Efficacy and safety of finerenone in non-diabetic CKD patients: a single-center, real-world, retrospective study

Efficacy and safety of finerenone in non-diabetic CKD patients: a single-center, real-world, retrospective study | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Efficacy and safety of finerenone in non-diabetic CKD patients: a single-center, real-world, retrospective study Yu Li, Jiaxing Feng, Xiaodan Guo, Wusijie Zhang, Ting Yang, Tianjun Guan, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-5729879/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 01 Jul, 2025 Read the published version in BMC Nephrology → Version 1 posted 14 You are reading this latest preprint version Abstract Background Finerenone, a novel non-steroidal mineralocorticoid receptor antagonist, has shown promising efficacy and safety profiles in the management of chronic kidney disease (CKD) associated with type 2 diabetes mellitus (T2DM). However, the effectiveness and safety of finerenone on non-diabetic CKD patients require further investigation. Methods This retrospective, real-world study involved non-diabetic CKD patients from April 2023 to June 2024. Participants received finerenone alongside standard CKD treatment. Primary clinical results included changes in the urinary albumin-to-creatinine ratio (UACR), estimated glomerular filtration rate (eGFR), and serum potassium (sK + ) levels. The data were collected initially and during follow-ups at 1, 3, 6, and 12 months. Results In total, 37 non-diabetic CKD patients were included in the population; 21 individuals (56.8%) were male, and the mean age was 48.84 ± 14.69 years. During the follow-up, there was a notable decrease in UACR, with a median reduction of 664.95 mg/g (IQR, 196.60-1226.70, P = 0.002). The baseline average eGFR was 70.80 ± 27.97 mL/min/1.73m 2 , with no notable alterations observed during the follow-up ( P > 0.05). In terms of safety analysis, the sK + levels were within the 3.5–5.5 mmol/L range, with no significant difference from the baseline ( P > 0.05). No patients discontinued treatment or were hospitalized because of hyperkalemia. Conclusion Real-world practice indicates that finerenone is effective and safe for non-diabetic CKD patients, but further large-scale, prospective studies are needed to confirm these findings. Finerenone chronic kidney disease non-diabetic Figures Figure 1 Figure 2 Figure 3 Introduction Chronic kidney disease (CKD) is a substantial burden threatening global health [1]. Aldosterone is one of the multiple factors contributing to the pathophysiological development of CKD [2]. Considerable evidence supports that aldosterone and overactivation of the mineralocorticoid receptor provoke inflammation, fibrosis, and eventual kidney dysfunction [3]. Currently, mineralocorticoid receptor antagonists (MRAs) have become a novel treatment strategy to alleviate the progression of CKD, the mechanism of which includes a reduction in renal collagen deposition and fibrosis, downregulation of proinflammatory mediators and cytokines, and a decrease in oxidative stress [4–6]. Spironolactone, a first-generation steroidal MRA, and eplerenone, a second-generation one, have demonstrated promise in improving renal outcomes and reducing CKD progression [7,8]. However, owing to apprehensions regarding potential complications such as hyperkalemia, worsening renal function, gynecomastia, impotence in men, and menstrual disorders in women, the use of these agents in CKD management is limited [9]. More recently, third-generation MRA has been successfully developed, and the alterations in receptor affinity and tissue tropism enable them to more selectively enhance efficacy and reduce risks [10]. Finerenone, a new non-steroidal MRA, offers better receptor selectivity compared to spironolactone and eplerenone and has demonstrated a more significant decrease in proteinuria and organ damage [11,12]. In the past few years, numerous clinical trials have proven the effectiveness and safety of finerenone in managing diabetic CKD [13–19]. The successful finerenone trials indicate its potential to revolutionize therapeutic approaches for CKD. In non-diabetic CKD, MRAs like spironolactone and eplerenone have been shown to protect the heart and kidneys. Research has found that eplerenone can decrease proteinuria and blood pressure in these patients [20]. These findings highlight the possible benefits of MRAs for this patient group and emphasize the necessity for more information on the effectiveness of finerenone in non-diabetic CKD. Currently, the