J. CardioRenal Med., Volume 2, Issue 1 (March 2026) – 5 articles

Background: Recent advancements in heart failure (HF) therapy have significantly enhanced the management of patients across all phenotypes of left ventricular ejection fraction. However, these multidrug regimens frequently induce alterations in renal function by influencing intrarenal hemodynamics, thereby modifying glomerular capillary pressure. This phenomenon could result in a mild to moderate decline in estimated glomerular filtration rate (eGFR), often classified as “worsening kidney function.” This nomenclature stems from consistent observations of eGFR reductions recorded during HF treatment in clinical trials. This narrative review aims to elucidate why the observed eGFR declines in clinical practice may represent either loss of functioning glomeruli or pharmacologically mediated reductions in intraglomerular pressure that ultimately safeguards long-term renal and cardiovascular outcomes. Methods: By a comprehensive re-examination of data from HF clinical trials conducted with various classes of medications, all affecting eGFR, we sought to provide evidence that the decline in eGFR is associated with the activation of specific mechanisms that collectively contribute to a reduction in glomerular filtration pressure, a prominent factor in maladaptive neurohormonal responses. Results: From the investigation of angiotensin-converting enzyme inhibitors to the more recent non-steroidal mineralocorticoid receptor antagonist, the renal effects of these therapeutic regimens correlate with improvements in patient outcomes. The data consistently indicate that an early decline in eGFR, when coupled with an enhancement in HF outcomes, is associated with a more gradual decline in eGFR during long-term follow-up. Conclusions: Clinicians should recognize early declines in eGFR as indicators of favorable intraglomerular hemodynamic adjustments that mitigate maladaptive neurohormonal responses and contribute to improved long-term outcomes in patients with HF. Full article

Cardio-renal syndrome (CRS) is a term referring to a bidirectional group of disorders in which there is a concomitant compromise of both organs, the heart and the kidney, leading to a significant increase in morbidity and mortality. In recent years, numerous publications have addressed this complex entity from different points of view. For better understanding, five subtypes have been established: depending on its form of presentation, acute or chronic; the organ initially affected; and whether there is another responsible systemic disease. CRS represents a complex interaction between both organs with several neurohormonal, inflammatory, and hemodynamic pathophysiological mechanisms involved. Because of its heterogeneous presentation and complex management, CRS requires a multidisciplinary approach targeting multiple pathogenic mechanisms. Throughout this review, we will analyze all relevant aspects of CRS from its classification to current diagnosis and treatment. Accordingly, this review provides a holistic overview of cardio-renal syndrome, emphasizing integrated pathophysiological mechanisms, contemporary diagnostic approaches, and their relevance for clinical management. Full article

Introduction: Advanced chronic kidney disease (CKD) patients undergoing percutaneous coronary intervention (PCI) face a high risk of renal injury. Given this vulnerability, zero- and ultra-low-contrast PCI techniques have been proposed to minimize renal damage while still enabling effective revascularization. On this basis, this meta-analysis tests whether these contrast-sparing strategies yield better clinical and renal outcomes compared with conventional PCI in CKD patients. Methods: A total of 3939 records were retrieved from PubMed, Embase, Scopus, ScienceDirect, and Cochrane from inception till November 2025. Eligible RCTs and comparative observational studies reporting renal or cardiovascular outcomes were included. Pooled analyses were conducted in RevMan Web using a random-effects model with p < 0.05 considered statistically significant. Results: Across nine included studies (464,815 patients) evaluating zero-contrast or ultra-low-contrast PCI versus conventional PCI, zero-contrast PCI significantly reduced contrast-induced acute kidney injury (CI-AKI) (OR 0.24, 95% CI 0.12–0.49; p = 0.002), decreased contrast volume (MD −110 mL, 95% CI −168.6 to −51.8; p = 0.005), lowered the need for repeat revascularization (OR 0.26, 95% CI 0.09–0.77; p = 0.005), and reduced the incidence of emergent hemodialysis (OR 0.25, 95% CI 0.13–0.49; p < 0.0001). All-cause mortality and repeat myocardial infarction were initially nonsignificant but became significant after excluding outlier studies (OR 0.49, 95% CI 0.47–0.51; p < 0.00001; OR 0.19, 95% CI 0.10–0.35; p = 0.007, respectively). No significant differences were observed for major adverse cardiovascular events, cardiovascular or non-cardiovascular mortality, renal replacement therapy, or dialysis requirement. Conclusions: Our findings demonstrate that zero- and ultra-low-contrast PCI significantly reduces the risk of CI-AKI while preserving cardiovascular and renal outcomes, supporting its use as a safe and effective alternative to conventional PCI in high-risk CKD patients. Full article

Hypertension has traditionally been viewed as a hemodynamic disorder leading to cardiac and renal injury; however, growing evidence suggests that, in many individuals, elevated blood pressure is instead the earliest clinical expression of subtle cardiorenal dysfunction. Early abnormalities—such as low-grade albuminuria, increased renal resistive index, arterial stiffness, and masked or nocturnal hypertension—can appear before estimated glomerular filtration rate decline or elevated office blood pressure, indicating early impairment of pressure–natriuresis, heightened tissue renin–angiotensin–aldosterone system (RAAS) activity, and increased renal microvascular impedance. The aim of this review is to summarize mechanistic, clinical, and phenotypic evidence supporting the concept that hypertension functions as an early biomarker along the cardiorenal continuum. Incorporating vascular and renal biomarkers, ambulatory blood pressure phenotyping, and targeted laboratory indices into routine assessment may identify individuals transitioning from functional disturbances to structural organ damage. These abnormalities reflect a mechanistic triad of arterial stiffening, salt-sensitive RAAS activation, and circadian blood pressure disruption, collectively defining the early cardiorenal–hypertensive phenotype. Viewing hypertension through a cardiorenal lens underscores a critical opportunity for earlier detection and mechanism-oriented intervention, which may modify disease trajectory and prevent progression to overt chronic kidney disease and heart failure. Full article

Heart failure (HF) and chronic kidney disease (CKD) are prevalent conditions in older adults, often coexisting and significantly increasing the risk of hospitalization, cardiovascular events, and mortality. Traditional hospital-based care, while essential for acute management, is often insufficient to ensure continuity of care and optimal long-term outcomes. Home-based care, although promising for improving quality of life and reducing hospital-acquired complications, faces challenges related to treatment adherence, monitoring, and caregiver support. Recent evidence highlights the potential of multidisciplinary, patient-centered care models integrating physicians, nurses, pharmacists, and family caregivers. Technological innovations, including telemedicine, remote monitoring, mobile health applications, and artificial intelligence, have shown efficacy in early detection of clinical deterioration, improving adherence, and reducing cardiovascular events in HF and CKD patients. Structured patient education, caregiver training, and proactive follow-up are key elements to optimize transitions from hospital to home and to improve long-term outcomes, including reduced rehospitalizations and better quality of life. Future care strategies should focus on personalized, integrated approaches that combine technology, education, and multidisciplinary collaboration to address the complex needs of HF and CKD patients, while mitigating healthcare costs and enhancing overall patient well-being. Full article