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Modular analyser

Manufactured by Roche
Sourced in Switzerland, Germany

The Modular Analyser is a versatile and automated laboratory instrument designed for clinical diagnostics. It is capable of performing a wide range of analytical tests efficiently and accurately. The core function of the Modular Analyser is to automate and streamline various clinical laboratory processes, enabling healthcare professionals to obtain reliable test results in a timely manner.

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15 protocols using modular analyser

1

Measuring Urinary and Serum Free Light Chains

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Serum and urine were processed immediately after collection according to pre-defined standard operating procedures and stored at -80°C until analysis.
Urinary FLCs were measured by turbidimetry on a Roche Modular P analyser using the Freelite immunoassay (The Binding Site Group Ltd, Birmingham, UK). To correct for variations in urine concentration, urinary FLCs were divided by urine creatinine concentration to give urinary FLC/creatinine (FLC/Cr) ratios in mg/mmol, i.e. a kappa/creatinine ratio (KCR) and a lambda/creatinine ratio (LCR). Serum creatinine measurements were performed on a Roche Modular analyser using a rate-blanked and compensated Jaffe reaction, and eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation [20 (link)]. Serum kappa (κ) and lambda (λ) FLC concentrations were measured by nephelometry on a Dade-Behring BN II System (Siemens AG, Erlangen, Germany) using the Freelite assay. Urine ACR was measured using a Roche Hitachi 702 analyser. Other biochemistry testing was performed by the local clinical laboratories in accordance with the current standard of care.
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2

Stress, Inflammation, and Physical Measures

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Waist circumference and height and weight (for calculation of BMI) were measured by trained Lifelines’ personnel during a physical visit of the second assessment. In addition to the level of psychological stress as determined by the LDI, we evaluated counts of different types of leukocytes and CRP levels as measures of inflammation and therefore indirect physical components of perceived stress (Del Giudice & Gangestad, 2018 (link); Dijkstra-de Neijs et al., 2020 (link)). Blood samples were also drawn during a physical visit of the second assessment. CRP levels were processed using a nephelometric assay in a Roche Modular analyser (Roche, Basel, Switzerland).
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3

Creatinine Measurement Protocol Conversion

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Serum creatinine was measured routinely in our central chemistry laboratory by an isotope dilution mass spectrometry (IDMS)-traceable enzymatic assay on the Roche Modular analyser (Roche, Mannheim, Germany) from 1 March 2006 onwards. Before this date, samples were measured by Jaffe alkaline picrate assay on the Merck Mega Analyzer (Merck, Darmstadt, Germany). Values obtained by the Jaffe method were converted to allow comparison with the Roche method by the formula (YRoche (µmol/L) = (XJaffe (µmol/L) – 8)/1.07) [16 ]. To make sure that this conversion would not influence our results, we separated the analyses into the group that donated before 2006 and the group that donated after 2006 and observed no discrepancies between the two groups nor compared with the total cohort (Supplementary data, Table S1). Creatinine clearance was calculated from the 24-h urine collected the day before the measurements.
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4

Measuring High-Sensitivity C-Reactive Protein

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Fasting blood samples from consenting LiLACS NZ participants were collected at baseline by trained phlebotomists. Samples were centrifuged and stored at -80 degrees Celsius required for processing. High sensitivity C-reactive protein (hs-CRP) was measured by a laboratory that met International Accreditation New Zealand standards, using the antigenantibody method, immunoturbidimetric reading and processed on the P module of the Roche Modular analyser (Roche Diagnostics GmbH, Mannheim, Germany).
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5

Lipidomics Quantification Validation

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A series of control blood plasma (sample volume: 1.25, 2.5, 5.0, 10.0, 15.0 μl) was measured to prove detection linearity of quantified lipid species for the expected total lipid concentrations of 2.0–28.3 mM. For the analyzed samples of this screen the total lipid concentration in blood plasma varied from 5.6–18.7 mM. Within the tested concentration range the adjusted R2 was greater 0.98 for the quantified lipid analytes.
Total triacylglycerol and cholesterol concentrations, as specified by lipidomics, were correlated with quantities obtained by standard enzymatic methods on a MODULAR analyser (Roche, Indianapolis, IN). The specified concentrations correlated well for total triacylglycerol (relative error = -5.48 ± 8.77%, adj. R2 = 0.9754, slope = 1.0151) and total cholesterol (relative error = 7.61 ± 5.44%, adj. R2 = 0.9362, slope = 0.9833). The data comparison uncovered 1 experimental outlayer in 91 analyzed plasma samples. For this sample total triglyceride differed by 7.9x; total cholesterol by 1.6x.
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6