effectiveness and safety of finerenone in non-diabetic CKD have been explored in a limited number of retrospective studies [21,22]. However, the evidence for finerenone's use in non-diabetic CKD patients is still not conclusive. Therefore, we conducted a real-world retrospective study investigating the efficacy and safety of finerenone in individuals with non-diabetic CKD. Methods Study design and patient population This single-center, real-world study was conducted retrospectively at the Department of Nephrology, Zhongshan Hospital of Xiamen University from April 2023 to June 2024. Criteria for inclusion: (1) patients aged 18 to 85 years; (2) patients diagnosed with CKD with a baseline eGFR ≥ 25 mL/min/1.73m 2 ; (3) patients undergoing finerenone treatment for CKD. Criteria for exclusion: (1) patients with diabetic nephropathy, or Addison's disease; (2) patients lacking complete medical records; (3) patients with severe hepatic impairment (Child-Push grade C). This study was approved by the Ethics Committee of Zhongshan Hospital of Xiamen University, with the requirement for informed consent waived. Treatment strategy Patients received standard CKD treatment tailored to their specific disease type and comorbidities, including hypertension, hyperlipidemia, hyperuricemia, and diabetes mellitus. Individualized regimes were implemented. The initial dose of finerenone was determined based on the patient's eGFR. Individuals with an eGFR equal to or greater than 60 mL/min/1.73m 2 were recommended to start with a daily dose of 20mg. In contrast, a lower starting dose of 10 mg per day is suggested for those with an eGFR between 25 and 60 mL/min/1.73m². Patients with an eGFR of less than 25 mL/min/1.73m² were contraindicated for finerenone. Serum potassium (sK + ) levels must be closely monitored and dosage adjustments made within four weeks following the commencement of treatment. If sK + levels were 4.8 mmol/L or lower, increasing the dose to 20 mg daily might be considered. Should sK + levels fall within the range of 4.8 to 5.5 mmol/L, it was advisable to maintain the current dosage regimen. Conversely, if sK + levels were higher than 5.5 mmol/L, finerenone should be discontinued temporarily until sK + levels were at or below 5.0 mmol/L; following this, therapy may be restarted with a lower dose of 10 mg daily. Clinical data collection The demographic and laboratory characteristics of patients include age, gender, serum creatinine, eGFR, UACR, and sK + levels. Clinical data collection will occur at baseline, and then at 1, 3, 6, and 12 months following treatment. The CKD-EPI formula was used to assess eGFR [23]. Statistical analysis Categorical data were expressed as frequencies and percentages. Continuous data that followed a normal distribution were presented as the mean ± standard deviation, whereas those that did not were presented as the median and interquartile range. Repeated measure ANOVA and the generalized estimating equation were employed to analyze the data with repeated measurements. Statistical analyses employed SPSS version 26.0 (Chicago, IL, USA), with a significance level established at P < 0.05 (two-tailed). Results Patient characteristics The baseline characteristics of the patients are presented in Table 1 . A total of 37 patients were included in the analysis (21 males, mean age 48.84 ± 14.69 years). The most frequent etiologic diagnoses were IgA nephropathy (54.1%) and membranous nephropathy (24.3%). Other etiologies included Henoch–Schönlein purpura nephritis, minimal change nephropathy, hepatitis B virus–associated nephritis, mesangial proliferative glomerulonephritis, and obesity-related glomerulopathy. The baseline median UACR was 1091.90 mg/g (IQR, 494.50-1860.05), and the mean eGFR was 69.04 ± 28.32 mL/min/1.73m 2 . The baseline mean serum potassium level was 4.30 ± 0.46 mmol/L. Table 1 Demographic and baseline characteristics of the patients Characteristics All (N = 37) Age (years) 48.84 ± 14.69 Male sex 21 (56.8%) Kidney diseases (etiological diagnosis) IgA nephropathy 20 (54.1%) Membranous nephropathy 9 (24.3%) Henoch-Schönlein purpura nephritis 2 (5.4%) Minimal change nephropathy 1 (2.7%) Hepatitis B virus-associated nephritis 1 (2.7%) Mesangial proliferative glomerulonephritis 1 (2.7%) Obesity-related glomerulopathy 1 (2.7%) Baseline UACR (mg/g) 1091.90 (494.50-1860.05) ≤ 300 5 (13.5%) > 300 32 (86.5%) Baseline eGFR (mL/min/1.73m 2 ) 69.04 ± 28.32 25–45 8 (21.6%) 45–60 8 (21.6%) > 60 21 (56.8%) Baseline serum potassium (mmol/L) 4.30 ± 0.46 Therapeutic outcomes