Introduction: Idiopathic membranous nephropathy (IMN) is a common cause of nephrotic syndrome in adults. It is an immune-mediated disease characterized by subepithelial immune complex deposition and alterations in the glomerular basement membrane. The Kidney Disease Improving Global Outcomes (KDIGO) guidelines recommend, for the treatment of this serious public health problem, rituximab or cyclophosphamide with steroids, or calcineurin inhibitor–based therapy. However, it is necessary to evaluate the efficacy of the currently proposed therapies. Methods: A search was conducted in the PubMed (MEDLINE) database using the MeSH terms “Glomerulonephritis, Membranous” and “Therapeutics,” applying the filters “Systematic Reviews” and “Free full text.” Studies published between 2020 and 2024 were selected, totaling 13 articles. Results: Rituximab proved to be effective, well-tolerated, and safe in the treatment of IMN, with the added advantage of being steroid-free. Most patients achieved complete remission during the follow-up period, with low rates of adverse events and relapses. Treatment with Tripterygium wilfordii poly-glycosides showed improvements, observed through essential markers for assessing renal function, such as 24-hour urinary protein levels, with significant clinical remission. Additionally, tacrolimus, both as monotherapy and combined with steroids, demonstrated a strong therapeutic effect in achieving overall and complete remission. However, the relapse rate with monotherapy was higher than with established therapies such as cyclophosphamide plus corticosteroids. Conclusions: IMN is a serious disease and a significant health problem for both patients and healthcare systems. In this context, rituximab therapies have shown high efficacy. Moreover, treatments with tacrolimus and Tripterygium wilfordii poly-glycosides have demonstrated potential effectiveness in treating IMN, as evidenced by renal function markers and good clinical remission, highlighting the need for further studies to ensure the safety and efficacy of these alternative therapies.

Abstract

Objective: This study aims to investigate the threshold effects and the shape of the association between dietary phosphorus intake and the prevalence of cardiovascular disease (CVD) in non-dialysis chronic kidney disease (CKD) patients. Understanding this relationship is crucial for dietary recommendations and clinical management in this vulnerable population.

Background: Phosphorus intake is strictly regulated in dialysis patients due to its significant impact on health outcomes. However, the association between phosphorus intake and CVD in non-dialysis CKD patients remains poorly understood. This knowledge gap prompted our investigation into whether dietary phosphorus intake influences CVD prevalence in this specific patient group.

Methods: The US National Health and Nutrition Examination Survey data from 2001 to 2018 were analyzed for this cross-sectional study. The diagnosis of chronic kidney disease is eGFR less than 60 (mL/min/1.73m²) or urinary albumin/creatinine ratio (ACR) greater than or equal to 30mg/g. Dietary phosphorus intake was evaluated using the 24 h dietary recall system.

Results: A total of 7,890 chronic kidney disease participants were included, divided into three groups according to dietary phosphorus intake: T1 (<1000 mg/day), T2 (1000-1200 mg/day), and T3 (>1200 mg/day). Of whom 2,198 (24.74%) reported having cardiovascular disease. Compared to T2 (1000-1200 mg/day), the adjusted odds ratios for CVD in T1 and T3 were 1.33 (95% confidence interval [CI]: 1.07-1.64, p = 0.01) and 0.98 (95% CI: 0.77-1.23, p = 0.834), respectively. Sensitivity analysis also showed an association between dietary phosphorus intake and cardiovascular disease.

Conclusion: Our analysis revealed an L-shaped relationship between dietary phosphorus intake and cardiovascular disease, indicating a higher risk at lower levels of intake.

Background: In septic patients, the interplay between macro-microcirculatory dysfunction and acute kidney injury (AKI) remains elusive. This study aimed to explore the association between hemodynamics and endothelial damage in sepsis associated AKI (SA-AKI) by evaluating the combined predictive value of renal resistive index (RRI) and plasma syndecan-1.

Methods: This prospective observational study enrolled 80 septic patients admitted to the intensive care unit of a tertiary hospital from May to December 2024. AKI was diagnosed according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Plasma syndecan-1 levels were measured at admission and RRI was assessed within 24 hours of ICU admission. Diagnostic performance was evaluated using receiver operating characteristic (ROC) curve analysis by calculating the area under the curve (AUC). Univariate and multivariate logistic regression models were applied to identify independent risk factors of SA-AKI. Predictive models were constructed to validate the effectiveness.

