Surgical resection is the only option of cure for patients with metastatic colorectal cancer. Risk of recurrence after metastasectomy is around 75%. Use of adjuvant chemotherapy after metastasectomy is controversial. Aim To address whether adjuvant systemic therapy after colorectal cancer metastasectomy offers any survival benefit compared with surgery alone. Methods Systematic review of literature and meta-analysis of all available randomised evidence. Relative hazards (RHs) were summarised across trials and heterogeneity was assessed with the Q and I2 statistics. Results Five trials were eligible. Three trials, all using single-agent fluoropyrimidine chemotherapy, presented data valuable for analyses. 482 patients were included in the meta-analysis: 238 randomly assigned to receive postoperative chemotherapy and 244 to metastasectomy only. We found no overall survival (OS) benefit with the use of postoperative single-agent fluoropyrimidines compared with surgery alone, even if a trend for benefit was observed (relative hazard (RH)=0.781, 95% CI 0.593 to 1.030, p=0.080). Significant disease-free survival benefit with the use of postoperative chemotherapy was observed (RH=0.645, 95% CI 0.509 to 0.818, p=0.001). No quality of life (QL) data were available. All trials showed accrual delay, two stopped and one recruiting after 10 years. Long follow-up needs were evidenced since OS curves split only after 3.5 years. Conclusions No OS benefit was documented from the use of postoperative monochemotherapy. Metastasectomy alone continues to be the standard of care. Combination chemotherapy regimens should be evaluated along with QL assessment in future trials appropriately designed for long-term accrual and follow-up.

Cardiovascular disease, particularly life-threatening ventricular arrhythmias and sudden cardiac death (SCD), remains the leading cause of death among haemodialysis (HD) patients, with an alarmingly higher incidence compared with the general population. By addressing key risk factors such as electrolyte imbalances, fluid overload and ultrafiltration rates, focusing on practical interventions and incorporating multidisciplinary care, clinicians can significantly reduce the risk of fatal arrhythmias. Here we propose 10 practical tips to guide clinicians in managing severe arrhythmias in HD patients. Each tip provides actionable insights for identifying high-risk individuals, with an emphasis on prevention and multidisciplinary care.

Introduction: Phosphate binders are commonly used in patients receiving kidney replacement therapy (KRT), aiming to reduce and maintain serum phosphorus. Chronic kidney disease‐mineral and bone disorder has been linked to reduced lifespan and worsened quality of life. This study aims to examine the efficacy and safety of sucroferric oxyhydroxide versus sevelamer carbonate in patients receiving KRT.Methods: The data sources examined were MEDLINE (PubMed), Scopus, and the Cochrane Central Register of Controlled Clinical Trials with a search deadline of October 2023. We examined randomized controlled trials that compared sucroferric oxyhydroxide versus sevelamer carbonate in the adult population receiving KRT. We performed a meta‐analysis combining the data from trials, using R‐studio.Findings: Inclusion criteria were met by five randomized trials. There was no statistically significant difference in the reduction of serum phosphorus between the two groups (MD: −0.07 mmol/L, 95% CI‐random effects: −0.15 to 0.02). In the same line, a non‐statistically significant difference was observed in serum i‐PTH reduction between the two drugs (MD = −1.53 mg/dL, 95% CI = (−4.45, 1.4), p = 0.26, random effects model). No statistically significant difference was observed in all adverse events between the two groups (odds ratio: 1.11, 95% CI: 0.65–1.88, random effects model). Further analysis of gastrointestinal adverse events revealed that sevelamer carbonate increases gastrointestinal adverse events by up to 60% (odds ratio: 1.60, 95% CI: 1.31–1.97, common (fixed) effect model).Discussion: This meta‐analysis of randomized trials showed that both drugs, sucroferric oxyhydroxide and sevelamer equally and effectively controlled serum phosphorus levels, whereas sucroferric oxyhydroxide revealed a better profile in terms of gastrointestinal adverse events. Sucroferric oxyhydroxide is a valuable option for patients receiving KRT when sevelamer carbonate is more difficult to tolerate.