The UACR was decreased compared with baseline at 3 months ( P = 0.018), 6 months ( P = 0.020), and a significant reduction of 664.95 mg/g (IQR, 196.60-1226.70, P = 0.002) was further observed at 12 months, as shown in Fig. 1 . The eGFR was lower at 6 months (66.99 ± 28.75 mL/min/1.73m 2 ), but there was no significant difference at baseline, 1, 3, 6, or 12 months (all P > 0.05), as shown in Fig. 2 . Safety For safety analysis, the levels of sK + remained within the 3.5–5.5 mmol/L range, with no significant differences compared to baseline ( P > 0.05), as shown in Fig. 3 . No treatment discontinuation or hospitalization occurred due to hyperkalemia. Discussion This real-world, observational retrospective study indicated the potential for finerenone in the clinical treatment of non-diabetic CKD patients. Our findings revealed that patients undergoing finerenone therapy experienced a notable reduction in UACR and maintained a stable eGFR throughout the treatment, indicating the drug might be conducive to alleviating the deterioration of renal function. Another crucial aspect of this study was the stable sK + levels in the non-diabetic CKD population during treatment, supporting the low hyperkalemia risk with finerenone, and manifesting acceptable safety and tolerability profile. Currently, the clinical evidence related to the utilization of finerenone in this patient population is extremely limited, and this study provided initial yet valuable evidence of both the efficacy and safety of finerenone in the treatment of non-diabetic CKD patients. The reduction of UACR implies an enhancement in renal function and a deceleration in the progression of kidney disease. Studies have reported that a decreased UACR is correlated with superior clinical outcomes [24,25]. Prior investigations have revealed that finerenone treatment leads to a reduction in UACR, demonstrating the renal protective effect in diabetic CKD patients [26]. The notable decrease in UACR seen in our group indicates that finerenone may effectively enhance kidney function in non-diabetic CKD patients. Pitt et al. [10] conducted an earlier study that examined the effectiveness of finerenone in individuals with heart failure and reduced left ventricular ejection fraction, in conjunction with mild or moderate CKD. In their study, two-thirds of the participants were non-diabetic, and a reduction in UACR was noted one month following finerenone therapy. The findings revealed a UACR reduction trend that matches our research. However, Pitt's study did not conduct a diabetes-based subgroup analysis, thereby limiting the applicability of the findings to non-diabetic CKD patients. In our cohort, a reduction in UACR was noted within the first month of treatment initiation; nevertheless, this decrease was not statistically significant, which might be attributed to the limited sample size. On later follow-up, significant UACR reductions at 3 months were sustained over 12 months. In CKD, renal function deterioration is usually marked by a gradual decrease in eGFR [27]. Previous meta-analysis on CKD indicated that while finerenone could slow down the deterioration of kidney function, patients still experienced a decrease in eGFR [28]. The FIDELIO-DKD study found that eGFR decline in diabetic CKD patients treated with finerenone followed a biphasic pattern [14]. In the initial stage, the finerenone group had a faster reduction in eGFR than the placebo group, but after 4 months, the decline rate slowed, causing the eGFR levels of the two groups to cross over. In our study, the average eGFR value moderately declined at the 6-month follow-up but subsequently moderately ascended at the 12-month follow-up. Despite the absence of statistically significant differences at various follow-up time points, the change in eGFR demonstrates a distinct pattern in non-diabetic CKD patients. Finerenone, functioning as an MRA, is capable of influencing the retention of sodium and the excretion of potassium, which might result in hyperkalemia, particularly among CKD patients with compromised excretion function. Hyperkalemia is one of the specific adverse events linked to the utilization of MRA drugs [10]. Previous studies have indicated that finerenone therapy was correlated with an elevated risk of hyperkalemia. Nevertheless, through monitoring and adjusting the dosage of the medication, the risk of hyperkalemia can be effectively mitigated in diabetic CKD patients [14–16]. In our cohort, the sK + level remained relatively stable throughout the 12-month follow-up period, and