Journal of CardioRenal Medicine

Obesity is a significant public health crisis with increasing rates worldwide. Chronic kidney disease (CKD) has also emerged as a leading cause of death worldwide. This review explores the intricate connection between obesity and CKD, discussing the underlying biological mechanisms, clinical consequences of their coexistence, and strategies for evidence-based management. We conducted an extensive literature review of peer-reviewed studies examining obesity–CKD relationships, including epidemiological studies, mechanistic research, clinical trials, and meta-analyses from major medical databases. Obesity serves as both a risk factor for de novo CKD development and a paradoxical protective factor observed in some studies of advanced CKD, particularly in dialysis populations. This review synthesizes current evidence on obesity-related glomerulopathy, the impact of obesity on CKD progression to end-stage renal disease, and the phenomenon known as the “obesity paradox”. Management approaches, including lifestyle interventions, pharmacological treatments, and bariatric surgery, show varying efficacy across different CKD stages. The multifaceted relationship between obesity and CKD necessitates individualized, multidisciplinary approaches to optimize patient outcomes while addressing the unique challenges presented by this complex comorbidity. Early intervention in obese patients may prevent CKD development, while careful management is required in advanced CKD stages where the obesity paradox may confer survival benefits. Full article

Background: Anticoagulation is the cornerstone of thromboembolic event prevention. Adversely, anticoagulants (ACs) are linked to a variety of adverse events. We aimed to assess the link between vitamin K antagonists (VKA) and direct anticoagulant (DOACs) use and acute kidney injury (AKI) using the FDA Adverse Events Reporting System (FAERS) Database. Methods: We conducted a disproportionality analysis on the adverse events (AEs) of interest in the FAERS database using the reporting odds ratio (ROR), proportional reporting ratio (PPR) with the Yates correction (x²yates), and the information component (IC). Results: A total of 20,253 cases of AKI associated with use of ACs were analyzed. Edoxaban, dabigatran and warfarin showed greater association with AKI (ROR 2.63; ROR 1.46; ROR). In cases with manifest bleeding, edoxaban, dabigatran, warfarin and rivaroxaban had a stronger statistical association with AKI. Rivaroxaban showed greater association with AKI compared to other ACs when used concomitantly with Aspirin (ROR 2.25). Conclusion: We showed increased odds of reporting AKI with use of edoxaban, dabigatran and warfarin compared to other anticoagulants. In cases with reported bleeding, AKI was more commonly reported with all five analyzed anticoagulants, except for apixaban, highlighting its favorable side-effect profile. Caution and clinical awareness are needed when prescribing ACs to vulnerable populations. Full article

Background: Uraemic cardiomyopathy (UCM), the cardiac manifestation of chronic kidney disease, represents a significant clinical challenge that is often underdiagnosed despite being one of the strongest predictors of mortality in the chronic kidney disease (CKD) population. It develops through pathophysiological mechanisms unique to the uraemic state—left ventricular hypertrophy, myocardial fibrosis, and diastolic dysfunction—that often progress silently, sometimes even without traditional cardiovascular risk factors. Purpose: This review synthesises nephrology-centric mechanisms with clinical phenotypes and contemporary imaging (including CMR T1/T2 mapping and ECV), and proposes a CKD-stage–tailored diagnostic–therapeutic framework. It offers a distinct perspective by integrating the complex pathophysiology of UCM with practical diagnostic approaches and evolving management strategies, differentiating it from prior cardiology-focused overviews. Methods: A comprehensive literature search was conducted across Ovid MEDLINE, Embase, PubMed, Google Scholar, BMJ Best Practice, and UpToDate for studies published up to March 2025. Key findings were extracted from the final evidence set and manually verified for relevance. This review introduces a patho-mechanical cascade model of uraemic cardiomyopathy, integrating toxin-driven, metabolic, and haemodynamic axes. Nephrology-led screening protocols are proposed, leveraging proteomics and strain echo, and advocate mineralocorticoid receptor antagonists with sodium–glucose co-transporter-2 (SGLT2) inhibitor initiation at CKD Stage 3a. Cardiorenal clinics are essential for improved outcomes. Key Insights: UCM develops from a multifactorial process. This involves neurohormonal activation, oxidative stress, chronic inflammation, and exposure to toxins such as indoxyl sulfate and p-cresyl sulfate, arising from uraemia. Diagnosis is challenging, masked by overlapping features of fluid overload and anaemia. SGLT2 inhibitors, non-steroidal mineralocorticoid antagonists, and renin–angiotensin–aldosterone system modulation offer promising interventions. The effect of the dialysis modality, its timing, and renal transplantation on cardiac remodelling also emerging from recent studies. Conclusions: UCM sits at the intersection of two failing organ systems. Managing it effectively requires a paradigm shift to incorporate pharmacological and early diagnostic interventions and the integration of cardiology and nephrology care, and the timely implementation of interventions. Full article