IntroductionBesides routine serum markers of inflammatory diseases, the diagnostic potential of selected urinary proteins has not been fully exploited yet. Former studies revealed that urinary orosomucoid (u-ORM) might have complementary information in inflammatory disorders. Our aim was to develop and validate a fully automated method for u-ORM measurements and to evaluate its potential clinical impact on systemic inflammatory diseases.Materials and methodsA particle-enhanced immune turbidimetric assay was validated for a Cobas 8000/c502 analyzer to determine u-ORM levels. Spot urine samples from 72 healthy individuals, 28 patients with Crohn’s disease and 30 septic patients were studied.ResultsOur assay time was 10 minutes and the detection limit of u-ORM was 0.02 mg/L. The intra- and inter-assay imprecision expressed as CV was less than 5%, and the recovery ranged between 95–103%. Within 10 to 60 years of age, a preliminary reference range for urinary orosomucoid/creatinine ratio (u-ORM/u-CREAT) was found to be 0.08 (0.01–0.24) mg/mmol [median (2.5–97.5 percentiles)]. Compared to controls, a five-fold increase of u-ORM/u-CREAT values in Crohn’s disease and approximately a 240-fold increase in sepsis were observed.ConclusionsWe set up a fast, sensitive and precise turbidimetric approach for automated u-ORM determination. Our highly sensitive assay is ideal for routine u-ORM measurements and might be a potential novel laboratory test in the management of systemic inflammatory processes.

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Aim: There is no commercially available urinary cystatin-C (u-CYSC) test in the market. Therefore, we optimized and validated an automated immune turbidimetric test for u-CYSC measurements and investigated u-CYSC concentrations in acute and chronic diseases which might lead to renal tubular disorders. Materials & methods: A particle-enhanced immune turbidimetric assay was adapted and validated on a Cobas 8000/c502 analyzer. Urine samples of different patient groups were also analyzed. Results: Our method showed excellent analytical performance. U-CYSC/u-creatinine (u-CREAT) was higher in sepsis-related acute kidney injury group (p < 0.001) compared with controls and to patients with chronic hypertension and Type 2 diabetes. Conclusion: We validated a fast, sensitive, fully automated u-CYSC assay which is ideal for routine use and might be a potential complementary laboratory test to evaluate renal tubular function.

The early and relevant increase of u-ORM in sepsis suggests that it might be a promising novel marker of sepsis and could be a valuable part of routine laboratory and clinical practice.

Both serum GSN and Gc globulin may have predictive values in sepsis. Considering the small sample size of our study, further measurements are needed to evaluate our results. Measurement of Gc globulin and GSN maybe useful in assessment of sepsis severity and in therapeutic decision-making.

Introduction A major complication of sepsis is the development of acute kidney injury (AKI). Recently, it was shown that intracellular actin released from damaged tissues appears in the urine of patients with multiple organ dysfunction syndrome. Our aims were to measure urinary actin (u-actin) concentrations of septic and control patients and to test if u-actin levels could predict AKI and mortality. Methods Blood and urine samples were collected from septic and sepsis-related AKI patients at three time points (T1-3): T1: within 24 hours after admission; T2: second day morning; T3: third day morning of follow-up. Patients with malignancies needing palliative care, end-stage renal disease or kidney transplantation were excluded. Serum and u-actin levels were determined by quantitative Western blot. Patients were categorized by the Sepsis-3 and KDIGO AKI classifications. Results In our study, 17 septic, 43 sepsis-induced AKI and 24 control patients were enrolled. U-actin levels were higher in septic patients compared with controls during follow-up (p<0.001). At T1, the septic and sepsis-related AKI groups also showed differences (p<0.001), yet this increase was not statistically significant at T2 and T3. We also detected significantly elevated u-actin concentrations in AKI-2 and AKI-3 septic patients compared with AKI-1 septic patients (p<0.05) at T1 and T3, along with a significant increase in AKI-2 septic patients compared with AKI-1 septic patients at T2 (p<0.01). This tendency remained the same when referring u-actin to urine creatinine. Parameters of first-day septic patient samples could discriminate AKI from non-AKI state (AUC ROC, p<0.001): u-actin: 0.876; se-creatinine: 0.875. Derived cut-off value for u-actin was 2.63 μg/L (sensitivity: 86.0%, specificity: 82.4%). Conclusion U-actin may be a complementary diagnostic biomarker to se-creatinine in sepsis-related AKI while higher u-actin levels also seem to reflect the severity of AKI. Further investigations may elucidate the importance of u-actin release in sepsis-related AKI.

Based on the results, our immune turbidimetric measurement offers a rapid and accurate quantitation of gelsolin in human serum samples. Serum gelsolin seems a promising additional diagnostic marker of sepsis which has to be further investigated.

Background Laboratory markers are essential tools in the follow‐up of patients with Crohn's disease (CD). Our aim was to investigate urinary concentrations of orosomucoid in relation to the inflammatory activity of CD and to compare it with clinical indices and conventional laboratory parameters. Materials and methods Blood and urine samples of 86 patients (55 adults and 31 children) with CD and 68 healthy individuals (38 adults and 30 children) as controls were analysed. Patients were categorized according to their clinical scores (Harvey‐Bradshaw Index [HBI] or Pediatric Crohn's Disease Activity Index [PCDAI]). Urinary orosomucoid (u‐ORM) was determined by automated immune turbidimetric assay, and values were referred to urinary creatinine (u‐ORM/u‐CREAT, mg/mmol). Results U‐ORM/u‐CREAT values were seven times higher in children with active CD (0.50 vs 0.07 mg/mmol, P < 0.001) and two times higher in adults (0.32 vs 0.14 mg/mmol, P = 0.01) compared with patients with inactive disease. U‐ORM/u‐CREAT showed good correlation with conventional inflammatory markers (hs‐CRP, serum ORM; P < 0.01) and activity indices (HBI, P = 0.018; PCDAI, P < 0.001). U‐ORM/u‐CREAT had similar discriminative performance to hs‐CRP and serum ORM in the differentiation of active from inactive paediatric CD patients. Conclusions Our findings suggest that u‐ORM/u‐CREAT might serve as a valuable additional marker in the follow‐up of CD patients, especially in children for whom the non‐invasive sampling is a further advantage.