no serious adverse events related to the treatment were noted, thereby confirming the favorable safety profile of finerenone in the non-diabetic CKD patient population. This study has certain important limitations. First, this research is a retrospective analysis from a single center, involving the inherent biases of study design. Second, the small sample size was also a limitation. Third, the current study design did not include a control group. Therefore, large-scale prospective randomized controlled trials are needed to confirm these findings among diverse populations and in different regions of the world. The FIND-CKD trial (NCT05047263) currently underway promises to further elucidate the prolonged effects of finerenone on renal function in the non-diabetic CKD patient population. In conclusion, finerenone demonstrates favorable efficacy and safety profiles in non-diabetic CKD patients within real-world clinical settings. This study offers significant insights and a promising perspective on the application of finerenone for non-diabetic CKD patients. Declarations Conflict of interest On behalf of all authors, the corresponding author states that there is no conflict of interest. Ethical approval Informed consent was waived due to the non-interventional design of the study and retrospective nature of data collection. Funding This study was funded by grants from the Xiamen Municipal Bureau of Science and Technology (Grant No. 3502Z20244ZD1061). Data Availability All data generated or analyzed in this study are included in this published article. Acknowledgements We are grateful for the subjects in our hospital. We also thank all colleagues who collected all medical information and clinical data. Author Contributions B.X., Y.L. and T.G. designed and conducted the study, acquired and analyzed data, and wrote the manuscript. J.F., X.G., W.Z, and T.Y. acquired and analyzed data. All authors read and approved the final manuscript. References Webster AC, Nagler EV, Morton RL, Masson P. Chronic Kidney Disease. Lancet. 2017;389(10075):1238-1252. Barrera-Chimal J, Girerd S, Jaisser F. Mineralocorticoid receptor antagonists and kidney diseases: pathophysiological basis. Kidney Int. 2019;96(2):302-319. Epstein M. Aldosterone and Mineralocorticoid Receptor Signaling as Determinants of Cardiovascular and Renal Injury: From Hans Selye to the Present. Am J Nephrol. 2021;52(3):209-216. Patel V, Joharapurkar A, Jain M. Role of mineralocorticoid receptor antagonists in kidney diseases. Drug Dev Res. 2021;82(3):341-363. Barrera-Chimal J, Lima-Posada I, Bakris GL, Jaisser F. Mineralocorticoid receptor antagonists in diabetic kidney disease - mechanistic and therapeutic effects. 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Tsuboi N, Kawamura T, Okonogi H, Ishii T, Hosoya T. The long-term antiproteinuric effect of eplerenone, a selective aldosterone blocker, in patients with non-diabetic chronic kidney disease. J Renin Angiotensin Aldosterone Syst. 2012;13(1):113-117. Zhou L, Li W. Effectiveness and safety of finerenone in Chinese CKD patients without diabetes: a retrospective, real-world study. Int Urol Nephrol. 2024;56(12):3877-3885. Wang X. WCN24-933 Effectiveness and safety of Finerenone in Chinese CKD patients without diabetes mellitus: A real-world retrospective study. Kidney International Reports. 2024;9(4, Supplement):S56-S7. Levey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604-612. Neuen BL, Weldegiorgis M, Herrington WG, Ohkuma T, Smith M, Woodward M. Changes in GFR and Albuminuria in Routine Clinical Practice and the Risk of Kidney Disease Progression. Am J Kidney Dis. 2021;78(3):350-360.e1. Levey AS, Gansevoort RT, Coresh J, et al. Change in Albuminuria and GFR as End Points for Clinical Trials in Early Stages of CKD: A Scientific Workshop Sponsored by the National Kidney Foundation in Collaboration With the US Food and Drug Administration and European Medicines Agency. Am J Kidney Dis. 2020;75(1):84-104. Agarwal R, Tu W, Farjat AE, et al. Impact of Finerenone-Induced Albuminuria Reduction on Chronic Kidney Disease Outcomes in Type 2 Diabetes : A Mediation Analysis. Ann Intern Med. 2023;176(12):1606-1616. Aklilu AM. Diagnosis of Chronic Kidney Disease and Assessing Glomerular Filtration Rate. Med Clin North Am. 2023;107(4):641-658. Bao W, Zhang M, Li N, Yao Z, Sun L. Efficacy and safety of finerenone in chronic kidney disease associated with type 2 diabetes: a systematic review and meta-analysis of randomized clinical trials. Eur J Clin Pharmacol. 2022;78(12):1877-1887. