Atypical hemolytic uremic syndrome (aHUS) is a rare, life-threatening thrombotic microangiopathy (TMA) characterized by complement dysregulation, leading to microvascular thrombosis and multi-organ injury. TMAs are defined by thrombocytopenia, microangiopathic hemolytic anemia and organ dysfunction caused by small-vessel thrombosis. Unlike thrombotic thrombocytopenic purpura, which results from severe ADAMTS13 deficiency, aHUS is driven by uncontrolled activation of the alternative complement pathway. While the kidneys are most frequently affected, other vital organs can also be involved. Genetic susceptibility contributes significantly to disease risk, but a trigger such as infection, pregnancy or autoimmune disease is usually required. Diagnosis is challenging due to overlapping features with other TMAs and relies on exclusion and complement testing. C5 inhibitors, such as eculizumab and ravulizumab, have revolutionized treatment but necessitate prophylactic vaccination and ongoing clinical surveillance. While these therapies provide effective disease control, discontinuing treatment remains complex, especially in patients with complement gene mutations. New therapies targeting various points in the complement cascade are under investigation and may offer safer, more cost-effective options. Progress in genetic profiling and biomarker discovery is essential for earlier diagnosis, individualized therapy and relapse prevention. This review highlights recent advances in the understanding of aHUS pathophysiology, clinical features and evolving therapeutic strategies aimed at improving patient outcomes.

Fat grafting has gained prominence in reconstructive and aesthetic surgery, necessitating accurate assessment methods for evaluating graft volume retention. This paper reviews various techniques for assessing fat and fat grafts, including their benefits and limitations. Three-dimensional (3D) scanning offers highly accurate, non-invasive volumetric assessments with minimal interference from breathing patterns. Magnetic resonance imaging (MRI) is recognized as the gold standard, providing precise volumetric evaluations and sensitivity to complications like oil cysts and necrosis. Computed tomography (CT) is useful for fat volume assessment but may overestimate retention rates. Ultrasonography presents a reliable, non-invasive method for measuring subcutaneous fat thickness. Other methods, such as digital imaging, histological analysis, and weight estimation, contribute to fat graft quantification. The integration of these methodologies is essential for advancing fat graft assessment, promoting standardized practices, and improving patient outcomes in clinical settings.

Nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a contributor to chronic kidney disease (CKD), yet its impact remains underappreciated in clinical practice. Recent studies reveal a strong association between NAFLD and CKD progression, with evidence linking hepatic dysfunction to renal impairment through metabolic and inflammatory pathways. NAFLD not only increases the risk of CKD but also accelerates its progression, leading to worse cardiovascular outcomes and higher mortality, particularly in patients with advanced fibrosis. Despite this growing evidence, NAFLD often goes undiagnosed in CKD patients and routine hepatic evaluation is rarely integrated into nephrology care. Emerging diagnostic tools, including noninvasive biomarkers and imaging techniques, offer potential for earlier detection, yet their clinical implementation remains inconsistent. Although lifestyle modifications remain the foundation of treatment, pharmacotherapeutic strategies, including SGLT2 inhibitors and GLP-1 receptor agonists, have demonstrated potential in mitigating both hepatic and renal impairment. Recognizing the interplay between NAFLD and CKD is essential for improving patient outcomes. A multidisciplinary approach, integrating hepatology and nephrology expertise, is crucial to refining screening strategies, optimizing treatment, and reducing the long-term burden of these coexisting conditions.

Background: Chronic kidney disease (CKD) represents a state of persistent, sterile low-grade inflammation in which sustained innate immune activation accelerates renal decline and cardiovascular complications. Diet-induced gut dysbiosis and intestinal barrier dysfunction lower mucosal immune tolerance, promote metabolic endotoxemia, and position the gut as an upstream modulator of systemic inflammatory signaling along the gut–kidney axis. Scope: Most studies address microbiota-derived metabolites, food-derived bioactive peptides, or omega-3 fatty acids separately. This review integrates evidence across these domains and examines their convergent actions on epithelial barrier integrity, immune polarization, oxidative-inflammatory stress, and inflammasome-dependent pathways relevant to CKD progression. Key mechanisms: CKD-associated dysbiosis is characterized by reduced short-chain fatty acid (SCFA) production and increased generation and accumulation of uremic toxins and co-metabolites, including indoxyl sulfate, p-cresyl sulfate, trimethylamine N-oxide, and altered bile acids. Reduced SCFA availability weakens tight junction-dependent barrier function and regulatory immune programs, favoring Th17-skewed inflammation and endotoxin translocation. Bioactive peptides modulate inflammatory mediator networks and barrier-related pathways through effects on NF-κB/MAPK signaling and redox balance, while omega-3 fatty acids and specialized pro-resolving mediators support resolution-phase immune responses. Across these modalities, shared control points include barrier integrity, metabolic endotoxemia, oxidative stress, and NLRP3 inflammasome activation. Conclusions: Although evidence remains heterogeneous and largely preclinical, combined nutritional modulation targeting these convergent pathways may offer greater immunomodulatory benefit than isolated interventions. Future multi-omics-guided, factorial trials are required to define responder phenotypes and translate precision immunonutrition strategies into clinical CKD care.