Results: Among 80 septic patients, 41 (51.25%) developed AKI. Syndecan-1 levels were significantly higher in the AKI group [109.95 (73.67,221.40) vs. 73.67（54.59,109.95）ng/ml, P =0.007], and RRI values were markedly elevated (0.69±0.08 vs. 0.60±0.06, P <0.001) compared to non-AKI patients. Univariate analysis revealed syndecan-1 (OR=2.68, 95%CI 1.29-5.59) and RRI (OR=1.18, 95%CI 1.09-1.28) as predictors of AKI. In multivariate models adjusted for confounders, both plasma syndecan-1 (OR=3.57, 95%CI 1.01-12.64, P =0.048) and RRI (OR=1.19, 95% CI 1.07-1.33, P =0.002) retained significance. The Predictive Model using a combination of plasma syndecan-1 and RRI achieved superior diagnostic performance (AUC 0.859, sensitivity 87.8%, specificity 92.3%).

Conclusions: In patients with SA-AKI, elevated plasma syndecan-1 and RRI were identified as independent risk factors for SA-AKI. The combination of syndecan-1 and RRI can serve as synergistic biomarkers for prediction of SA-AKI.

Inflammation is increasingly recognized in the pathogenesis of hypertension (HTN), and the neutrophil-to-lymphocyte ratio (NLR) has emerged as a simple, low-cost inflammatory marker. Yet published data on the NLR and HTN relationship are conflicting and virtually absent for Jordan. Clarifying this association could refine risk stratification and guide future anti-inflammatory interventions. Guided by the immuno-inflammatory model of HTN, we performed a cross-sectional analysis of 352 adult inpatients at the University of Jordan Hospital (February–July 2024). A minimum of three blood pressure readings were taken on different days. The HTN stage was assigned per ACC guidelines. Neutrophils and lymphocytes were measured using complete blood counts to calculate the NLR. Group differences were tested with independent-sample t-tests; Spearman correlation assessed relations between NLR, hemoglobin (Hb), and systolic/diastolic BP across age strata (young 18–35, middle-aged 36–55, older 56–75, elderly 76–90 yrs). NLR did not differ significantly between hypertensive and normotensive participants (p = 0.131) and showed only weak inverse correlations with systolic (r = –0.166, p = 0.039) and diastolic (r = –0.128, p = 0.113) pressures. Among hypertensive patients, mean NLR increased with age (p = 0.0116). Hb correlated positively with both systolic (r = 0.238, p = 0.003) and diastolic BP (r = 0.366, p < 0.0001). No significant associations were found between NLR and HTN stage. Hemoglobin demonstrated a clinically significant association with blood pressure in this Jordanian inpatient population, although NLR was not a significant predictor of the incidence or severity of HTN. These results raise uncertainty on NLR's ability to be used alone for HTN monitoring in comparable clinical contexts and suggest Hb as a potential marker. More extensive, multicenter research in a range of demographics is necessary to identify age-specific inflammatory profiles and investigate whether combining Hb with conventional risk factors will improve the treatment of hypertension.

Introduction: Sodium-glucose co-transporter 2 (SGLT2) inhibitors have become known as cornerstone therapies, demonstrating glycemic and cardiorenal benefits. While their role on glycemic control is established, real-world data on their impact on renal function (serum creatinine, serum urea, estimated glomerular filtration rate–eGFR) in different stages of chronic kidney disease (CKD) remains limited. This study evaluates the changes in kidney function following SGLT2 inhibitors in adults with varying stages of CKD, including both diabetic and non-diabetic patients.

Methods: This retrospective observational study included CKD patients aged 35 years and older. Patients on dialysis and patients who had side effects (UTI, diarrhea) or intolerance (shortness of breath and palpitations) to therapy were excluded. Kidney function was the primary endpoint, and secondary were glycemic control and electrolytes (natrum and potassium). Measurements were recorded at baseline, one month, and three to six months after the treatment initiation.

Results: Participants (38-80 years), consist of both males and females, predominantly CKD stages 3b-4. After six months of SGLT2 inhibitor therapy, eGFR responses varied. Some patients showed stabilization or improvement, and others experienced initial decline followed by stabilization or a sustained decline. SCr changes paralleled eGFR changes. Reduction in proteinuria wass observed. Patients with diabetes mellitus marked significant improvements in both glucose and HgA1C, while electrolytes remained stable. Metabolic and renal parameters were similar between diabetic and non-diabetic patients.

Conclusions: This real-world retrospective study shows that SGLT2 inhibitors may promote renal stabilization, with metabolic benefits in patients with chronic kidney disease. While individual renal varied, the overall data supports the metabolic and renal benefits of these agents.

