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Treatment of patients with lupus nephritis (LN) requires judicious use of immunosuppression. Novel biomarkers may be useful for monitoring disease activity and treatment response. We assessed the utility of urinary monocyte chemoattractant protein-1 (uMCP-1) and urinary tumour necrosis factor-like weak inducer of apoptosis (uTWEAK) for disease activity and treatment response monitoring in South Africans with LN. We recruited consenting patients with active LN confirmed on kidney biopsy. Urinary levels of MCP-1 and TWEAK were assayed at baseline and after completion of induction therapy using ELISA methods. We also collected relevant demographic, clinical and biochemical data for patients included in this study. The mean age of patients in this study was 29.8 ± 10.7 years, 60% were patients of mixed ancestry, 70% had proliferative LN and mean spot urine proteinuria at baseline was 0.37 (0.18–0.59) g/mmolCr. At completion of induction therapy, the level of uMCP-1 had reduced to 314.5 (IQR: 197.0–622) pg/mgCr from a baseline of 1092.7 (IQR 578.6–1848) pg/mgCr (P = 0.06) while uTWEAK had reduced to 36.0 (IQR 17.0–88.0) pg/mgCr from 159.0 (IQR: 88.5–295.5) pg/mgCr (P = 0.03). For patients reaching early complete or partial remission (n = 17), both biomarkers had significantly declined in their urine: uMCP-1 (P = 0.018) and uTWEAK (P = 0.015). There was no reduction of both biomarkers in patients not achieving remission and no association between uMCP-1 or uTWEAK with renal histological features. Our study shows that uMCP-1 and uTWEAK are elevated in patients with active LN, correlated with the remission status (response to treatment) at the end of induction therapy and can, therefore, be useful for monitoring disease activity and treatment response.

Treatment of patients with lupus nephritis (LN) requires judicious use of immunosuppression. Novel biomarkers may be useful for monitoring disease activity and treatment response. We assessed the utility of urinary monocyte chemoattractant protein-1 (uMCP-1) and urinary tumour necrosis factor-like weak inducer of apoptosis (uTWEAK) for disease activity and treatment response monitoring in South Africans with LN.We recruited consenting patients with active LN confirmed on kidney biopsy. Urinary levels of MCP-1 and TWEAK were assayed at baseline and after completion of induction therapy using ELISA methods. We also collected relevant demographic, clinical and biochemical data for patients included in this study.The mean age of patients in this study was 29.8 ± 10.7 years, 60% were patients of mixed ancestry, 70% had proliferative LN and mean spot urine proteinuria at baseline was 0.37 (0.18-0.59) g/mmolCr. At completion of induction therapy, the level of uMCP-1 had reduced to 314.5 (IQR: 197.0-622) pg/mgCr from a baseline of 1092.7 (IQR 578.6-1848) pg/mgCr (P = 0.06) while uTWEAK had reduced to 36.0 (IQR 17.0-88.0) pg/mgCr from 159.0 (IQR: 88.5-295.5) pg/mgCr (P = 0.03). For patients reaching early complete or partial remission (n = 17), both biomarkers had significantly declined in their urine: uMCP-1 (P = 0.018) and uTWEAK (P = 0.015). There was no reduction of both biomarkers in patients not achieving remission and no association between uMCP-1 or uTWEAK with renal histological features.Our study shows that uMCP-1 and uTWEAK are elevated in patients with active LN, correlated with the remission status (response to treatment) at the end of induction therapy and can, therefore, be useful for monitoring disease activity and treatment response.

Biomarkers assist in diagnosing neonatal sepsis but often provide results 6 to 48 h later. Bedside C-reactive protein (CRP) test may help to expedite clinical management. We assessed the performance of point of care test (POCT) CRP against routine laboratory analysis and determined the time difference in obtaining results.A prospective observational study was conducted over 4 months. Neonates clinically indicated, had CRP simultaneously tested using the POCT and laboratory assays.Using similar decision cut-off values of 10 mg/l, POCT compared favourably to laboratory testing. The median times to POCT result was 4 min whereas laboratory results were entered at a median of 4.1 h (95th percentile 8 h) but only checked after 5.5 h (95th percentile 19.8 h).POCT may be a quick and reliable method to determine CRP. It may rationalize antibiotic usage, allow for earlier patient discharge and reduce overall patient management cost.

