Real-world study of finerenone in patients with heart failure with preserved ejection fraction in Spain

Abstract

Purpose

To evaluate the effects of finerenone in patients with Heart failure with preserved ejection fraction (HFpEF), diabetes, chronic kidney disease, and albuminuria in Spain.

Methods

This observational, retrospective multicenter study included adults with HFpEF, type 2 diabetes, chronic kidney disease, and albuminuria who started finerenone between June 1, 2024, and January 1, 2025. The patients were monitored over a six-month period. Hyperkalemia was defined as a serum potassium level > 5.5 mEq/L, and renal function deterioration as a >  25% decrease in baseline estimated glomerular filtration rate.

Results

The study included 96 participants with a median age [IQR] of 78.50 [74.00, 83.00] years; 64.4% were male. Hypertension was present in 88.5% of subjects, type 2 diabetes in 94.8%, and ischemic heart disease in 32.3%. Regarding treatments, 93.8% of patients were prescribed SGLT2 inhibitors, 59.4% renin-angiotensin system inhibitors, and 64.6% beta blockers. During follow-up, significant improvements in NYHA functional class and albuminuria were observed, together with a trend toward lower natriuretic peptide levels. There was no significant change in systolic blood pressure or glomerular filtration rate. At study end, 5.2% of patients died, 8.3% had a hospitalization related to HF, 13.5% discontinued finerenone, 5.2% experienced symptomatic hypotension, 10.4% developed hyperkalemia, and 16.7% showed a decline in renal function (>50%: 4.2%).

Conclusions

In Spanish clinical practice, finerenone appears safe and is associated with improvements in functional class and albuminuria in patients with HFpEF, type 2 diabetes, CKD, and albuminuria.

Introduction

Heart failure with preserved ejection fraction (HFpEF) represents a considerable clinical challenge given its high prevalence and association with poor patient outcomes. HFpEF constitutes approximately 40–60% of all HF cases. Current epidemiological evidence demonstrates a worldwide increase in both incidence and prevalence of HFpEF, primarily driven by an aging population and the rising prevalence of comorbid conditions such as hypertension, obesity, and diabetes. Affected individuals are generally older, and often present with a substantial burden of cardiometabolic and non-cardiac comorbidities. Patients with HFpEF experience poor clinical outcomes. Thus, recent analyses report annual hospitalization rates of about 1.3–1.5 per patient-year and annual mortality rates between 10% and 20% [1–3].

Traditionally, treatment for HFpEF has focused on relieving symptoms and congestion with diuretics and managing associated conditions [4]. However, recent randomized clinical trials have broadened the range of evidence-based therapies available. Sodium-glucose cotransporter-2 inhibitors (SGLT2i), such as empagliflozin and dapagliflozin, have been shown to notably reduce hospitalizations due to HF and enhance patients’ quality of life [5, 6]. As a result, these medications are now recommended as core treatments in the latest HFpEF guidelines [7].

Activation of the renin-angiotensin-aldosterone system plays a central role in the progression of cardiac and vascular dysfunction associated with HFpEF. This mechanism promotes inflammation, fibrosis, and oxidative stress. Finerenone, a selective nonsteroidal mineralocorticoid receptor antagonist, has demonstrated clinical efficacy in this patient population [8]. The FINEARTS-HF study indicated that the addition of finerenone to standard therapy significantly reduced the risk of cardiovascular mortality and HF decompensation events relative to placebo in patients with HFpEF [9]. Additionally, finerenone has been shown to reduce the risk of cardiovascular and renal outcomes in patients with chronic kidney disease and albuminuria who have type 2 diabetes [10], as well as in the cardiovascular-kidney-metabolic syndrome [11]. Although on 26 March 2026 the European Medicines Agency approved the use of finerenone among patients with HF EF ≥ 40% [12], in Spain, finerenone is currently approved and reimbursed for use in patients with type 2 diabetes, chronic kidney disease, and albuminuria. At the moment of manuscript publication, finerenone cannot be prescribed in Spain according to HF EF ≥40% indication, as reimbursement conditions are still under discussion.