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Published Journal Publication published 01 Jul, 2025 Read the published version in BMC Nephrology → Version 1 posted Editorial decision: Revision requested 04 Feb, 2025 Reviewers agreed at journal 30 Jan, 2025 Reviewers agreed at journal 26 Jan, 2025 Reviews received at journal 25 Jan, 2025 Reviewers agreed at journal 25 Jan, 2025 Reviewers agreed at journal 25 Jan, 2025 Reviewers agreed at journal 24 Jan, 2025 Reviews received at journal 22 Jan, 2025 Reviewers agreed at journal 22 Jan, 2025 Reviewers invited by journal 08 Jan, 2025 Editor invited by journal 31 Dec, 2024 Editor assigned by journal 30 Dec, 2024 Submission checks completed at journal 30 Dec, 2024 First submitted to journal 29 Dec, 2024 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-5729879","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":396181587,"identity":"fca77bfe-9008-4f6b-b8ff-094abf89d29d","order_by":0,"name":"Yu Li","email":"","orcid":"","institution":"Zhongshan Hospital of Xiamen University","correspondingAuthor":false,"prefix":"","firstName":"Yu","middleName":"","lastName":"Li","suffix":""},{"id":396181588,"identity":"07f2c3f9-083b-4a56-acf3-8e06466e98be","order_by":1,"name":"Jiaxing Feng","email":"","orcid":"","institution":"Zhongshan Hospital of Xiamen 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reported.","formattedTitle":"Efficacy and safety of finerenone in non-diabetic CKD patients: a single-center, real-world, retrospective study","fulltext":[{"header":"Introduction","content":"\u003cp\u003eChronic kidney disease (CKD) is a substantial burden threatening global health [1]. Aldosterone is one of the multiple factors contributing to the pathophysiological development of CKD [2]. Considerable evidence supports that aldosterone and overactivation of the mineralocorticoid receptor provoke inflammation, fibrosis, and eventual kidney dysfunction [3].\u003c/p\u003e \u003cp\u003eCurrently, mineralocorticoid receptor antagonists (MRAs) have become a novel treatment strategy to alleviate the progression of CKD, the mechanism of which includes a reduction in renal collagen deposition and fibrosis, downregulation of proinflammatory mediators and cytokines, and a decrease in oxidative stress [4\u0026ndash;6]. Spironolactone, a first-generation steroidal MRA, and eplerenone, a second-generation one, have demonstrated promise in improving renal outcomes and reducing CKD progression [7,8]. However, owing to apprehensions regarding potential complications such as hyperkalemia, worsening renal function, gynecomastia, impotence in men, and menstrual disorders in women, the use of these agents in CKD management is limited [9]. More recently, third-generation MRA has been successfully developed, and the alterations in receptor affinity and tissue tropism enable them to more selectively enhance efficacy and reduce risks [10].\u003c/p\u003e \u003cp\u003eFinerenone, a new non-steroidal MRA, offers better receptor selectivity compared to spironolactone and eplerenone and has demonstrated a more significant decrease in proteinuria and organ damage [11,12]. In the past few years, numerous clinical trials have proven the effectiveness and safety of finerenone in managing diabetic CKD [13\u0026ndash;19]. The successful finerenone trials indicate its potential to revolutionize therapeutic approaches for CKD. In non-diabetic CKD, MRAs like spironolactone and eplerenone have been shown to protect the heart and kidneys. Research has found that eplerenone can decrease proteinuria and blood pressure in these patients [20]. These findings highlight the possible benefits of MRAs for this patient group and emphasize the necessity for more information on the effectiveness of finerenone in non-diabetic CKD.\u003c/p\u003e \u003cp\u003eCurrently, the effectiveness and safety of finerenone in non-diabetic CKD have been explored in a limited number of retrospective studies [21,22]. However, the evidence for finerenone's use in non-diabetic CKD patients is still not conclusive. Therefore, we conducted a real-world retrospective study investigating the efficacy and safety of finerenone in individuals with non-diabetic CKD.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy design and patient population\u003c/h2\u003e \u003cp\u003eThis single-center, real-world study was conducted retrospectively at the Department of Nephrology, Zhongshan Hospital of Xiamen University from April 2023 to June 2024. Criteria for inclusion: (1) patients aged 18 to 85 years; (2) patients diagnosed with CKD with a baseline eGFR\u0026thinsp;\u0026ge;\u0026thinsp;25 mL/min/1.73m\u003csup\u003e2\u003c/sup\u003e; (3) patients undergoing finerenone treatment for CKD. Criteria for exclusion: (1) patients with diabetic nephropathy, or Addison's disease; (2) patients lacking complete medical records; (3) patients with severe hepatic impairment (Child-Push grade C).