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Rivaroxaban should not be recommended for cardiovascular prevention in patients with advanced CKD

Low-dose rivaroxaban did not improve cardiovascular outcomes in patients with advanced chronic kidney disease (CKD) compared with placebo, but was associated with an increased risk of major bleeding events.

Prof. Sunil Badve (University of New South Wales, Australia) presented results from TRACK (NCT03969953), a phase 3, investigator-initiated, multicentre, randomised, double-blind, placebo-controlled, multinational trial that evaluated low-dose rivaroxaban (2.5 mg twice daily) versus placebo in patients with advanced CKD [1]. Patients were eligible if they had stage 4 or 5, including those receiving dialysis, and were at high cardiovascular risk. Patients with bleeding disorders or at high risk of bleeding were excluded. The primary endpoint was a composite of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, or a non-fatal peripheral artery disease event.

A total of 1,458 patients were randomised. However, the independent safety data monitoring committee recommended early termination of the trial because of “concerns about increased bleeding and a low probability of demonstrating efficacy,” said Prof. Badve. The primary outcome occurred in 20.7% of patients receiving placebo (11.8 events per 100 person-years) and in 22.6% of patients receiving rivaroxaban (13.0 events per 100 person-years; HR 1.09; 95% CI 0.87–1.36; P=0.46). Analysis of the individual components of the primary endpoint showed no benefit of rivaroxaban over placebo for any of the 4 outcomes. However, rivaroxaban significantly increased the incidence of major bleeding compared with placebo (5.1 vs 3.4 events per 100 patient-years; HR 1.51; 95% CI 1.02–2.22; P=0.04). The gastrointestinal tract was the most common site of major bleeding, and 6.3% of patients receiving low-dose rivaroxaban required hospitalisation due to bleeding compared with 4.7% of those receiving  placebo.

“In patients with advanced CKD at high cardiovascular risk, low-dose rivaroxaban did not reduce the risk of the composite cardiovascular outcome,” concluded Prof. Badve. “Major bleeding events were significantly more frequent with low-dose rivaroxaban than with placebo.”

  1. Badve S, et al. Low-dose rivaroxaban in patients with advanced kidney disease and high cardiovascular risk: an international randomised, placebo-controlled trial. ERA 2026, 3–6  June. Glasgow, Scotland.

 Copyright ©2026 Medicom Education B.V.

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Nurandociguat shows preliminary efficacy in patients with CKD

Nurandociguat, a soluble guanylate cyclase (sGC) activator, significantly improved urinary albumin-to-creatinine ratio (UACR) after 16 weeks of treatment compared with placebo, while increasing the incidence of hypotension and syncope.

Prof. Christoph Wanner (University Hospital of Würzburg, Germany) presented data from ALPINE 1 (NCT06522997), a phase 2b, prospective, randomised, controlled trial evaluating multiple dose levels of nurandociguat compared to placebo in patients with chronic kidney disease (CKD) [1]. Participants were eligible if they had an estimated glomerular filtration rate (eGFR) between 20 and 75 mL/min/1.73 m2, a UACR between 200 and 3500 mg/g, and were receiving the maximally tolerated labelled dose of standard-of-care therapy, including angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) plus sodium-glucose cotransporter 2 (SGLT2) inhibitors, finerenone, or glucagon-like peptide-1 receptor (GLP-1R) agonists. Patients with a systolic blood pressure of <100 mmHg or clinically relevant hypotension were excluded. The primary endpoint was the mean change in UACR at week 16. Overall, 751 patients were included.

A statistically significant reduction in UACR was observed with every nurandociguat dose compared with placebo (P<0.05). However, the minimum dose required to achieve a 30% improvement in UACR compared with placebo could not be determined. Treatment-emergent adverse events of special interest occurred more commonly with nurandociguat, including syncope, symptomatic hypotension, and worsening kidney function, with event rates increasing at higher dose levels.

“The study met its primary efficacy endpoint, demonstrating a statistically significant dose-response relationship,” concluded Prof. Wanner. “A statistically significant reduction in UACR was observed through week 16 across all dose groups. Nurandociguat was generally well tolerated, with a dose-dependent increase in treatment-related adverse events.”

  1. Wanner C, et al. Effect of nurandociguat on albuminuria in patients with CKD: A phase 2, randomized dose-finding clinical trial. ERA 2026, 3–6 June. Glasgow, Scotland.

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Finerenone slows eGFR decline in patients with CKD due to glomerular disease

Compared with placebo, finerenone slowed the decline in estimated glomerular filtration rate (eGFR) in patients with non-diabetic chronic kidney disease (CKD) due to glomerular disease.