Real-world data plays a critical role in HF research by supplementing findings from randomized controlled trials and providing insight into the complexity, variability, and comorbidity profiles of patients observed in routine clinical settings [13]. The aim of this study was to evaluate the effects of finerenone in patients with HFpEF, diabetes, chronic kidney disease, and albuminuria treated in the cardiology, internal medicine, and nephrology departments across three hospitals in Spain.

Methods

This was an observational, retrospective multicenter study that included adults with type 2 diabetes, chronic kidney disease, and albuminuria who started finerenone between June 1, 2024, and January 1, 2025. Within this cohort, patients with an established diagnosis of HFpEF defined according to European guidelines (signs and symptoms of HF, elevated natriuretic peptides and specific echocardiographic alterations) [4] were selected. The patients were monitored over a six-month period. Patients were included from the cardiology, internal medicine and nephrology departments of Consorcio Hospital General Universitario de Valencia, and from the internal medicine departments of hospital de Leon and Hospital Universitario Central de Asturias. The study was carried out in accordance with the ethical principles of the Declaration of Helsinki and the regulations in force. The study was approved by the Research Ethics Committee for Medicinal Products of Fundación de Investigación del Hospital General Universitario de Valencia (Valencia, Spain). The committee approved the exemption of informed consent, as it was an observational and retrospective study, without any intervention on the patient.

The primary objective of the study was to determine the incidence of hyperkalemia during the observation period, defined as the proportion of patients who developed hyperkalemia, as well as to evaluate changes in renal function based on estimated glomerular filtration rate (eGFR). Hyperkalemia was defined as a serum potassium concentration greater than 5.5 mEq/L. Renal function deterioration was characterized by a > 25% decrease in eGFR from baseline, as measured by the CKD-EPI 2021 equation.

In addition, assessments were conducted on changes in New York Heart Association (NYHA) functional classification, blood pressure, NT-proBNP levels, albuminuria, electrolytes, as well as rates of HF readmission and mortality throughout the follow-up period. The proportion of patients who experienced side effects and the rate of withdrawal from finerenone treatment were also evaluated.

Study variables were extracted from medical records and entered into standardized case report forms by the investigators. Baseline data collection encompassed biodemographic variables (age, sex, hospital of origin, blood pressure), comorbidities (type 2 diabetes, hypertension, atrial fibrillation, obesity, ischemic heart disease), and treatments for HF, including SGLT2i, beta blockers, angiotensin-converting enzyme inhibitors (ACEi), angiotensin II receptor blockers (ARB), and diuretics. Additionally, therapies for diabetes (metformin, insulin, glucagon-like peptide-1 receptor agonists [GLP1-RA]) and other medications (statins, potassium binders, oral potassium) were documented. Biochemical parameters such as N-terminal pro-B-type natriuretic peptide (NT-proBNP), eGFR, urine albumin-to-creatinine ratio (UACR), sodium, and potassium levels were also recorded.

NYHA functional class, blood pressure, and biochemical markers (NT-proBNP, eGFR, UACR, sodium, and potassium) were measured at 3 and 6 months after starting finerenone. The dosage of finerenone (10 or 20 mg daily) during the follow-up period and the proportion of patients who discontinued treatment were evaluated. Additionally, the occurrence of adverse effects was assessed, with particular attention to symptomatic hypotension, hyperkalemia, and renal function deterioration. HF hospitalizations at 1, 3, and 6 months, together with cardiovascular and all-cause mortality during follow-up, were recorded.