\u003c/p\u003e \u003cp\u003e This study was approved by the Ethics Committee of Zhongshan Hospital of Xiamen University, with the requirement for informed consent waived.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eTreatment strategy\u003c/h3\u003e\n\u003cp\u003ePatients received standard CKD treatment tailored to their specific disease type and comorbidities, including hypertension, hyperlipidemia, hyperuricemia, and diabetes mellitus. Individualized regimes were implemented.\u003c/p\u003e \u003cp\u003eThe initial dose of finerenone was determined based on the patient's eGFR. Individuals with an eGFR equal to or greater than 60 mL/min/1.73m\u003csup\u003e2\u003c/sup\u003e were recommended to start with a daily dose of 20mg. In contrast, a lower starting dose of 10 mg per day is suggested for those with an eGFR between 25 and 60 mL/min/1.73m\u0026sup2;. Patients with an eGFR of less than 25 mL/min/1.73m\u0026sup2; were contraindicated for finerenone. Serum potassium (sK\u003csup\u003e+\u003c/sup\u003e) levels must be closely monitored and dosage adjustments made within four weeks following the commencement of treatment. If sK\u003csup\u003e+\u003c/sup\u003e levels were 4.8 mmol/L or lower, increasing the dose to 20 mg daily might be considered. Should sK\u003csup\u003e+\u003c/sup\u003e levels fall within the range of 4.8 to 5.5 mmol/L, it was advisable to maintain the current dosage regimen. Conversely, if sK\u0026thinsp;+\u0026thinsp;levels were higher than 5.5 mmol/L, finerenone should be discontinued temporarily until sK\u0026thinsp;+\u0026thinsp;levels were at or below 5.0 mmol/L; following this, therapy may be restarted with a lower dose of 10 mg daily.\u003c/p\u003e\n\u003ch3\u003eClinical data collection\u003c/h3\u003e\n\u003cp\u003eThe demographic and laboratory characteristics of patients include age, gender, serum creatinine, eGFR, UACR, and sK\u003csup\u003e+\u003c/sup\u003e levels. Clinical data collection will occur at baseline, and then at 1, 3, 6, and 12 months following treatment. The CKD-EPI formula was used to assess eGFR [23].\u003c/p\u003e \u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003eStatistical analysis\u003c/h2\u003e \u003cp\u003eCategorical data were expressed as frequencies and percentages. Continuous data that followed a normal distribution were presented as the mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation, whereas those that did not were presented as the median and interquartile range. Repeated measure ANOVA and the generalized estimating equation were employed to analyze the data with repeated measurements. Statistical analyses employed SPSS version 26.0 (Chicago, IL, USA), with a significance level established at \u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;0.05 (two-tailed).\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003ePatient characteristics\u003c/h2\u003e \u003cp\u003eThe baseline characteristics of the patients are presented in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e. A total of 37 patients were included in the analysis (21 males, mean age 48.84\u0026thinsp;\u0026plusmn;\u0026thinsp;14.69 years). The most frequent etiologic diagnoses were IgA nephropathy (54.1%) and membranous nephropathy (24.3%). Other etiologies included Henoch\u0026ndash;Sch\u0026ouml;nlein purpura nephritis, minimal change nephropathy, hepatitis B virus\u0026ndash;associated nephritis, mesangial proliferative glomerulonephritis, and obesity-related glomerulopathy. The baseline median UACR was 1091.90 mg/g (IQR, 494.50-1860.05), and the mean eGFR was 69.04\u0026thinsp;\u0026plusmn;\u0026thinsp;28.32 mL/min/1.73m\u003csup\u003e2\u003c/sup\u003e. The baseline mean serum potassium level was 4.30\u0026thinsp;\u0026plusmn;\u0026thinsp;0.46 mmol/L.