytical interference identified on one immunoassay should raise the possibility of other affected results. Characterization of interference may help to identify other potentially affected immunoassays. In the case of anti-streptavidin antibodies, the pattern of interference mimics that due to biotin ingestion. However, the degree of interference varies between individual assays and between patients.
This report demonstrates that potentially significant consequences can arise from the failure to consider heterophile antibody interference. Clinicians who interpret test results need to be aware of the potential for interference in immunoassays by heterophile antibodies.
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