Statistical analysis

A descriptive analysis of the cohort was conducted. Categorical variables were reported as absolute and relative frequencies (percentages), while continuous variables were expressed as mean ± standard deviation if normally distributed or as median and interquartile range (IQR) otherwise. The chi-squared test was used to compare proportions. The Shapiro-Wilk test was employed to assess the normality of continuous variables. To compare means over two periods (0–3 months or 0–6 months), the paired t-test was used for normally distributed data, or the Wilcoxon matched-pairs signed-rank test for non-normal distributions. In order to control for type I error due to multiple comparisons within each variable, p-values were adjusted using the Bonferroni correction, considering three independent comparisons per variable. Effect size (r) was reported for each comparison. All tests were two-tailed, with significance defined as p < 0.05. Analyses were performed using R or SPSS statistical software.

Results

A total of 96 patients were included. At baseline, the study population had a median age of 78.50 years, with women representing 39.6% of participants. Mean systolic blood pressure was 134.39 ± 21.56 mmHg. Comorbidities were highly prevalent, including type 2 diabetes (94.8%), hypertension (88.5%), atrial fibrillation (61.5%), obesity (45.8%), and ischemic heart disease (32.3%). Regarding treatment, the majority received SGLT2i (93.8%), as well as diuretics (83.3%), predominantly furosemide (71.9%). Beta blockers and renin angiotensin system inhibitors were used in 64.6% and 59.4% of patients, respectively. Biochemical assessment revealed elevated NT-proBNP levels (median 2233.0 pg/mL), impaired renal function (median eGFR 40.64 mL/min/1.73 m²), and increased albuminuria (median UACR 183.85 mg/g), while serum sodium and potassium concentrations remained within normal ranges (Table 1).

Table 1.

Baseline characteristics of the cohort (n = 96)

Biodemographic data
Age, years2	78.50 [74.00, 83.00]
Sex (women), n (%)	38 (39.6)
Hospital of origin, n (%)
Asturias	38 (39.6)
Leon	10 (10.4)
Valencia	48 (50.0)
Systolic blood pressure, mmHg1	134.39 (21.56)
Diastolic blood pressure, mmHg2	71.00 [65.00, 78.00]
Comorbidities
Type 2 diabetes, n (%)	91 (94.8)
Hypertension, n (%)	85 (88.5)
Atrial fibrillation, n (%)	59 (61.5)
Obesity, n (%)	44 (45.8)
Ischemic heart disease, n (%)	31 (32.3)
Treatments
Heart failure
SGLT2i, n (%)	90 (93.8)
Diuretics, n (%)	80 (83.3)
Furosemide	69 (71.9)
Hydrochlorothiazide	36 (37.5)
Beta blockers, n (%)	62 (64.6)
ACEi/ARB, n (%)	57 (59.4)
Diabetes
SGLT2i, n (%)	90 (93.8)
Metformin, n (%)	41 (42.7)
Insulin, n (%)	37 (38.5)
GLP1-RA, n (%)	22 (22.9)
Others
Statins, n (%)	76 (79.2)
Potassium binders, n (%)	5 (5.2)
Oral potassium, n (%)	4 (4.2)
Biochemical parameters
NT-proBNP, pg/mL2	2233.00 [900.75, 4025.75]
eGFR, mL/min/1.73 m2 2	40.64 [31.83, 54.25]
UACR, mg/g2	183.85 [66.25, 481.25]
Sodium, mEq/L2	141.00 [139.00, 143.00]
Potassium, mEq/L2	4.30 [4.00, 4.65]

¹Mean (SD); ²Median [IQR]

ACEi angiotensin-converting enzyme inhibitors, ARB angiotensin II receptor blockers, DPP4i dipeptidyl peptidase-4 inhibitors, eGFR estimated glomerular filtration rate (CKD-EPI 2021), GLP-1 RA glucagon like peptide-1 receptor agonists, IQR interquartile range, NT-proBNP N-terminal pro-B-type natriuretic peptides, NYHA New York Heart Association, SD standard deviation, SGLT2 i sodium-glucose cotransporter-2 inhibitors, UACR Urine Albumin-to-Creatinine Ratio

Regarding the distribution of finerenone dosing over time (Fig. 1), at 1 month, nearly all patients were receiving finerenone 10 mg (98.2%), with only 1.8% treated with the 20 mg dose. By 3 months, the proportion of patients on 20 mg increased to 8.2%, while 91.8% remained on 10 mg. At 6 months, further dose escalation was observed, with 18.9% of patients receiving finerenone 20 mg and 81.1% continuing on 10 mg.

