Renal fibrosis is a leading cause of chronic allograft nephropathy. While renal biopsy remains the gold standard for diagnosing fibrosis, it is an invasive procedure with potential for severe complications. Elastography, an emerging ultrasound imaging technique, appears to be a valuable tool for quantifying tissue stiffness, which correlates with fibrosis. Indeed, numerous studies have demonstrated a strong correlation between increased tissue stiffness, measured by elastography, and the degree of fibrosis detected in biopsy. Over the past few years, various elastography techniques have been evaluated, including strain elastography, shear wave elastography, and acoustic radiation force impulse. However, challenges such as operator dependence, tissue heterogeneity, and the lack of standardized protocols persist. Despite these limitations, elastography presents itself as a valuable tool for the non-invasive monitoring of renal transplant function and could facilitate the early detection of fibrosis, allowing for timely interventions. Future research should focus on standardizing acquisition protocols, establishing robust reference values, and exploring the clinical utility of elastography in guiding therapeutic decisions. The aim of this review is to explore the current state of elastography in the assessment of fibrosis in renal transplantation.

Fracture risk is a serious yet underrecognized complication among patients with chronic kidney disease (CKD), especially in those with stages G3-G5D. The overlap between CKD-Mineral and Bone Disorder (CKD-MBD) and osteoporosis leads to complex bone changes that increase the likelihood of fragility fractures. Studies show that 18% to 32% of CKD patients also have osteoporosis, and these individuals are more than 2.5 times as likely to suffer from fractures compared to those without CKD. In the advanced stages of the disease, fracture risk is up to four times higher than in the general population, with the femur, forearm, and humerus being the most commonly affected sites. Hip fractures are of particular concern as they are linked to longer hospital stays and higher rates of morbidity and mortality. Furthermore, dialysis patients who experience hip fractures have a mortality rate 2.4 times higher than those in the general population with similar fractures. This increased risk underscores the need for proactive bone health maintenance in CKD patients to prevent fractures and related complications. This review explores the underlying pathophysiological mechanisms, diagnostic challenges, and treatment options related to bone fragility in CKD. Diagnostic tools, such as bone mineral density (BMD) assessments, the trabecular bone score (TBS), and biochemical markers, remain underused, especially in advanced CKD stages. Recent treatment strategies emphasize a multidisciplinary, stage-specific approach, incorporating calcium and vitamin D supplements, anti-resorptive agents like denosumab, and anabolic therapies such as teriparatide and romosozumab. Effective management needs to be tailored to the patient’s bone turnover status and stage of CKD. Despite progress in understanding bone fragility in CKD, significant gaps remain in both diagnosis and treatment. Personalized care, guided by updated KDIGO recommendations and based on an interdisciplinary approach, is essential to reduce fracture risk and improve outcomes in this vulnerable population. Further research is needed to validate risk assessment tools and refine therapeutic protocols.

Surgically created native arteriovenous fistulas (AVFs) remain the preferred vascular access for chronic hemodialysis, yet they are limited by substantial early failure and progressive consumption of venous capital. Endovascular arteriovenous fistulas (endoAVFs, also referred to as percutaneous AVFs) have become a catheter-based alternative to surgical AVF (sAVF). We conduct an updated narrative, practice-oriented review of the literature on endoAVF creation, and we qualitatively synthesize evidence. Two devices are currently available in contemporary clinical practice: a dual 4 Fr-catheter, fluoroscopy-guided radiofrequency system (WavelinQ) and a single 6 Fr-catheter, ultrasound-guided thermal resistance system (Ellipsys). Across prospective studies and real-world series, endoAVF creation is consistently reported to have high technical success, with low major complication and infection rates. Clinical usability can often be achieved within weeks when ultrasound-based surveillance and protocol-driven maturation assistance are implemented; however, adjunctive procedures are frequently required and should be anticipated in program planning and informed consent. Observational comparisons and pooled analyses indicate broadly comparable functional outcomes versus surgery in selected cohorts, while estimates of primary patency and maintenance burden vary substantially across studies. Overall, endoAVFs represent a feasible, minimally invasive, vessel-sparing option that can be integrated into multidisciplinary access pathways in anatomically suitable candidates and experienced centers, complementing rather than replacing surgical strategies within a distal-first plan. Recent society practice guidance further emphasizes standardized mapping, expectation setting, troubleshooting algorithms for non-maturation, and dialysis-unit cannulation training to support consistent implementation. Pragmatic comparative studies and long-term registries using standardized endpoints, paired with healthcare-system-specific economic analyses, are needed to better define durability, resource use, and patient-centered outcomes over the full-access life cycle.