Prof. Brendon Neuen (The George Institute for Global Health, Australia) presented a prespecified subgroup analysis of the phase 3 FIND-CKD trial (NCT05047263) in patients with CKD due to glomerular disease [1]. Of the overall FIND-CKD population, 57.0% had glomerular disease as the underlying cause of CKD, including 26.3% with immunoglobulin A (IgA) nephropathy, 13.6% with focal segmental glomerulosclerosis, 5.7% with membranous nephropathy, 1.6% with membranoproliferative glomerulonephritis, and 9.8% with other causes.

The eGFR curves in patients with glomerular disease showed a trend similar to that observed in the overall FIND-CKD population. In the placebo group, eGFR declined linearly, reaching an annualised decline of 4.2 mL/min/1.73 m2/year by month 36. In the finerenone group, eGFR showed an initial steep decline before stabilising, resulting in an annualised decline of 3.5 mL/min/1.73 m2/year by month 36, corresponding to a between-group difference of 0.7 mL/min/1.73 m2/year (95% CI 0.2–1.2). Furthermore, urinary albumin-to-creatinine ratio (UACR) decreased by 42% from baseline with finerenone, whereas it remained stable with placebo (0% change) at month 12, corresponding to a between-group difference of -42% (95% CI -48% to -35%). Regarding safety, finerenone demonstrated a profile in patients with glomerular diseases that was consistent with that observed in the overall FIND-CKD population.

“In this prespecified subgroup analysis from the FIND-CKD trial, finerenone compared with placebo slowed the annualised rate of eGFR decline and reduced albuminuria,” concluded Prof Neuen. “Finerenone was overall well-tolerated, with a safety profile consistent with that of the overall FIND-CKD population.”

  1. Neuen B, et al. Finerenone in patients with glomerulonephritis. ERA 2026, 3–6 June. Glasgow, Scotland.

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Finerenone is a treatment option in non-diabetic kidney disease

Compared with placebo, finerenone slowed the decline of the annualised estimated glomerular filtration rate (eGFR) while increasing rates of hyperkalaemia in patients with non-diabetic chronic kidney disease (CKD), according to results reported by Prof. David Cherney (University of Toronto, Canada) and Prof. Hiddo J.L. Heerspink (University of Groningen, the Netherlands) [1].

FIND-CKD (NCT05047263) is a phase 3, randomised, double-blind, placebo-controlled trial assessing the effect of finerenone in patients with non-diabetic CKD. Patients were eligible if they were at risk of disease progression despite optimised angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) therapy and were randomised 1:1 to receive either finerenone 10 mg once daily (eGFR ≥25 to <60 mL/min/1.73 m2), finerenone 20 mg once daily (eGFR ≥60 mL/min/1.73 m2), or placebo for a total treatment duration of 36 months. The primary endpoint was the mean annual rate of change in eGFR assessed as the total eGFR slope from baseline to month 32. Overall, 793 patients were included in the finerenone group and 791 in the placebo group.

Compared with placebo, finerenone significantly slowed eGFR decline, as demonstrated by the eGFR slope analysis. Subgroup analyses showed that the effect of finerenone on eGFR slope was consistent across subgroups defined by primary CKD cause (hypertension/ischemic nephropathy, chronic glomerulonephritis, and other), baseline eGFR, baseline urinary albumin-to-creatinine ratio (UACR; ≤1000 and >1000 mg/g), and concomitant sodium-glucose cotransporter 2 (SGLT2) inhibitor use. Finerenone also significantly reduced the risk of the composite kidney-cardiovascular endpoint (sustained ≥57% decrease in eGFR for >4 weeks, kidney failure, hospitalisation for heart failure, or cardiovascular death) compared with placebo (HR 0.77; 95% CI 0.60–0.99; P=0.043). Adverse events leading to discontinuation were more common with finerenone, whereas those leading to death were more common with placebo (1.3% vs 0.8%). Hyperkalaemia, a known class effect, was reported in 17.0% of patients receiving finerenone and 13.3% of those receiving placebo.

“This international, phase 3 clinical trial met its primary endpoint,” concluded Prof. Heerspink. “Finerenone reduced the mean annual rate in eGFR from baseline to month 32 and reduced the risk of the composite kidney-cardiovascular endpoint compared with placebo. Although there was a higher incidence of hyperkalaemia, the clinical impact was minimal.”

  1. Heerspink HJL, et al. Finerenone in patients with chronic kidney disease. ERA 2026, 3–6  June. Glasgow, Scotland.

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