Background/Objectives: Type 2 diabetes mellitus (T2DM), is a rapidly growing global health concern, often accompanied by chronic kidney disease (CKD) and metabolic disturbances. Obesity-related indices, such as the visceral adiposity index (VAI) and body adiposity index (BAI), have been linked to cardiovascular and renal complications in diabetic patients. However, studies integrating both the atherogenic coefficient (AC) and prognostic nutritional index (PNI) for evaluating diabetic nephropathy (DN) remain limited. This study aimed to assess the associations of obesity-related indices with immunological and nutritional factors in patients with T2DM and prediabetes (PreDM). Methods: A retrospective, cross-sectional study was conducted over six months at a university clinical hospital in Dolj County, Romania. The study enrolled 268 newly diagnosed T2DM patients and 150 PreDM patients. Anthropometric parameters, laboratory tests, and demographic data were collected. AC and PNI were calculated using standard formulas, and statistical analyses were performed to determine their associations with metabolic and inflammatory markers. Results: Our study found that T2DM patients had significantly lower PNI values, indicating mild malnutrition, while PreDM patients maintained a normal nutritional status. AC was significantly higher in T2DM patients, correlating with lipid profile alterations and systemic inflammation. Obesity indices, particularly VAI, were significantly elevated in T2DM patients with higher AC values. Statistically significant differences in total cholesterol, low-density lipoprotein cholesterol (LDL-c), and triglycerides were observed between AC subgroups, reinforcing its role in cardiovascular risk assessment. Conclusions: The findings highlight the potential of AC and PNI as biomarkers for assessing nutritional, inflammatory, and lipemic status in diabetic patients. The significant associations between obesity-related indices, lipid profiles, and inflammation markers suggest that early assessment of these parameters may potentially aid in predicting diabetic complications. Further studies are needed to explore the clinical utility of AC and PNI in managing T2DM and CKD progression. Future research should investigate how the lipidic spectrum alters the progression of DN across various patient groups with diabetes and prediabetes

Chronic kidney disease (CKD) is a multifactorial disorder increasingly recognized as a systemic condition marked by persistent inflammation, oxidative stress, dyslipidemia, and endothelial dysfunction. Diabetic nephropathy, a leading cause of CKD, amplifies cardiovascular risk through intertwined mechanisms beyond traditional risk factors. This review synthesizes current evidence on the interplay between inflammation, oxidative stress, and atherosclerosis in CKD, with a special focus on emerging molecular biomarkers—PCSK9, EPHX2, AOPPs, and TBARSs—and their integration with clinical indices. These markers illuminate pathophysiological networks underlying CKD progression and cardiovascular complications, offering novel insights into risk stratification, disease monitoring, and targeted therapy. By exploring molecular and clinical intersections, this review underscores the potential of a personalized, biomarker-driven approach to CKD management.

We compared oxidative markers and their links to inflammation in diabetic nephropathy and hemodialysis to identify independent determinants. We studied 180 adults, 90 patients with type 2 diabetes and diabetic nephropathy and 90 patients on hemodialysis. We measured serum advanced oxidation protein products (AOPP) and thiobarbituric acid reactive substances (TBARS) by enzyme-linked immunosorbent assay (ELISA). Partial correlations were adjusted for age, sex, and albumin with false discovery rate (FDR) control. Principal component analysis (PCA) summarized inflammatory indices and linear models tested predictors of AOPP and TBARS. Oxidative damage was higher in hemodialysis, with AOPP median 25.80 versus 5.06 and TBARS 8.49 versus 1.89, p less than 0.0001. C reactive protein (CRP) and mean corpuscular volume-to-lymphocyte ratio (MCVL) were higher in patients ongoing hemodialysis; systemic immune-inflammation index (SII) was higher in diabetic nephropathy. PCA yielded a dominant inflammation axis in both cohorts, 74.73 percent in hemodialysis and 85.20 percent in diabetic nephropathy. In regression, creatinine (β = 2.47, p = 0.026) predicted AOPP in hemodialysis. Dialysis vintage inversely predicted TBARS, β = −0.2305, p = 0.0209. In diabetic nephropathy, the PCA inflammation score predicted AOPP, β = 1.134, p = 0.0003. Protein oxidation tracked systemic inflammation in diabetic nephropathy, but not in hemodialysis. AOPP outperformed TBARS as an inflammatory partner and a practical monitoring candidate in diabetic kidney disease. Prospective studies should test for prognostic value and therapy sensitivity.

In patients diagnosed with multiple myeloma (MM), the primary complaints at the time of diagnosis are often related to bone involvement, significantly impacting quality of life and increasing both morbidity and mortality. Obesity is associated with a chronic inflammatory state that results in the production of various cytokines and adipokines, which may promote bone destruction. Adiponectin, an adipokine predominantly secreted by adipocytes, is notably diminished in circulation among individuals with obesity, a phenomenon that has also been observed in MM. This reduction may contribute to the disruption of an already compromised bone architecture. The increase in adipose tissue is associated with heightened leptin production, a key adipokine, which can play a significant role in the pathophysiology of MM and its related bone complications. Obesity is associated with hyperinsulinemia and increased levels of free IGF-1. In MM, IGF-1 plays a critical role as a growth factor, produced by both myeloma cells and osteoclasts within the bone marrow microenvironment. Our gathered data indicates a significant relationship between the adipokines produced by adipose tissue and the bone matrix, particularly in the context of obesity and MM. However, it is important to note that the existing body of research on this topic is relatively sparse, with the majority of studies conducted on murine models rather than human subjects. This limitation highlights a critical need for further investigation to elucidate the precise mechanisms that contribute to bone destruction under these conditions.