Creatinine, eGFR, and CRP Measurements

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Serum creatinine measurements were performed on a Roche Modular Analyser using a blank rated compensated Jaffe reaction, and eGFR was estimated using the creatinine-based CKD-EPI equation33 (link). Urinary creatinine was measured using the ADVIA 1800 Chemistry System (Bayer HealthCare). Urinary ACR was measured using a Roche Hitachi 702 analyser. C-reactive protein (CRP) was measured using the Full Range C-Reactive Protein Kit on a SPATM automated PLUS turbidimeter (The Binding Site Group Ltd, UK). The normal range for CRP is between 0.1 and 9 mg/L, with 90 percent below 3 mg/L34 (link).
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7

Bone Turnover Markers Assessment

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Blood samples were collected from all participants for analysis. Serum bone formation marker osteocalcin (OC) (normal reference value: 26.5 (12.8–55.0 95% CI) ng/ml) and bone resorption marker C-terminal telopeptides of type 1 collagen (CTX) (normal reference value: 0.439 (0.142–1.351 95% CI) ng/ml) were measured using enzyme-linked immunosorbent assay (ELISA) (Immunodiagnostics Systems Ltd (IDS); intra-assay CV was 1.8% & 4.7%; respectively). Serum total alkaline phosphatase was quantified by Roche Modular Analyser and expressed as a bone formation marker (u/L). Urinary bone resorption markers CTX (normal reference range: 324 (121–874 95% CI) µg/mmol/Cr) and deoxypyridinoline (DPD) (7.56 (2.27)/7.94 (3.25) nmol DPD/mmol Cr) were measured using enzyme immunosorbent assay (EIA) (Urine CrossLaps EIA, IDS, intra-assay CV was 4.7% and Urine DPD EIA, Metra DPD EIA kit; Quidel, intra-assay CV was 4.3%). Urinary CTX and DPD results were both corrected for urinary concentrations of creatinine (Cr). CTX:OC ratio was calculated. A high CTX:OC ratio means higher bone resorption relative to bone formation.
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8

Calculating eGFR and Assessing Albuminuria

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The CKD‐EPI (Chronic Kidney Disease Epidemiology Collaboration) equation incorporating creatinine was used to calculate eGFR (Levey et al., 2009). Serum creatinine was measured using a Roche Modular Analyser using a blank rated compensated Jaffe reaction. Albuminuria was assessed using urine ACR, which was measured using the ADVIA 1800 Chemistry System (Bayer HealthCare).
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9

Serum and Bile Acid Biochemical Analysis

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Serum biochemical markers [alkaline phosphatase (ALP), alanine aminotransferase (ALT), bilirubin] were determined in an automatic analyser (Modular analyser; Roche Diagnostics GmbH, Mannheim, Germany) by using standard assays. Total serum and biliary BA levels were determined spectrophotometrically by using a Bile Acids kit (Trinity Biotech, Jamestown, NY, USA). BA levels in urine were determined by gas chromatographic/mass spectrophotometric method as previously described 34 .
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10

Renal Function and Complement Levels in Lupus Nephritis

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Serum creatinine was analysed according to clinical routine at the Karolinska University Hospital Clinical Chemistry Department and expressed as micromoles/liter (μmol/L). Renal function (estimated glomerular filtration rate, eGFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation (CKD-EPI).24 (link)Complement levels were determined on a modular analyser (Roche), with normal ranges of 0.67–1.29 g/L for C3 and 0.13–0.32 g/L for C4.
In the LN group, a subset of patients was sampled before establishing this method. Such samples were analysed by nephelometry array (Beckman Coulter). The normal level using this method was 0.5–1.2 g/L for C3 and of 0.1–0.4 g/L for C4.
Anti-dsDNA antibodies were routinely analysed over the years using different methods at the Department of Clinical Immunology at the Karolinska University Hospital.
For statistical purposes, and considering the changes in laboratory methods, C3, C4 and anti-dsDNA were considered as categorical variables in this study, based on their being outside or within reference ranges.
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