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eDemographic and baseline characteristics of the patients\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"2\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCharacteristics\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAll (N\u0026thinsp;=\u0026thinsp;37)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge (years)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e48.84\u0026thinsp;\u0026plusmn;\u0026thinsp;14.69\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMale sex\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21 (56.8%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eKidney diseases (etiological diagnosis)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIgA nephropathy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e20 (54.1%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMembranous nephropathy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e9 (24.3%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHenoch-Sch\u0026ouml;nlein purpura nephritis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2 (5.4%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMinimal change nephropathy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (2.7%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHepatitis B virus-associated nephritis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (2.7%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMesangial proliferative glomerulonephritis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (2.7%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eObesity-related glomerulopathy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (2.7%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBaseline UACR (mg/g)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1091.90 (494.50-1860.05)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;300\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5 (13.5%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;300\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e32 (86.5%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBaseline eGFR (mL/min/1.73m\u003csup\u003e2\u003c/sup\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e69.04\u0026thinsp;\u0026plusmn;\u0026thinsp;28.32\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e25\u0026ndash;45\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e8 (21.6%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e45\u0026ndash;60\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e8 (21.6%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;60\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21 (56.8%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBaseline serum potassium (mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4.30\u0026thinsp;\u0026plusmn;\u0026thinsp;0.46\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eTherapeutic outcomes\u003c/h3\u003e\n\u003cp\u003eThe UACR was decreased compared with baseline at 3 months (\u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.018), 6 months (\u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.020), and a significant reduction of 664.95 mg/g (IQR, 196.60-1226.70, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.002) was further observed at 12 months, as shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e. The eGFR was lower at 6 months (66.99\u0026thinsp;\u0026plusmn;\u0026thinsp;28.75 mL/min/1.73m\u003csup\u003e2\u003c/sup\u003e), but there was no significant difference at baseline, 1, 3, 6, or 12 months (all P\u0026thinsp;\u0026gt;\u0026thinsp;0.05), as shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e\n\u003ch3\u003eSafety\u003c/h3\u003e\n\u003cp\u003eFor safety analysis, the levels of sK\u0026thinsp;+\u0026thinsp;remained within the 3.5\u0026ndash;5.5 mmol/L range, with no significant differences compared to baseline (\u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026gt;\u0026thinsp;0.05), as shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e. No treatment discontinuation or hospitalization occurred due to hyperkalemia.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis real-world, observational retrospective study indicated the potential for finerenone in the clinical treatment of non-diabetic CKD patients. Our findings revealed that patients undergoing finerenone therapy experienced a notable reduction in UACR and maintained a stable eGFR throughout the treatment, indicating the drug might be conducive to alleviating the deterioration of renal function. Another crucial aspect of this study was the stable sK\u003csup\u003e+\u003c/sup\u003e levels in the non-diabetic CKD population during treatment, supporting the low hyperkalemia risk with finerenone, and manifesting acceptable safety and tolerability profile. Currently, the clinical evidence related to the utilization of finerenone in this patient population is extremely limited, and this study provided initial yet valuable evidence of both the efficacy and safety of finerenone in the treatment of non-diabetic CKD patients.