Fig. 1.

Proportion of patients on finerenone 10 or 20 mg during the study

The evolution of NYHA functional class over time was reported in Fig. 2. At baseline, most patients were classified as NYHA class III (52.1%), followed by class II (39.6%). At 3 months, a shift toward lower symptom burden was observed, with class II becoming predominant (54.8%), while class III decreased to 35.5% (P = 0.532). By 6 months, further improvement was evident, with 80.0% of patients in class II, 16.7% in class III, and no patients in class IV (P = 0.008). Despite higher baseline NYHA class was associated with worse clinical outcomes, among patients who completed follow-up evaluations, improvement in NYHA class was observed over time, regardless of baseline NYHA functional class.

Fig. 2.

Changes in functional class (NYHA) over the follow-up period. P_{0−3 months} =0.532; P_{0−6 months} =0.008, the chi-squared test was used to compare proportions. NYHA: New York Heart Association

Over the 6-month follow-up, no significant changes were observed in systolic blood pressure. NT-proBNP levels showed a progressive numerical decline from baseline to 6 months, although these changes did not reach statistical significance. Renal function, assessed by eGFR, demonstrated a modest but significant decline from baseline to 3 months (r = 0.31, P = 0.005), with no significant difference between baseline and 6 months. Albuminuria, measured by UACR, decreased markedly at both 3 and 6 months compared with baseline, with strong and significant correlations for both time intervals (0–3 months: r = 0.77, P < 0.001; 0–6 months: r = 0.63, P < 0.001). Serum sodium levels showed a small but statistically significant reduction at 3 months (r = 0.30, P = 0.008), returning to baseline values at 6 months. In contrast, serum potassium levels increased significantly at both 3 and 6 months (0–3 months: r = 0.49, P < 0.001; 0–6 months: r = 0.41, P = 0.001), although median values remained within clinically acceptable ranges. These trends persisted after Bonferroni correction (Table 2).

Table 2.

Changes in biochemical parameters over the follow-up period

	Baseline	3 months	6 months	0–3 months		0–6 months
				r	P	r	P
Systolic blood pressure, mmHg1	134.39 (21.56)	131.73 (21.76)	132.83 (20.67)	0.11	0.432	0.09	0.570
NT-proBNP, pg/mL2	2233.00 [900.75, 4025.75]	1933.00 [843.00, 3484.00]	1469.00 [599.00, 2287.00]	0.20	0.169	0.25	0.077
eGFR, mL/min/1.73 m2 2	40.64 [31.83, 54.25]	37.00 [28.47, 58.95]	37.70 [26.56, 58.25]	0.31	0.005	0.18	0.152
UACR, mg/g2	183.85 [66.25, 481.25]	67.55 [25.70, 245.32]	96.40 [38.40, 229.25]	0.77	< 0.001	0.63	< 0.001
Sodium, mEq/L2	141.00 [139.00, 143.00]	140.50 [139.00, 142.00]	141.00 [140.00, 142.50]	0.30	0.008	0.02	0.900
Potassium, mEq/L2	4.30 [4.00, 4.65]	4.70 [4.40, 5.00]	4.60 [4.30, 5.05]	0.49	< 0.001	0.41	0.001

Means over two periods (0–3 months or 0–6 months) were compared using the paired t-test and the Wilcoxon matched-pairs signed-rank test was used to compare medians. Effect size (r) was reported for each comparison

¹Mean (SD); ²Median [IQR]

eGFR estimated glomerular filtration rate (CKD-EPI 2021), IQR interquartile range, NT-proBNP N-terminal pro-B-type natriuretic peptide, SD standard deviation, UACR Urine Albumin-to-Creatinine Ratio