Breast thread lifting is a minimally invasive technique for correcting mild to moderate ptosis, offering aesthetic enhancement with reduced morbidity compared to traditional mastopexy. This review examines the anatomical underpinnings, clinical indications, technical nuances and limitations of breast thread lifting. The breast’s fascial architecture, particularly the role of Cooper’s ligaments and the retromammary space, critically influences thread trajectory and vector planning. Classification systems assist in proper patient selection, highlighting the suitability of thread lifts for Grades I–II ptosis with minimal skin excess. Advances in ultrasonography have improved preoperative planning, thread placement accuracy and postoperative monitoring. Various thread types, including PDO, PLLA, PCL and Silhouette Soft, offer different lifting capacities and collagen-stimulatory properties, necessitating tailored material selection. Although thread lifts offer immediate improvements, their transient nature necessitates careful patient counseling to manage expectations regarding durability and potential maintenance sessions. Innovative techniques, including clavicular anchoring and multi-level subdermal scaffolding, have expanded the procedural repertoire. Despite certain limitations, breast thread lifting remains a valuable tool within the aesthetic surgeon’s armamentarium, particularly for patients seeking minimally invasive options with shortened recovery periods and favorable psychosocial outcomes. Future developments are expected to further enhance safety, reproducibility and long-term results.

Background/Objectives: Capsular contracture (CC) is the most frequent complication of breast implant surgery, affecting up to 20% of augmentation and up to 40% of post-mastectomy reconstruction patients. Diagnosis relies on the Baker classification with poor interobserver reliability (κ = 0.55). This study evaluated shear-wave elastography (SWE) as an objective diagnostic tool for CC via quantitative measurement of periprosthetic capsule stiffness. Methods: A prospective single-center comparative study (Romania) enrolled 26 augmentation patients (50 breasts) with asymptomatic Baker I/II CC as controls, and 25 breasts with confirmed Baker III/IV CC in post-mastectomy reconstruction patients as the study group. Stiffness was measured using the SuperSonic MACH 30 platform (mean, median, min, max, SD in kPa). Analysis included Mann-Whitney U tests, ROC curves with bootstrapped 95% CIs, and Youden’s J index. Confounder analyses (Spearman correlations, multivariable logistic regression, partial correlations) assessed the independence of SWE findings from implant depth, periprosthetic tissue thickness, region-of-interest (ROI) diameter, and body mass index (BMI). Results: All four primary stiffness parameters differed significantly between groups (p < 10⁻¹¹, r > 0.97). Control median stiffness was 32.6 kPa versus 138.0 kPa in the study group. All four parameters achieved outstanding discriminative performance (AUC 0.988–0.994); SWE median yielded the highest AUC (0.994; 95% CI 0.980–1.000). A threshold of 82 kPa provided 100% sensitivity, 98% specificity, and 100% NPV. Baker Grades III (~92 kPa) and IV (~147 kPa) also differed significantly (p = 0.0001). No covariate (implant depth, periprosthetic tissue thickness, ROI diameter, BMI) significantly influenced SWE values within either group (all intra-group Spearman ρ p > 0.05), and SWE median stiffness remained the sole significant predictor in the fully adjusted multivariable model (adjusted OR = 1.18, 95% CI 1.08–1.31, p < 0.001). Conclusions: SWE objectively differentiates normal periprosthetic capsules from clinically significant CC with outstanding accuracy. An 82 kPa median stiffness threshold offers a reproducible, non-invasive complement to the Baker classification and provides a foundation for elastography-based CC staging.