Background Biomarkers assist in diagnosing neonatal sepsis but often provide results 6 to 48 h later. Bedside C-reactive protein (CRP) test may help to expedite clinical management. We assessed the performance of point of care test (POCT) CRP against routine laboratory analysis and determined the time difference in obtaining results. Methods A prospective observational study was conducted over 4 months. Neonates clinically indicated, had CRP simultaneously tested using the POCT and laboratory assays. Results Using similar decision cut-off values of 10 mg/l, POCT compared favourably to laboratory testing. The median times to POCT result was 4 min whereas laboratory results were entered at a median of 4.1 h (95th percentile 8 h) but only checked after 5.5 h (95th percentile 19.8 h). Conclusions POCT may be a quick and reliable method to determine CRP. It may rationalize antibiotic usage, allow for earlier patient discharge and reduce overall patient management cost.

Background: Immunoassays are prone to interference by various substances which may cause inaccurate results. This type of interference is difficult to detect analytically. Objective: A case of CARDIAC Troponin T Quantitative reader (Roche Diagnostics) assayfailure was detected and investigated in order to ascertain the likely cause. Method: Patient whole blood was mixed with cardiac troponin T-positive blood, patient and control sera were denuded of immunoglobulin G by protein A-affinity chromatographyand patient sera were mixed with mouse serum. Samples were analysed on a CARDIAC Troponin T Quantitative reader. Results: A mixture of patient whole blood and cardiac troponin T-positive blood resultedin assay failure; removal of immunoglobulin G from patient sera reversed the cardiactroponin T assay failure; the addition of mouse serum as a heterophile antibody blocking agent had no effect. Conclusion: It is proposed that the interference resulting in assay failure may not be because of a heterophile antibody, but rather a result of a circulating autoantibody to cardiactroponin T, which may compete with antibody assay reagents for binding sites.

Background Non-esterified fatty acid (NEFA) levels are an important diagnostic tool in the investigation of neonatal hypoglycaemia. NEFA reference intervals have not been reported for neonates previously. Methods The objective of this study was to determine an NEFA reference interval for neonates. Results Heparinized plasma obtained from 106 healthy neonates in the first week of life was analysed using the Roche “Free fatty acid, Half-micro test” kit. Results were then analysed statistically for normality (Shapiro–Wilk test) and reference interval determined non-parametrically (bootstrap method). Conclusions NEFA levels displayed a non-Gaussian distribution and the reference interval (2.5th and 97.5th percentiles) was 0.2–1.5 mmol/L (90% confidence intervals 0.1–0.3 and 1.4–2.0 mmol/L, respectively). The NEFA reference interval in South African neonates less than a week old is similar to that described in infants (1–12 months), indicating that this reference range can be used over the entire neonatal period.

Clinicians use several approaches in the interpretation of laboratory results. These include comparison with predetermined cut-off values or reference values, or a comparison between two sequential results for a specific analyte.1 Each has its own merits. The latter is the focus of this commentary. A simple comparison between two sequential results is not as straightforward as it seems. It should be remembered that each result is associated with its own inherent random variation, meaning that each result obtained is, in fact, a dispersion rather than a singular value. This random variation comprises both variation associated with laboratory activity (pre-analytical and analytical variation) and inherent biological variation (intra-individual) (see box 1). #### Box 1: Total variation CVT = (CVP2+ CVA2+ CVI2)1/2 CVP is considered negligible due to standardised collection protocols, therefore: CVT = (CVA2+ CVI2)1/2 The total variation consists of the sum of all associated variations, where CVP = pre-analytical variation, CVI = intra-individual biological variation, CVA = analytical variation, and CVT = total variation. Therefore, a numerical change is an expected occurrence in sequential testing.1 Whether this numerical change is significant is a question answered by determining the reference change value (RCV) as proposed by Harris and Brown.2 The RCV, defined as the critical difference that must be exceeded between two sequential results for a significant (or true) change to occur,3 incorporates the total variation associated with both results and is demonstrated by the equation in box 2. #### Box 2: Reference change value RCV = Z × [(CVA2+ CVI2) + (CVA2+ CVI2)]½RCV = 2½× Z × (CVA2+ CVI2)½ The …