University Hospital Dubrava

Abstractsurinary sediment, and cylindruria was observed exclusively in this group (p=0.007).In proliferative LN, the median NIH activity index was 7 (IQR 4-8), whereas the chronicity index was low at 1 (IQR 0-2).Interstitial fibrosis and tubular atrophy were absent in most cases and, when present, were uniformly mild.At the end of follow-up, 12 of 13 patients with proliferative LN maintained preserved renal function (eGFR >60 mL/min/1.73m 2 ).Conclusions Proliferative lupus nephritis is common in patients with SLE and proteinuria <500 mg/day and, in this cohort, occurred exclusively at proteinuria >300 mg/day.Integration of proteinuria with clinical and serological activity,particularly SLEDAI, anti-double-stranded DNA antibodies and complement levels,improves identification of patients at risk.Early kidney biopsy allows detection of active proliferative LN before irreversible renal damage and is associated with favourable renal outcomes.

Rosacea is increasingly recognized as a complex inflammatory disorder extending beyond isolated cutaneous pathology, involving dysregulated interactions between the skin, gastrointestinal system, and central nervous system. The skin-gut-brain axis has emerged as a relevant conceptual framework for understanding this multifactorial disease, integrating gut microbiota dysbiosis, neuroimmune signaling, autonomic nervous system dysfunction, and stress-related mechanisms. The aim of this narrative hypothesis-driven overview is to reframe rosacea as a neuroimmune disorder in which central nervous system involvement plays an active regulatory role, rather than as a purely peripheral or dermatological condition. We synthesize the mechanistically relevant evidence linking gastrointestinal inflammation and microbial imbalance with neurogenic inflammation, mast cell activation, sebaceous gland dysfunction, and aberrant innate immune responses in the skin, with particular emphasis on neurovascular and trigeminal pathways. A key novelty of this perspective lies in highlighting brain-centered mechanisms, including central sensitization, autonomic dysregulation, and stress-related neural modulation, as integral components of the skin-gut-brain axis in rosacea. By integrating peripheral and central processes, we propose rosacea as a model condition for studying neuroimmune dysregulation across interconnected regulatory systems. Finally, we discuss the clinical and translational implications of this framework and outline future research directions, focusing on autonomic regulation, patient stratification, and personalized, multidisciplinary therapeutic approaches.

Background: In patients with ST-segment elevation myocardial infarction (STEMI), apelin is upregulated and exerts cardioprotective effects against ischemia-reperfusion injury (IRI). The present study aimed to investigate serum apelin-36 levels in STEMI patients and their relationship with the no-reflow phenomenon. Methods: In this study, 161 patients presenting with STEMI within 12 h of symptom onset and undergoing primary percutaneous coronary intervention (pPCI) were enrolled. Biochemical parameters, including apelin-36, troponin T, creatine kinase (CK), the MB fraction of creatine kinase (CK-MB), total cholesterol, triglycerides, and other routine laboratory parameters, were measured. Two-dimensional echocardiography was performed in all patients. Thereafter, patients were divided into two groups according to their level of aaapelin-36. Results: Among the 161 consecutive STEMI patients, 115 (71.42%) had Apelin-36 levels ≤ 0.58 ng/mL (group 1), whereas 46 (28.57%) had Apelin-36 levels > 0.58 ng/mL (group 2). In total, 51 (31.67%) STEMI patients experienced no-reflow phenomenon after PCI: 29 (25.21%) of patients with apelin-36 ≤ 0.58 ng/mL and 22 (47.82%) of those with a value > 0.58 ng/mL (p < 0.001). In terms of Gensini score, the mean value in group 1 was 70.29 (±28.76), while in group 2, it was 81.95 (±23.82) (p = 0.004). Overall, a positive correlation between apelin-36 and Gensini score was observed in both groups using Kendall's correlation analysis (group 1: p = 0.05; group 2: p < 0.0001). Binary logistic regression analysis identified apelin-36 and diabetes mellitus as significant predictors at the 5% level, with p-values of 0.045 and 0.036, respectively. Patients with apelin-36 levels ≤ 0.58 ng/mL had troponin T levels of 290.0 (8.5-9510.0), while those with a value > 0.58 ng/mL had troponin T levels of 132.15 (9.4-5190.0) (p < 0.012). The receiver operating characteristics (ROC) curve of apelin-36 was used to plot the true positive rate against the false positive rate at different cut-off points, with AUC = 0.77 (95% CI, 0.69-0.84), and the cut-off value for apelin-36 was 0.58 ng/mL, with p = 0.001. Conclusions: Significant associations were observed between apelin-36 and the no-reflow phenomenon in patients with STEMI. An apelin-36 cut-off value of 0.58 ng/mL, measured at admission, could be used to identify patients who were at increased risk of no-reflow phenomenon/reperfusion injury.

