Journal of CardioRenal Medicine

Heart failure (HF) remains a prevalent, high-risk condition particularly common among the elderly population. The impairment of systolic function, secondary dysregulation of maladaptive neurohormonal systems and HF therapies lead to electrolyte disturbances. Hyponatremia is a well-studied, robust marker of adverse prognosis in HF. Serum chloride has emerged as a promising prognostic marker, accurately predicting adverse outcomes in both acute and chronic settings. Hypochloremia reflects a compound of maladaptive neurohormonal, renal and acid–base mechanisms, frequently worsened by diuretic therapy. In the context of HF, low chloride levels are independently associated with increased cardiovascular mortality, HF hospitalization and diuretic resistance. Urinary chloride (uCl⁻) has recently been shown to serve as a dynamic biomarker of HF severity, Renin–Angiotensin–Aldosterone-system (RAAS) activation, and poor outcomes, offering incremental prognostic value. Our review synthesizes the latest evidence on serum and urinary chloride disturbances in HF, framing key distinctions between acute versus persistent electrolyte disturbances. We also explore the interrelationship between chloride and sodium, the differential impact of hypochloremia in Heart Failure with Preserved Ejection Fraction (HFpEF) versus Heart Failure with Reduced Ejection Fraction (HFrEF), and clinical outcomes stratified by the temporary vs. persistent nature of chloride imbalance. We have also included visual flowcharts for classifying and managing hypochloremia based on the underlying etiology.

Introduction: The prevalence of cardiorenal syndrome (CRS) and its management might be challenging, so an interdisciplinary approach is advocated. The aim of this study was to identify and describe the population which might profit from such an interdisciplinary clinic at the University Hospital of Zürich. Methods: We screened 551 patients who were seen at least once in the nephrology and cardiology outpatient clinics from 2015 to 2022. Patients with kidney (87) or heart (47) transplantation, on dialysis (179), without concomitant chronic kidney disease (CKD) and heart failure (HF) (179), and those who died before the end of follow-up (94), were excluded, resulting in a cohort of 150 patients. Characteristics related to the type and cause of renal and cardiac disease, cardiovascular risk factors, adequacy of therapy, and incidence of hospitalization for HF were recorded. Results: The median age of the population was 71 years, with one-third having diabetes and two-thirds being male. The median BMI was 28 kg/m². The predominant cause of chronic kidney disease (CKD) was cardiorenal syndrome type 2, affecting 44% (66 out of 150 patients). At the start of the follow-up, the distribution of CKD stages was as follows: 52 patients (34.7%) had CKD stage 2, 30 (20%) had CKD stage 3a, 21 (14%) had CKD stage 3b, 11 (7.3%) had CKD stage 4, and 1 (0.6%) had CKD stage 5. Notably, 81 patients (54%) had moderate or severe albuminuria. Ischemic cardiomyopathy was the leading cause of heart failure, affecting 36.4% (47 patients). Among the heart failure classifications, 73 patients (48.7%) had HFrEF, 32 (21.3%) had HFmrEF, and 45 (30%) had HFpEF. A total of 54 patients (36%) were treated with SGLT2 inhibitors, while 116 (77.3%) received RAAS inhibitors, including 32 patients (21.3%) on an ARNI. Those using both RAAS inhibitors and SGLT2 inhibitors were younger (average age 66 vs. 73 years, p = 0.005) and had a higher prevalence of diabetes (44% vs. 30%) and HFrEF compared to HFpEF (70% vs. 7%, p = 0.002). The hospitalization rate was notably high at 2.2 admissions per patient per year, with an incidence of acute kidney injury (AKI) at 0.23 events per patient per year. Conclusions: We identified a high-risk patient population with cardiorenal disease that might particularly benefit from evidence-based and patient-centered interdisciplinary care.

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.