Introduction:

Obstructive sleep apnea (OSA) is a chronic disorder leading to intermittent hypoxia, oxidative stress and vascular inflammation. These mechanisms are recognized contributors to atherosclerotic cardiovascular disease (CVD). The objective of this study was to evaluate the correlation between the severity of obstructive sleep apnea (OSA) and the presence of coronary artery disease (CAD) that necessitates revascularization procedures.

Materials and Methods:

A restrospective analysis was conducted on 70 patients treated between 2022 and 2024. Demographic data, comorbidities, sleep polygraphy results were reviewed. Patients were divided into two groups: mild/no OSA (apnea–hypopnea index [AHI] < 15 events/h) and moderate to severe OSA (AHI ≥15 events/h).

Results:

Group I (n=35) included patients with no to mild OSA, while group II (n=35) comprised patients with moderate to severe OSA. The prevalence of ischemic heart disease requiring revascularization was more frequent in patients with moderate to severe OSA compared with those with mild/no OSA (52.9% vs. 47.1%). A subgroup analysis demonstrated that patients with severe OSA had a significantly higher prevalence of coronary artery disease requiring revascularization (41.2%) compared to those without OSA (14.7%), with mild OSA (32.3%), or moderate OSA (11.8%), with these differences being statistically significant (p = 0.01). No statistically significant association was found between the severity of sleep apnea and either the number of affected vessels or the involvement of a specific coronary artery by atherosclerotic lesions.

Conclusions:

The prevalence of CAD requiring revascularization was higher in patients with moderate to severe OSA. These findings emphasize the importance of systematic screening and management of OSA, particularly in patients with advanced CAD undergoing coronary interventions.

Background

Lipoprotein(a) [Lp(a)] is a genetically inherited lipid marker associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD). Unlike LDL-C, Lp(a) is minimally responsive to lifestyle modification or statins. Management becomes especially challenging in patients with statin intolerance and co-existing cardiac conditions. PCSK9 inhibitors offer a therapeutic option by modestly lowering Lp(a) levels in addition to LDL-C. This case highlights the management of a patient with elevated Lp(a), statin intolerance, and a history of transcatheter aortic valve implantation (TAVI).

Case Presentation

A 65-year-old female with a history of chronic coronary syndrome and severe aortic valve stenosis underwent successful TAVI with a Sapien 3 bioprosthetic valve in November 2022. She was diagnosed with familial hyperlipoproteinemia and significantly elevated Lp(a) levels (801 mmol/L), alongside intolerance to high-dose statins. Due to her high cardiovascular risk, she was enrolled in the RDTL drug reimbursement program and initiated on evolocumab (a PCSK9 inhibitor) at 140 mg every 14 days.

At follow-up in December 2024, clinical assessment revealed stable cardiovascular status. Echocardiography showed preserved left ventricular ejection fraction (EF 60%) with good function of the implanted aortic valve. Blood pressure was 120/70 mmHg, ECG demonstrated sinus rhythm, and her Lp(a) level had decreased to 585 mmol/L, indicating a partial but significant response to therapy. Her medications included perindopril, metoprolol, rosuvastatin/ezetimibe (5/10 mg), metformin, clopidogrel, and evolocumab.

Conclusion

This case illustrates the long-term benefit of PCSK9 inhibitor therapy in a statin-intolerant patient with elevated Lp(a) and post-TAVI status. Partial biochemical response and clinical stability highlight the role of targeted lipid-lowering therapy and structured follow-up in managing genetically driven dyslipidemia in high-risk cardiac patients.

Introduction:

Mediastinal widening on chest X-ray is an alarming finding that requires further investigation. In infants and young children, it usually reflects physiological thymic enlargement. In older children, however, it may result from germ cell tumors, thymic disease, infections, vascular anomalies, or hematopoietic malignancies. We present three pediatric cases in which proliferative disorders of the hematopoietic and lymphatic systems manifested as very similar mediastinal enlargement on radiographs.

Case reports:

Case 1: A 14-year-old girl presented with fever, pruritus, and neck contour changes. Examination revealed hard, painless lymphadenopathy in the supraclavicular and cervical regions. Laboratory tests showed leukocytosis of 13,000/µl, hemoglobin 11.1 g/dl, and platelets 405,000/µl. Chest X-ray demonstrated a mediastinal shadow of 105 mm. Histopathology confirmed stage IVB Hodgkin’s lymphoma, nodular sclerosis subtype.