SGLT2 inhibitors have transformed the care of patients with diabetes, chronic kidney disease (CKD), and cardiovascular disease. Nevertheless, the efficacy of SGLT2 inhibitors as well as potential associated risks remains to be further clarified in the setting of advanced diabetic kidney disease. Indirect evidence and secondary analyses from the landmark SGLT2 trials as well as emerging data from recent studies including exclusively patients with diabetes and advanced CKD, indicate that the renal and cardiovascular benefits of SGLT2 inhibitors persist even in these patients. Although the use of SGLT2 inhibitors in patients with diabetes undergoing dialysis remains investigational, preliminary evidence from experimental and clinical studies seems promising in terms of multifaceted positive outcomes, including preservation of residual kidney function. Furthermore, the available data until now does not indicate an increase in risk in patients with diabetes and advanced CKD regarding acute impairment of kidney function or other adverse outcomes of interest including diabetic ketoacidosis, infections, fractures risk and amputations. The aim of this review is to present the current knowledge available on the utility of SGLT2 inhibitors in patients with diabetes and advanced CKD so as to provide a foundation for their implementation in clinical practice. Future experimental research shall further elucidate the pleiotropic effects of SGLT2 inhibitors so as to expand their indications in the setting of diabetes and advanced CKD. Finally, the results of ongoing clinical trials in patients with diabetes and kidney failure as well as in dialysis patients are much anticipated.

Aberrant signaling pathways of the acquired immune system are implicated in the development of cardiovascular disease (CVD) and chronic kidney disease (CKD) phenotypes. Understanding the complex abnormalities of lymphocyte subpopulations in CKD is a prerequisite for elucidating their implication in uremic cardiomyopathy. T cell subsets display various patterns of association with indices of myocardial function in both experimental and clinical CKD models. The role of Tregs in CVD and CKD has attracted significant research interest. Although experimental data suggest a protective role of Tregs from the development of arterial hypertension- and pressure overload-induced myocardial hypertrophy, there might be a change in the regulatory T cell (Treg) phenotype towards a profibrotic one in the settings of CKD and heart failure. Depletion of B lymphocytes is a hallmark of CKD and heart failure, bearing adverse prognostic significance, yet evidence of B lymphocytes’ involvement in the pathogenesis of myocardial damage is currently lacking. Considering that myocardial remodeling is the final outcome of diverse pathogenic processes targeting the heart, the aim of this review is to present the evidence available up to now regarding the role of acquired immune cells in the pathogenesis of the structural and functional alterations of the myocardium in CKD.

Primary membranous nephropathy (pMN) is an antibody-mediated podocytopathy, most commonly caused by autoantibodies against the M-type phospholipase A2 receptor (PLA2R1). Rituximab (RTX), an anti-CD20 monoclonal antibody, is a first-line treatment for moderate-to-high-risk pMN, inducing partial or complete remission in about 60% of patients within 24 months. However, treatment response varies considerably, and current biomarkers, including anti-PLA2R1 titers and peripheral B cell counts, have limited predictive value for non-response or relapse. Beyond B cell depletion, RTX exerts broader immunomodulatory effects by influencing T cell subsets, monocytes, and natural killer (NK) cells involved in antibody-dependent cellular cytotoxicity. This review examines the peripheral immune cell changes that accompany anti-CD20 therapy and their value as candidate biomarkers. Total CD19+ B cell depletion is the standard pharmacodynamic measure of drug effect but correlates only loosely with clinical outcome. A specific B cell reconstitution profile was associated with pending relapse. Class-switched memory B cells remain depleted during sustained remission, and their premature re-expansion has been associated with subsequent relapse. Regulatory T cells are reduced in active disease and rise within days of infusion in patients who later respond. The systemic inflammation response index, derived from the routine differential count, has been associated with both 6- and 12-month remission. These observations derive from small, mostly single-center cohorts using heterogeneous panels and different RTX regimens. On the available evidence, immune cell profiling cannot yet be recommended for routine disease monitoring, and larger prospective studies with standardized panels are required.