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Chronic kidney disease (CKD) is diagnosed when glomerular filtration rate (GFR) falls below 60 ml/min/1.73 m2 or urinary albumin:creatinine ratio (UACR) reaches ≥30 mg/g, as these two thresholds indicate a higher risk of adverse health outcomes, including cardiovascular mortality. CKD is classified as mild, moderate or severe, based on GFR and UACR values, and the latter two classifications convey a high or very high cardiovascular risk, respectively. Additionally, CKD can be diagnosed based on abnormalities detected by histology or imaging. Lupus nephritis (LN) is a cause of CKD. Despite the high cardiovascular mortality of patients with LN, neither albuminuria nor CKD are discussed in the 2019 European League Against Rheumatism (EULAR)/European Renal Association–European Dialysis and Transplant Association recommendations for the management of LN or the more recent 2022 EULAR recommendations for cardiovascular risk management in rheumatic and musculoskeletal diseases. Indeed, the proteinuria target values discussed in the recommendations may be present in patients with severe CKD and a very high cardiovascular risk who may benefit from guidance detailed in the 2021 European Society of Cardiology guidelines on cardiovascular disease prevention in clinical practice. We propose that the recommendations should move from a conceptual framework of LN as an entity separate from CKD to a framework in which LN is considered a cause of CKD and evidence generated from large CKD trials applies unless demonstrated otherwise. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is a risk factor for premature cardiovascular disease. As kidney function declines, the presence of left ventricular abnormalities increases such that by the time kidney replacement therapy is required with dialysis or kidney transplantation, more than two-thirds of patients have left ventricular hypertrophy. Historically, much research in nephrology has focussed on the structural and functional aspects of cardiac disease in CKD, particularly using echocardiography to describe these abnormalities. There is a need to translate knowledge around these imaging findings to clinical outcomes such as unplanned hospital admission with heart failure and premature cardiovascular death. Left ventricular hypertrophy and cardiac fibrosis, which are common in CKD, predispose to the clinical syndrome of heart failure with preserved left ventricular ejection fraction (HFpEF). There is a bidirectional relationship between CKD and HFpEF, whereby CKD is a risk factor for HFpEF and CKD impacts outcomes for patients with HFpEF. There have been major improvements in outcomes for patients with heart failure and reduced left ventricular ejection fraction as a result of several large randomized controlled trials. Finding therapy for HFpEF has been more elusive, although recent data suggest that sodium-glucose cotransporter 2 inhibition offers a novel evidence-based class of therapy that improves outcomes in HFpEF. These observations have emerged as this class of drugs has also become the standard of care for many patients with proteinuric CKD, suggesting that there is now hope for addressing the combination of HFpEF and CKD in parallel. In this review we summarize the epidemiology, pathophysiology, diagnostic strategies and treatment of HFpEF with a focus on patients with CKD. [ABSTRACT FROM AUTHOR]

Arteriovenous fistula (AVF) is the preferred type of vascular access for maintenance haemodialysis but it may contribute to maladaptive cardiovascular remodelling. We studied the effect of AVF creation on cardiac structure and function in patients with chronic kidney disease (CKD). In this prospective cohort study patients with CKD listed for first AVF creation underwent cardiac magnetic resonance (CMR) imaging at baseline and at 6 weeks. All participants had ultrasound measurements of fistula blood flow at 6 weeks. The primary outcome was the change in left ventricular (LV) mass. Secondary outcomes included changes in LV volumes, LV ejection fraction, cardiac output, LV global longitudinal strain and N-terminal-pro B-type natriuretic peptide (NT-proBNP). A total of 55 participants were enrolled, of whom 40 (mean age 59 years) had AVF creation and completed both scans. On the second CMR scan, a mean increase of 7.4 g (95% CI 1.1–13.7, p = 0.02) was observed in LV mass. Significant increases in LV end-diastolic volumes (p = 0.04) and cardiac output (p = 0.02) were also seen after AVF creation. No significant changes were observed in LV end-systolic volumes, LV ejection fraction, NT-proBNP and LV global longitudinal strain. In participants with fistula blood flows ≥ 600 mL/min (n = 22) the mean increase in LV mass was 15.5 g (95% CI 7.3–23.8) compared with a small decrease of 2.5 g (95% CI − 10.6 to 5.6) in participants with blood flows < 600 mL/min (n = 18). Creation of AVF for haemodialysis resulted in a significant increase of LV myocardial mass within weeks after surgery, which was proportional to the fistula flow. [ABSTRACT FROM AUTHOR]

The article described a series of successful autogenous arteriovenous fistula (AVF) creations for hemodialysis. It mentions Left ventricular hypertrophy (LVH) is primarily an adaptive remodeling process as a response to increased cardiac workload aiming to minimize ventricular wall stress and is almost universal in new dialysis patients; and also mention the hemodynamic effects after AVF creation include decreased peripheral resistance and thus increased cardiac output.

• First CFD-based flow analysis of proximal vasculature to arteriovenous fistula (AVF) • First use of ferumoxytol-enhanced magnetic resonance angiography (FeMRA) with CFD • FeMRA-CFD workflow generates accurate patient-specific haemodynamic profiles • 2-3-fold wall shear stress (WSS) increase in proximal arteries following AVF creation • WSS in feeding artery juxta-anastomosis increased by a factor of 10 post-AVF Despite arteriovenous fistulae (AVF) being the preferred vascular access for haemodialysis, high primary failure rates (30-70%) and low one-year patency rates (40-70%) hamper their use. Furthermore, AVF creation has been associated with haemodynamic changes causing maladaptive cardiac remodelling leading to cardiovascular (CV) complications. In this study, we present a new workflow for characterising the haemodynamic profile prior to and following surgical creation of a successful left radiocephalic AVF in a 20-year-old end-stage kidney disease patient. The reconstructed vasculature was generated using multiple ferumoxytol-enhanced magnetic resonance angiography (FeMRA) datasets. Computational fluid dynamics (CFD) simulations utilising a scale-resolving turbulence model were completed to investigate the changes in the proximal haemodynamics following AVF creation, in addition to the post-AVF juxta-anastomosis flow patterns, which is impractical to obtain in-vivo. Following AVF creation, a significant 2-3-fold increase in blood flow rate was induced downstream of the left subclavian artery. This was validated through comparison with post-AVF patient-specific phase-contrast data. Proximal to the anastomosis, the increased flow rate yielded an increase in time-averaged wall shear stress (WSS), which is a key marker of adaptive vascular remodelling. In the juxta-anastomosis region, the success of the AVF was discussed with respect to the National Kidney Foundation's vascular access guidelines, where the patient-specific AVF met the flow rate and geometry criterion. The AVF venous diameter exceeded 6mm and the venous flow rate surpassed 600mL/min. This workflow may potentially be significant clinically when applied to multi-patient cohorts, with population-wide patient-specific conclusions being ascertained for the haemodynamic assessment of AVFs and improved surgical planning. [ABSTRACT FROM AUTHOR]