Abstract Objectives Calprotectin and pentraxin 3 (PTX3) have emerged as potential biomarkers of central nervous system inflammatory diseases, yet evidence based analytical verifications in cerebrospinal fluid (CSF) is lacking. This study aimed to verify the manufacturer’s claims for precision, limit of quantitation (LoQ) and stability for calprotectin using fCAL turbo reagent (Bühlmann Laboratories AG, Schonenbuch, Switzerland); precision and linearity for PTX3 using Human PTX3 ELISA Kit (BioVendor Group, Brno, Czech Republic) in CSF. Methods Samples were collected in additive-free tubes and centrifuged at 400 g, 10 min. Calprotectin was measured on Atellica Solution analyser (Siemens), PTX3 was determined by ELISA method on the Thunderbolt analyser (Gold Standards Diagnostics). The verification protocol was carried out according to Clinical and Laboratory Standards Institute (CLSI) guidelines: precision by EP15-A3, LoQ verification by EP17-A2, and linearity by EP6-A. Calprotectin stability at −20 °C for 7 days was assessed in three CSF samples. Results The CV%s for calprotectin precision were 4.52 % and 1.66 %; for PTX3 were 6.0 % and 8.9 %, respectively. The declared LoQ for fCAL turbo of 50.0 μg/L (CV%<20 %) was verified. The stability equation for calprotectin did not exceed the MPD (41.6 %), and it was y=−0.15× (95 % Cl −0.49 to 0.19), indicating stability at −20 °C for 7 days. The method for PTX3 was linear over the manufacturer declared ranges (3,212.0–406.0 and 3,315.0–411.0 ng/L). Conclusions This study showed that Bühlmann fCAL turbo reagent and the Biovendor Human PTX3 ELISA kit support the determination of calprotectin and PTX3 in CSF for research purposes, with potential future clinical applications.
Abstract The Kidney Failure Risk Equation (KFRE) is a validated tool for predicting the risk of kidney failure in patients with chronic kidney disease (CKD) and is increasingly recommended to guide referral pathways, monitoring, and treatment decisions. As its clinical use expands, laboratories play a central role in ensuring accurate, standardized, and harmonized implementation. However, important methodological questions remain regarding the selection of estimated glomerular filtration rate (eGFR) equations, additional laboratory biomarkers, reporting practices, and analytical considerations, while current guidance remains heterogeneous. This document reviews the available evidence and international guidance on the laboratory implementation of the KFRE, with a particular focus on eGFR equations, creatinine and cystatin C, albuminuria measurement, measured GFR, analytical performance, and reporting considerations. Based on this evidence, the Nephrology Commission of the Spanish Society of Laboratory Medicine (SEMEDLAB) presents consensus recommendations for standardized implementation of the KFRE in routine clinical laboratory practice. By distinguishing the available evidence from expert consensus, this document aims to support harmonized laboratory practice, facilitate consistent KFRE reporting, and promote reliable risk stratification to improve the care of patients with CKD.
Abstract Objectives The aim of this study was to evaluate the performance of serum anti-Müllerian hormone (AMH) concentrations and the luteinizing hormone (LH) to follicle-stimulating hormone (FSH) ratio and to propose a sequential algorithm for identifying polycystic ovarian morphology (PCOM) in women with menstrual irregularity. Methods This retrospective study included 149 women aged 18–40 years evaluated between 2018 and 2023. Participants were classified into control, ovulatory dysfunction (OD), and polycystic ovarian morphology with ovulatory dysfunction (PCOM + OD) groups based on menstrual status and transvaginal ultrasound findings. Serum AMH, LH and FSH were measured by automated immunoassays, and diagnostic performance was evaluated using ROC curve analysis. A new dataset of 42 patients was used to validate the diagnostic performance of AMH and the LH/FSH ratio. Results Women with PCOM + OD had significantly higher serum AMH concentrations and LH/FSH ratios than the OD and control groups, while AMH was also higher in the OD group than in controls. AMH and a regression model combining AMH and LH/FSH had moderate to strong diagnostic performance for identifying PCOM in women presenting with OD, with an AUC of 0.783 and 0.811, respectively. Conclusions Comparing women with PCOM and OD to women with OD alone could provide a more meaningful assessment of biomarker performance than comparisons with healthy controls, as it reflects the real diagnostic challenge encountered in routine practice. A sequential strategy using the LH/FSH ratio as an initial test followed by AMH measurement could improve the selection of patients requiring transvaginal ultrasound.
Abstract Objectives Medullary thyroid carcinoma (MTC) is a rare neuroendocrine malignancy monitored with serum calcitonin (CT) and carcinoembryonic antigen (CEA), whose doubling times guide imaging and treatment decisions. CT interpretation is constrained by analytical and biological variability, prompting interest in complementary biomarkers. Pro-gastrin releasing peptide (ProGRP) shows a low within-subject biological variation, making it attractive for serial monitoring. Methods In this single-centre retrospective study, 43 post-thyroidectomy MTC patients (complete response [CR], n=20; partial response [PR], n=10; progressive disease [PD], n=13) with serial ProGRP, CT and CEA were analysed using patient-level median concentrations. Groups were compared using the Kruskal–Wallis test with Dunn–Holm correction, and biomarkers were correlated at patient level (Spearman). Reference change values (RCV95) were derived from EFLM within-subject biological variation and local analytical imprecision. Biomarker-specific doubling times were estimated in PD as an exploratory analysis. Results All three biomarkers increased stepwise across CR, PR and PD (p<0.001). On single-timepoint comparison, CT showed the broadest discrimination, separating CR from PR and PR from PD, whereas ProGRP and CEA separated only PD from CR. ProGRP correlated strongly with CT (ρ=0.80). RCV95 was narrowest for ProGRP (16.6 %) vs. CEA (25.1 %) and CT (38.2 %). Doubling times were estimable in only a few patients and did not clearly distinguish biomarkers. Conclusions ProGRP behaves as a disease burden biomarker that tracks calcitonin and, through its narrow RCV95, may serve as a fine-grained longitudinal complement for CT and CEA. These hypothesis-generating findings warrant prospective, multicentre validation.