Adverse events occurred in 21.9% of patients during follow-up, mainly eGFR decline (>25%: 16.7%; >50%: 4.2%), hyperkalemia (10.4%), and symptomatic hypotension (5.2%). Finerenone was discontinued in 13.5% of cases. At the conclusion of the study, total mortality was observed at 5.2%, with 2.1% attributable to cardiovascular causes and 3.1% resulting from non-cardiovascular causes. Only 8 patients (8.3%) were hospitalized for HF during the study period, 2 at one month, 5 at three months, and 1 at six months (Table 3). Patients who were readmitted for HF during follow-up tended to be older, had higher initial NT-proBNP levels, and more often belonged to advanced functional classes (NYHA III–IV) compared to those who did not experience events. By contrast, patients who remained event-free consistently showed lower baseline NT-proBNP values and a greater proportion were in NYHA I–II functional classes. There were only slight differences in initial renal function (eGFR and serum creatinine), with no clear patterns distinguishing these groups.

Table 3.

Events and adverse events with finerenone over the follow-up period

Adverse events with finerenone
Any, n (%)	21 (21.9)
Decline in eGFR, n (%)	16 (16.7)
Hyperkalemia, n (%)	10 (10.4)
Symptomatic hypotension, n (%)	5 (5.2)
Discontinuation, n (%)	13 (13.5)
Events
Death, n (%)	5 (5.2)
Cardiovascular	2 (2.1)
No cardiovascular	3 (3.1)
HF hospitalization, n (%)
1 month	2 (2.1)
3 months	5 (5.2)
6 months	1 (1.0)

eGFR estimated glomerular filtration rate, HF heart failure

Discussion

In this cohort of elderly patients with significant cardiometabolic comorbidities, finerenone was mostly prescribed at 10 mg with gradual dose increases. Over 6 months, it was linked to clinical and biological improvements, including better functional status and reduced albuminuria. Renal function declined slightly initially but stabilized, while serum potassium rose yet stayed within acceptable limits. Adverse events, treatment discontinuation, mortality, and HF hospitalizations were all relatively rare.

In the RICA registry, which included patients consecutively admitted for HF in internal medicine departments across Spain, 46% of those diagnosed with HFpEF, comprising 62% of the total HF population, had diabetes mellitus [14]. Another registry based on the BIG-PAC database in Spain, including adults with at least one inpatient or outpatient HF diagnosis, reported that approximately 40% had HFpEF and nearly 30% of them had diabetes [15]. Although in Spain finerenone is currently approved for individuals with type 2 diabetes, chronic kidney disease, and albuminuria, but not specifically for patients with HFpEF, it is evident that finerenone may be applicable to a broad spectrum of patients with HFpEF. Whereas some studies have analyzed the role of finerenone in real-world patients with diabetic nephropathy [16–18], and the FINEARTS-HF trial has established its efficacy in a broad HFpEF population [9], real-world evidence specifically in patients with HFpEF who meet the criteria for finerenone use in routine clinical practice (i.e., those with type 2 diabetes and CKD with albuminuria) is lacking. Although the indication of finerenone has been recently extended to the whole population with HFpEF [12] and the limited number of patients included, our study provided important insights into the effects and safety of finerenone in this relevant subgroup of patients with HFpEF.