IntroductionCoronary artery bypass grafting remains the preferred method for surgicalmyocardial revascularization. The use of extracorporeal circulation duringsurgery has been linked to myocardial damage and a systemic inflammatoryresponse. To mitigate these adverse effects, off-pump coronary artery bypassgrafting was introduced as an effective and safe alternative. However, thecomparison between these two procedures has yielded ambiguous results. Theaim of our study was to determine the differences in myocardial damage andthe intensity of the inflammatory response by measuring concentrations oftroponin, cardiac isoenzyme of creatine kinase, leukocytes, and C-reactiveprotein at multiple time points within the first 24 hourspostoperatively.MethodsThis single-center, prospective study involved 61 patients diagnosed withcoronary artery disease and divided into two groups based on the type ofsurgery performed.ResultsOur results indicated that coronary artery bypass grafting withextracorporeal circulation is associated with greater myocardial damage, asevidenced by higher levels of troponin and cardiac isoenzyme of creatinekinase. Additionally, extracorporeal circulation was linked to a morepronounced increase in leukocyte count postoperatively. Unexpectedly,C-reactive protein levels were higher in the off-pump coronary artery bypassgrafting group. There were no significant differences in hospital stay orin-hospital mortality between the two groups.ConclusionFurther research is necessary to clarify these controversies regarding thedifferences in systemic inflammatory responses between the two surgicalapproaches.

Diabetes mellitus and its microvascular complications, including diabetic retinopathy (DR), present significant health challenges. DR is a leading cause of vision impairment and blindness among working-age individuals in developed countries. The prevalence of DR continues to rise, underscoring the need for more precise diagnostic and therapeutic strategies. Due to its multifactorial nature and despite advancements in understanding DR pathophysiology, predicting its onset and progression remains challenging. Traditional screening and treatment methods often fall short of addressing the heterogeneous nature of the disease, underscoring the need for personalised therapeutic strategies. Recent research has highlighted the vital role of genetic biomarkers in the development and progression of DR, paving the way for a precision medicine approach. Personalised eye care in patients with diabetes aims to accurately predict the risk of DR progression and visual loss in real time. A precision medicine approach that utilises genetic biomarkers offers a promising pathway for personalised diagnosis and treatment strategies. Each DR case is distinct in phenotype, genotype, and therapeutic response, making personalised therapy crucial for optimising outcomes. Advancements in genomics, including genome-wide association studies (GWAS) and next-generation sequencing (NGS), have identified numerous genetic markers associated with DR susceptibility and severity. Emerging evidence underscores the critical role of genetic factors, which account for 25–50% of the risk of developing DR. Advances in identifying genetic markers, such as gene polymorphisms and human leukocyte antigen associations, along with the development of targeted drugs, highlight a promising future for personalised medicine in DR. By identifying specific genetic variants associated with DR, we can enhance prevention and early diagnosis, tailor personalised treatment plans, and more accurately predict disease progression. This represents a critical step toward personalised medicine in DR management. Integrating genetic and epigenetic biomarkers into clinical models may transform DR care through earlier diagnosis and precision-guided interventions, gearing it toward precision ophthalmology.

The role of nurse educators in academia requires balancing teaching, research, and administrative responsibilities, often with limited institutional recognition or support. These demands can influence job satisfaction, professional relationships and faculty retention. In Croatia, where nursing education is still developing within the higher education system, little is known about the experiences of nurse educators. This study explored job satisfaction and professional relationships of nurse educators employed full time in higher education institutions in Croatia. An exploratory descriptive qualitative study was conducted in 2024 among full-time nurse educators from 12 higher education institutions offering accredited nursing programs in Croatia. Data were collected through semi-structured online interviews. The interview guide included questions on job satisfaction and professional relationships. Data were analysed using reflexive thematic analysis. The study included 52 participants. Participants generally reported high job satisfaction, associated with autonomy in academic work, opportunities for professional development, and meaningful interaction with students. However, dissatisfaction stemmed from administrative overload, limited financial incentives, and uneven task distribution among colleagues. Institutional support and collegiality emerged as key factors sustaining motivation and professional identity, while many educators expressed a desire for closer integration of academic and clinical roles to strengthen both teaching relevance and clinical competence. This study highlighted the complex interplay between job satisfaction, professional expectations, and institutional support of nurse educators employed as full-time faculty. The findings emphasise the need for institutional and policy reforms to enhance the working conditions and recognition of nurse educators. Reducing administrative demands, providing fair financial and professional rewards, and establishing structured mentorship and development programs could foster career sustainability and faculty retention. Strengthening institutional support for academic nurses is essential for maintaining a competent and motivated teaching workforce, ultimately improving the quality and continuity of nursing education and practice in Croatia. Not applicable. This study was not a clinical trial.