Heart failure affects more than 64 million people worldwide, and admissions for acute decompensation account for a substantial proportion of cardiovascular healthcare expenditure. Achieving complete decongestion remains the principal objective of inpatient management, yet many patients are discharged with persistent volume overload, a consistent predictor of early rehospitalization and mortality. Loop diuretics have remained the cornerstone of decongestive therapy for more than six decades; however, their effectiveness is frequently limited by diuretic resistance, leaving many patients incompletely decongested despite dose escalation. Diuretic resistance reflects adaptive sodium retention distributed across multiple nephron segments, a process that extends well beyond the loop itself. Distal-tubular-remodeling-enhanced proximal sodium reabsorption, neurohormonal activation, post-diuretic sodium retention, and impaired tubular drug delivery collectively blunt natriuretic responsiveness, explaining why progressive loop–dose escalation often yields diminishing returns. Sequential nephron blockade provides a physiology-based strategy that matches the adjunct agent to the predominant mechanism of sodium retention. We integrate contemporary randomized evidence with renal tubular physiology to propose a mechanism-based approach: acetazolamide for patients with hypochloremic metabolic alkalosis and enhanced proximal sodium reabsorption, thiazide-type diuretics when distal cotransporter escape predominates, vasopressin antagonists for dilutional hyponatremia complicating congestion, and sodium–glucose cotransporter 2 inhibitors as foundational therapy that combines modest acute natriuresis with durable cardiorenal protection. Early assessment of natriuretic response using spot urine sodium further enables individualized treatment escalation. Together, these concepts move sequential nephron blockade beyond empirical combination diuretic therapy toward a mechanism-based strategy for overcoming diuretic resistance. We propose a personalized, phenotype-driven framework in which early urinary sodium response, kidney function, serum chloride, acid–base status, serum sodium, background SGLT2 inhibitor therapy, and venous congestion imaging guide the selection, escalation, and de-escalation of adjunctive therapy, with the goal of more complete and safer decongestion in acute decompensated heart failure. Matching adjunct choice to a patient’s individual biochemical phenotype, rather than applying diuretics in a fixed sequence, exemplifies precision medicine applied to acute decongestive therapy.

In many immune-mediated kidney diseases, tissue injury is driven by dysregulated B-cell immunity, with autoantibodies and complement acting as key effectors at the glomerulus. Corticosteroids and conventional immunosuppressants control these diseases only in part, and they do so at the price of cumulative toxicity and frequent relapse. Anti-CD20 antibodies deplete circulating B cells but spare plasmablasts and CD19+ plasma cells that sustain autoantibody production, leaving a residual autoreactive compartment that may contribute to refractory disease and relapse. Anti-CD19 chimeric antigen receptor (CAR) T cells target a broader spectrum of B-cell populations, and early clinical studies suggest that this deeper depletion extends into secondary lymphoid tissues. The clinical evidence, however, is uneven. It is strongest in systemic lupus erythematosus and refractory lupus nephritis, where case series and early-phase trials report clinical and serological remission together with discontinuation of immunosuppression and treatment-free remission. In multiple myeloma and immunoglobulin light-chain (AL) amyloidosis with renal involvement, anti-B-cell maturation antigen (anti-BCMA) CAR-T products are increasingly used in real-world cohorts of patients with reduced estimated glomerular filtration rate (eGFR) or on dialysis, while bispecific T-cell engagers such as teclistamab offer an off-the-shelf alternative. The toxicity of these agents concerns the nephrologist directly. Cytokine release syndrome, immune effector cell-associated neurotoxicity syndrome, tumor lysis syndrome, and the immune effector cell-associated hemophagocytic lymphohistiocytosis-like syndrome (IEC-HS) (IEC-HS) can each involve the kidney, as can the newly defined local immune effector cell-associated toxicity syndrome (LICATS). This review explores the immunological basis of CAR-T constructs, the evidence by disease, the renal toxicity profile, and the criteria for candidate selection and nephrological monitoring.

Background: Patients with chronic kidney disease (CKD) have a substantially higher risk of developing cognitive impairment (CI) than the general population. Patients with CKD undergoing haemodialysis (HD) treatment also have an elevated risk of developing cerebrovascular and cardiovascular diseases. This study aims to investigate the relationship between the cognitive performance of haemodialysis patients and cerebral and carotid haemodynamic indices. Methods: This study was a non-interventional observational study; the sample consisted of 32 patients (age 65 ± 12 years) undergoing chronic HD treatment. The patients underwent neuropsychological and haemodynamic instrumental investigations, including Supra-Aortic Trunk Echodoppler (SAT) and Transcranial Doppler (TCD). Results: Patients were 17% deficient at Montreal Cognitive Assessment (MoCA), 45% deficient at Frontal Assessment Battery (FAB), 55% deficient at Trail-Making Test-A (TMT-A) and 65% deficient at TMT-B. The TCD investigation detected a decrease in flow (MFV) and an increase in Breath Hold Index (BHI) predominantly in the right cerebral arterial district. The SAT investigation revealed an altered IMT, plaques and the presence of severe carotid stenosis. A strong association between cerebral and carotid indices and cognitive scores was also observed. Correlation analyses reported statistically significant correlations between TMT-A and TMT-B and cerebral flow indices. Conclusions: Among haemodialysis patients, there is a high percentage of cognitive impairment associated and correlated with alterations in cerebral and carotid haemodynamics. Cerebral haemodynamics are a factor to be taken into consideration as a possible pathological mechanism underlying cognitive impairment in haemodialysis.