Introduction: Although quadruple therapy in the induction of treatment for Multiple Myeloma has become standard, autologous stem cell transplant (ASCT) remains indicated in eligible patients (Rajkumar SV et al. Multiple myeloma: 2022 update on diagnosis, risk stratification, and management. Am J Hematol. 2022). However, 6-27% of patients with Multiple Myeloma will fail to harvest the desired amount of CD34+ stem cells, thus will require a second mobilization strategy, increasing the costs and time the patient is hospitalized (Hsu TL et all, Risk Factors and Outcomes of Stem Cell Mobilization Failure in Multiple Myeloma Patients. Transfus Med Hemother. 2022 Sep). With poor mobilizers, some essential traits that need to be considered are age, prior radiotherapy, use of immunomodulatory drugs, and monoclonal CD38 antibodies (He X et all., Predictive factors for peripheral blood stem cell mobilization in multiple myeloma in the era of novel therapies: A single-center experience. Cancer Med. 2024). Therefore, we conducted a retrospective analysis to evaluate the mobilization outcome in patients diagnosed with Multiple Myeloma and to determine how the various treatment options influenced the amount of CD34+ stem cells collected. Methods: We conducted a retrospective study of 154 patients who performed peripheral stem cell (PBSC) harvest at the Bone Marrow Transplant at Fundeni Clinical Institute, Bucharest, Romania, between January 2020 and June 2024. Harvest was conducted using 10-15 µg/kg/day, sub-cutaneous G-CSF for 4-5 days. Poor mobilizers were considered patients who were not able to harvest a PBCS of at least 2 x10^6 CD34/kgc after G-CSF. Poor mobilizers were readmitted to hospitalization after at least 4 weeks, and Plerixafor or Cyclophosphamide (CFS) was used. Results: Of the 154 patients, 47 (31%) failed to mobilize with G-CSF-alone. Patients at risk for poor mobilizer were considered those who received prior treatment with Radiotherapy (15/154), treatment with Daratumumab (59/154), immunomodulator (94/154), respectively, double therapy with both immunomodulator and anti-CD38 (15/154). Also, the presence of extramedullary disease at diagnosis, the number of induction cycles used, patient age, and disease status before harvest were analyzed. The risk of harvest failure was 41% (24/59) among patients receiving anti-CD38 (p=0.031), 21% (20/94) in those with an immunomodulator therapy (p= 0.161), and 67% (10/15) for those with both of them (p=0.001); but immunomodulator treatment was stopped within 14 days before harvest. Plerixafor was used in 30/47 cases and CFS in 17/47 patients. Graft quality analyses showed that Plerixafor comes with a better graft - mean 6.3±2.7 (2.4-13) versus CFS - mean 4.9 ±2.5 (2.0-12.6) but without statistically significant differences (p=0.773). Conclusion: In the era of quadruple therapy, the increased rate of poor mobilizers makes harvesting challenging. Scientific research acknowledged that immunomodulators and anti-CD38 agents both raise the risk; however, using both in the same treatment regimen introduces an additional risk. Early recognition of patients at risk indicate using Plerixafor or CFS from the first admission, with reducing hospitalization costs and readmissions for a new harvest. Further studies are needed to determine the best moment for harvest in patients with MM who receive quadruple therapy, and which, Plerixafor or CFS, is preferable and at what time.

Background/Objectives: Inflammatory and hematologic indices derived from routine blood tests have been increasingly investigated as prognostic biomarkers in multiple myeloma (MM). However, their clinical utility remains inconsistent, and data on novel composite indices, such as the mean corpuscular volume-to-lymphocyte ratio (MCVL) and the cumulative inflammatory index (IIC), are lacking in MM. Methods: We conducted a retrospective study including 122 patients with newly diagnosed MM. Hematologic and inflammatory indices were evaluated at baseline and after four cycles of induction therapy. Associations with progression-free survival (PFS) and overall survival (OS) were assessed using Kaplan–Meier analysis, Cox regression models, and receiver operating characteristic (ROC) curve analysis. Results: Baseline inflammatory biomarkers, including NLR, PLR, MLR, SII, as well as MCVL and IIC, were not significantly associated with PFS or OS. ROC analysis demonstrated poor discriminative ability for all evaluated markers at both baseline and post-induction timepoints (AUC values close to or below 0.50). In contrast, post-induction inflammatory indices, particularly PLR, MLR, AISI, and SIRI, were significantly associated with PFS in both univariable and multivariable Cox regression analyses. Neither baseline nor post-induction MCVL and IIC showed independent prognostic value. Conclusions: Baseline inflammatory and erythrocyte-derived indices, including the novel composite markers MCVL and IIC, have limited prognostic utility in MM. In contrast, dynamic changes in inflammatory biomarkers during treatment may provide more clinically relevant information regarding disease progression. These findings support the integration of longitudinal biomarker assessment into future risk stratification models in MM.