Tianjin University of Traditional Chinese Medicine

In recent years, Raman spectroscopy analysis of hematological diseases is increasingly applied in research, but its application in serum analysis of myeloid neoplastic diseases represented by myeloproliferative neoplasms (MPN), myelodysplastic/myeloproliferative neoplasms (MDS/MPN), and acute myeloid leukemia (AML) has not been fully tested. To establish an oversimplified non-invasive serum test approach for MPN, MDS/MPN and AML, we systematically examined peripheral blood serum samples from 8 patients diagnosed with MPN, 4 patients with MDS/MPN, 3 patients with AML, and 9 control participants. A laser Raman spectroscopy was utilized together with orthogonal partial least squares discriminant analysis (OPLS-DA). Next, a differentiation model for MPN, MDS/MPN, AML, and the control was constructed. Compared with the healthy participants, the serum spectral data of patients with myeloid tumors were specific, and the intensities of Raman peaks representing nucleic acids (786, 1579 cm^-1), proteins (643, 759, 1031, 1260, 1603, 1616 cm^-1), lipids (1437, 1443, 1446 cm^-1), and β-carotene (957 cm^-1) were significantly decreased, while the intensity of the Raman peak representing collagen (1345 cm^-1) was significantly increased. Metabolic serum marker analysis revealed consistent patterns across MPN, MDS/MPN, and AML patients: adenosine deaminase (ADA) levels were significantly elevated, while both total protein and low-density lipoprotein concentrations showed marked reductions compared to controls. This provides spectroscopic evidence that will guide early differentiation of massive serum test data of patients with MPN, MDS/MPN and AML, and simultaneously uncovers crucial details for rapid and rudimentary differentiating them. This exploratory study show that the Raman spectroscopy analysis is an innovative non-invasive clinical instrument for the detection of MPN, MDS/MPN and AML.

Abdominal aortic calcification (AAC) is prevalent in chronic kidney disease (CKD) patients and linked to elevated cardiovascular disease (CVD) risk. Obesity, linked to both CKD and CVD, can be better assessed by A Body Shape Index (ABSI), a novel index measuring central obesity and fat distribution. We posit that ABSI may correlate with AAC risk in CKD patients. This research explores the association using 2013-2014 National Health and Nutrition Examination Survey (NHANES) data.

From the 2013-2014 NHANES dataset, we excluded participants lacking data on AAC or ABSI A total of 961 CKD subjects remained. Before analyzing ABSI as a continuous variable, we standardized it, denoting the result as ABSI^a. We then plotted restricted cubic splines (RCS). Follow-up univariate and multivariate regression, subgroup, and interaction analyses were conducted to explore the ABSI^a-AAC relationship.

The analysis revealed a significant positive relationship between ABSI^a and AAC in CKD patients (OR = 1.41, 95% CI: 1.23-1.61, p < 0.001). Even after adjustment for multiple confounders, ABSI^a remained independently associated with AAC (OR = 1.38, 95%CI: 1.17-1.64, p < 0.001). Subgroup analyses further validated this association across various patient subgroups.

In patients with CKD, this cross-sectional study identified a significant positive association between ABSI and AAC, persisting after adjusting for confounders. This suggests ABSI may be a biomarker for AAC risk assessment and CVD risk stratification in CKD patients.

Chronic kidney disease-associated pruritus (CKD-aP) is a common complication in peritoneal dialysis (PD) patients. Whether serum phosphate is associated with CKD-aP is controversial. We identified the serum phosphate trajectories of PD patients in the last 3 months and investigated the effects of serum phosphate persistence on CKD-aP.

A total of 407 PD patients from the PD Center of the First Teaching Hospital of Tianjin University of Traditional Chinese Medicine were included. The 14-item UP-Dial was used to investigate the prevalence and clinical characteristics. PD patients were identified with different trajectories of serum phosphate by group-based trajectory modeling.

The prevalence of CKD-aP in PD patients was 51.8%. Among 407 PD patients, four distinct serum phosphate trajectories were identified. Both transient serum phosphate and serum phosphate status were associated with CKD-aP. Transient serum phosphate was associated with an increased risk of CKD-aP [OR (95%CI): 2.28 (1.30-4.02), 2.24 (1.22-4.10), 3.04 (1.66-5.58), 2.12 (1.21-3.70), respectively]. Compared with the persistent low-level group, the gradual increase group was not associated with an increased risk of CKD-aP [OR (95%CI): 1.59 (0.77-3.26)]. Both the gradual decrease group and the persistent high-level group were positively associated with an increased risk of CKD-aP [OR (95%CI): 2.18 (1.30-3.66), 3.19 (1.60-6.36), respectively].

Our study confirmed the relationship between serum phosphate and CKD-aP within the past 3 months, to some extent explaining the controversy generated by previous studies. These results may help clinicians better understand the relationship between serum phosphate and CKD-aP and the importance of controlling serum phosphate.