A single-center, retrospective study in the United States examined 250 patients with HFpEF and type 2 diabetes, separating groups based on their use of SGLT2i. The average age was about 70, and almost half of the participants had both chronic kidney disease and coronary artery disease. Nearly all had hypertension. In terms of medication, approximately two-thirds were on renin angiotensin system inhibitors, 60% used beta blockers, and 15–20% took mineralocorticoid receptor antagonists (spironolactone) [19]. Another study analyzed 31 individuals with diabetic kidney disease. Among those with HFpEF (71%), the mean age was 70, with men comprising 73%, obesity present in 41%, almost all hypertension, and coronary artery disease in half. Treatment regimens included SGLT2i for 91%, beta blockers for 91%, ACEi/ARB for 100%, diuretics for 77%, and statins for 86% [20]. Our cohort comprised about 100 patients with a median age of 78.5 years; 89% had hypertension, one third had coronary artery disease, and 46% were obese. Among HF treatments, 94% received SGLT2i, 83% diuretics, two thirds beta blockers, and 60% ACEi/ARB. The clinical characteristics of our cohort were consistent with those reported in previous studies, including patients with HFpEF and diabetes, supporting the applicability of our findings across broader contexts. These studies also highlight that HF treatments, especially for patients with HFpEF and diabetes, have been improving in the last years. Consequently, most patients currently receive SGLT2i, renin–angiotensin system blockers, beta-blockers, and diuretics as part of guideline-directed therapy [19, 20]. However, although there has been progress, mineralocorticoid receptor antagonists continue to be underused. Importantly, the FINEARTS-HF study found that adding finerenone to standard therapy offered further benefits, which were unaffected by diabetes status [9, 21, 22]. Furthermore, the impact of finerenone on lowering the combined incidence of cardiovascular death and overall HF events was consistent across baseline eGFR and UACR levels [9, 23]. In this context, determining the effects of finerenone in our study population is of significant interest.

In FINEARTS-HF, patients with baseline eGFR of 25–60 mL/min/1.73 m² were assigned to low-dose finerenone (10 mg daily, up to 20 mg) or placebo, while those with eGFR > 60 mL/min/1.73 m² received high-dose finerenone (20 mg daily, up to 40 mg) or placebo. The mean achieved dose was 32.3 mg in the high eGFR group and 15.6 mg in the low eGFR group [24]. Despite median eGFR and potassium levels were 40.6 mL/min/1.73 m² and 4.3 mEq/L at baseline, less than 20% of patients achieved the target dose of finerenone over time, reflecting clinical inertia rather than the impossibility to up titrate finerenone dosage according to the characteristics of the patients. Consistent with our study, real-world dosing is more conservative than in clinical trials [20]. In this context, more efforts are required to emphasize the importance of attaining the target dose to obtain the maximum benefit of finerenone.

While there have been concerns about potential side effects, our study involving chronic kidney disease patients found that adverse events such as eGFR decline, hyperkalemia, and symptomatic hypotension were uncommon. The decrease in eGFR seen after 3 months is actually linked to a predictable and harmless hemodynamic response, which can indicate renal protection, followed by stabilization. Other researchers have reported similar findings [20]. In the FINEARTS-HF trial, increases in creatinine and potassium levels occurred more frequently with finerenone compared to placebo; however, only 3% of participants had potassium levels > 6.0 mmol/L, with no reports of fatal hyperkalemia and just 0.5% requiring hospitalization [9]. In our study, although serum potassium levels exhibited a significant upward trend over time, the median values consistently stayed within clinically acceptable parameters. Additionally, in the FINEARTS-HF trial, at six months, mean systolic blood pressure was 3.4 mmHg lower in the finerenone group than in the placebo group [9]. By contrast, our study did not identify any notable alterations in systolic blood pressure. On the other hand, in the FINEARTS-HF trial, finerenone was associated with a significantly slower decline in chronic eGFR slope among patients with HFpEF and macroalbuminuria, compared to placebo [25]. Importantly, our study showed that albuminuria markedly decreased over time. Albuminuria is a strong, independent predictor of HF risk, hospitalization, and mortality [26]. These findings suggest that finerenone may provide additional benefits in patients with HFpEF and chronic kidney disease.

Our data indicated that finerenone treatment significantly enhanced patients’ functional status over time, regardless baseline status. In addition, a trend towards a reduction in natriuretic peptide levels was also observed, that did not reach statistical significance likely due to insufficient statistical power and the high proportion of patients with atrial fibrillation. In the FINEARTS-HF trial, despite both the finerenone and placebo groups experienced similar improvements in NYHA functional class up to 12 months, finerenone consistently lowered the primary endpoint regardless of the initial NYHA functional class, providing greater absolute benefits for those in NYHA class III/IV compared to class II [27].