Case 2: An 11-year-old boy was admitted with progressive dyspnea, cough, and neck swelling lasting one month. Chest X-ray revealed mediastinal widening of 83 mm, narrowing the airway to 1 mm. Due to respiratory failure, tracheostomy and biopsy were performed. Laboratory results showed leukocytosis of 10,100/µl and elevated D-dimers. Final diagnosis was stage IV T-cell lymphoblastic lymphoma.

Case 3: A 13-year-old boy presented with gastrointestinal bleeding and generalized petechiae. Ultrasound revealed splenomegaly. Laboratory findings included hyperleukocytosis (170,000/µl) with 80% blasts, thrombocytopenia (23,000/µl), and elevated transaminases. Physical exam showed hepatosplenomegaly and generalized lymphadenopathy. Chest X-ray demonstrated mediastinal widening of 77 mm. Myelogram and immunophenotyping confirmed acute T-cell lymphoblastic leukemia.

Conclusions:

Although chest X-ray is an important initial tool, it cannot differentiate the causes of mediastinal widening. In adolescents with alarming symptoms, further evaluation with blood counts, imaging, and histopathology is essential. These cases demonstrate that nearly identical radiological appearances may correspond to distinct hematologic malignancies, each requiring targeted treatment.

Hemoglobin (Hb) is an essential hematological parameter, and its deviations from the physiological range can have important implications for cardiovascular health. Anemia is associated with chronic inflammation, oxidative stress, and endothelial dysfunction, increasing the risk of cardiovascular events, while elevated hemoglobin levels can cause high blood viscosity, tissue hypoxia, and thrombotic risk. A retrospective study was conducted on 100 adult patients, using data from standard hemograms. The parameters analyzed included Hb, hematocrit (Hct), leukocytes (WBC), platelets (PLT), age, and gender. The prevalence of anemia (Hb <12 g/dL in women, <13 g/dL in men) and elevated Hb values (>16 g/dL in men, >15 g/dL in women) was evaluated, as well as the correlations between Hb and other hematological parameters. Anemia was identified in 18% of patients, being more frequent in women over 65 years of age. Elevated Hb values were observed in 7% of patients, predominantly in young men. Hb showed a strong correlation with Hct (r=0.82, p<0.001), while the correlations with WBC (r=0.24) and PLT (r=0.18) were moderate and statistically insignificant. Extreme Hb values were associated with hematological changes suggestive of increased cardiovascular risk, including tissue perfusion disturbances and thrombotic predisposition. Hemoglobin values, either low or high, may constitute adjunctive hematological markers of cardiovascular risk. Integrating Hb into clinical evaluation, together with other hematological parameters and traditional risk factors, may support the identification of patients at high risk and the orientation of preventive interventions. These results provide a solid basis for future research on the role of Hb as a clinical marker in cardiovascular risk stratification.

Introduction: Subclinical atherosclerosis (SA) is a silent preclinical stage of atherosclerotic cardiovascular disease, particularly in individuals with high-risk metabolic disorders. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have shown cardiovascular benefits in supplementation trials; however, evidence from habitual intake is limited particularly in people with diabetes mellitus (DM). We aimed to assess the association between dietary EPA and DHA and the presence of carotid atherosclerotic plaque(s) (SA) in adults with and without DM.

Methods: A cross-sectional study was conducted in adults with and without DM. EPA and DHA intake were assessed with a validated 101-item Spanish food frequency questionnaire. Ultrasound was used to detect the SA in the common, bulb and internal carotid arteries, by a blinded operator. Statistical analyses included group comparisons and multivariable logistic regression adjusted for age, sex, hypertension, dyslipidemia, smoking, waist circumference, glycemic control, and renal function, conducted in the overall sample and restricted to participants with DM (both type 1 and type 2).

Results: Out of 1,221 participants, 429 (35.1%) had AP (median age: 57 years), while 792 (64.9%) did not (median age: 45 years). DM was more frequent in the group with SA (57.3% vs. 36.4%). EPA intake was slightly higher in individuals with AP (0.14 vs. 0.13 g/day; p = 0.061), while DHA intake showed no difference (0.26 vs. 0.24 g/day; p = 0.202). In adjusted models, higher EPA intake was associated to lower odds of AP in analyses including all subjects (OR: 0.18; p = 0.018) and in those restricted to DM (OR 0.13; p=0.034). DHA intake was inversely associated with AP in all subjects (OR 0.37; p=0.010), with an association even stronger in DM (OR 0.25; p=0.008).

Conclusion: Higher dietary intake of EPA and DHA was associated with a lower likelihood of SA, particularly in subjects with diabetes.