By study end, total mortality was 5.2%, with cardiovascular deaths accounting for 2.1% and only 8.3% had HF-related hospitalizations, indicating low clinical worsening rates. In FINEARTS-HF, 8.1% of finerenone-treated patients died from cardiovascular causes and 28% had worsening HF over 32 months. Pooled analysis of FIDELIO-DKD, FIGARO-DKD, and FINEARTS-HF (FINE-HEART, 18,991 participants, mean age 67, 35% women) found that after 2.9 years, finerenone significantly reduced all-cause mortality (11% vs. 12%, HR: 0.91; 95% CI 0.84–0.99), and HF hospitalizations (7.4% vs. 8.8%, HR: 0.83; 95% CI 0.75–0.92) and numerically cardiovascular mortality (4.4% vs. 5.0%; HR 0.89; 95% CI 0.78–1.01) compared to placebo [11]. Although there are relevant differences between the study populations, these numbers suggest that in clinical practice, even rates may be lower than in clinical trials. In addition, our data showed that patients with higher NT-proBNP and worse functional status had poorer outcomes, highlighting the need for early intensified treatment in high-risk subgroups.

There are some limitations associated with this study. It is a retrospective investigation lacking a control group, which means that some data may be missing and the relative effectiveness of finerenone cannot be established. Nevertheless, this approach best mirrors real-world clinical practice, and factors like patient numbers and the multicenter setup may help minimize bias. In addition, the relatively small sample size may reduce statistical power and limit the generalizability of the findings. In Spain, finerenone is currently approved only for individuals with chronic kidney disease, albuminuria, and type 2 diabetes; therefore, our findings are applicable solely to patients with HFpEF within this specific population. As a result, larger prospective real-world studies are needed. In this context, the ongoing FINE registry in Spain, which matches HF patients regardless of EF with controls not receiving finerenone, is expected to definitely clarify the clinical role of finerenone in this population [28].

In summary, finerenone appears to be safe in Spanish patients with HFpEF, type 2 diabetes, chronic kidney disease, and albuminuria, showing low rates of side effects and events. In addition, its use is associated with improvements in functional class and albuminuria levels, as well as a trend toward reduced natriuretic peptide levels.

Abbreviations

ACEi

Angiotensin-converting enzyme inhibitors

ARB

Angiotensin II receptor blockers

CHMP

Committee for Medicinal Products for Human Use

DPP4i

Dipeptidyl peptidase-4 inhibitors

eGFR

Estimated glomerular filtration rate

GLP-1 RA

Glucagon like peptide-1 receptor agonists

HF

Heart failure

HFpEF

Heart failure with preserved ejection fraction

IQR

Interquartile range

NT-proBNP

N-terminal pro-B-type natriuretic peptide

NYHA

New York Heart Association

SD

Standard deviation

SGLT2 i

Sodium-glucose cotransporter-2 inhibitors

UACR

Urine Albumin-to-Creatinine Ratio

Authors' contributions

The study conception and design were written by Ana Lamilla Álvarez, Miriam Ripoll Martínez, Sofía Russo Botero, David García Escrivá, Lorenzo Fácila Rubio, Sergio Bea Granell and José Pérez Silvestre. Material preparation, data collection and analysis were performed by Ana Lamilla Álvarez, Miriam Ripoll Martínez, Sofía Russo Botero, Alberto Muela Molinero, Azucena López Álvarez, Carolina García Lamigueiro, Elisa Esther Rodríguez Ávila and José María Fernández Rodríguez. The first draft of the manuscript was written by Content ed Net and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Funding

The authors declare that no funds, grants, or other support were received for developing the study.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

The study was carried out in accordance with the ethical principles of the Declaration of Helsinki and the regulations in force. The study was approved by the Research Ethics Committee for Medicinal Products of Fundación de Investigación del Hospital General Universitario de Valencia (Valencia, Spain). The committee approved the exemption of informed consent, as it was an observational and retrospective study, without any intervention on the patient.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.