\u003c/p\u003e \u003cp\u003eThe reduction of UACR implies an enhancement in renal function and a deceleration in the progression of kidney disease. Studies have reported that a decreased UACR is correlated with superior clinical outcomes [24,25]. Prior investigations have revealed that finerenone treatment leads to a reduction in UACR, demonstrating the renal protective effect in diabetic CKD patients [26]. The notable decrease in UACR seen in our group indicates that finerenone may effectively enhance kidney function in non-diabetic CKD patients. Pitt et al. [10] conducted an earlier study that examined the effectiveness of finerenone in individuals with heart failure and reduced left ventricular ejection fraction, in conjunction with mild or moderate CKD. In their study, two-thirds of the participants were non-diabetic, and a reduction in UACR was noted one month following finerenone therapy. The findings revealed a UACR reduction trend that matches our research. However, Pitt's study did not conduct a diabetes-based subgroup analysis, thereby limiting the applicability of the findings to non-diabetic CKD patients. In our cohort, a reduction in UACR was noted within the first month of treatment initiation; nevertheless, this decrease was not statistically significant, which might be attributed to the limited sample size. On later follow-up, significant UACR reductions at 3 months were sustained over 12 months.\u003c/p\u003e \u003cp\u003eIn CKD, renal function deterioration is usually marked by a gradual decrease in eGFR [27]. Previous meta-analysis on CKD indicated that while finerenone could slow down the deterioration of kidney function, patients still experienced a decrease in eGFR [28]. The FIDELIO-DKD study found that eGFR decline in diabetic CKD patients treated with finerenone followed a biphasic pattern [14]. In the initial stage, the finerenone group had a faster reduction in eGFR than the placebo group, but after 4 months, the decline rate slowed, causing the eGFR levels of the two groups to cross over. In our study, the average eGFR value moderately declined at the 6-month follow-up but subsequently moderately ascended at the 12-month follow-up. Despite the absence of statistically significant differences at various follow-up time points, the change in eGFR demonstrates a distinct pattern in non-diabetic CKD patients.\u003c/p\u003e \u003cp\u003eFinerenone, functioning as an MRA, is capable of influencing the retention of sodium and the excretion of potassium, which might result in hyperkalemia, particularly among CKD patients with compromised excretion function. Hyperkalemia is one of the specific adverse events linked to the utilization of MRA drugs [10]. Previous studies have indicated that finerenone therapy was correlated with an elevated risk of hyperkalemia. Nevertheless, through monitoring and adjusting the dosage of the medication, the risk of hyperkalemia can be effectively mitigated in diabetic CKD patients [14\u0026ndash;16]. In our cohort, the sK\u003csup\u003e+\u003c/sup\u003e level remained relatively stable throughout the 12-month follow-up period, and no serious adverse events related to the treatment were noted, thereby confirming the favorable safety profile of finerenone in the non-diabetic CKD patient population.\u003c/p\u003e \u003cp\u003eThis study has certain important limitations. First, this research is a retrospective analysis from a single center, involving the inherent biases of study design. Second, the small sample size was also a limitation. Third, the current study design did not include a control group. Therefore, large-scale prospective randomized controlled trials are needed to confirm these findings among diverse populations and in different regions of the world. The FIND-CKD trial (NCT05047263) currently underway promises to further elucidate the prolonged effects of finerenone on renal function in the non-diabetic CKD patient population.\u003c/p\u003e \u003cp\u003eIn conclusion, finerenone demonstrates favorable efficacy and safety profiles in non-diabetic CKD patients within real-world clinical settings. This study offers significant insights and a promising perspective on the application of finerenone for non-diabetic CKD patients.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eConflict of interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOn behalf of all authors, the corresponding author states that there is no conflict of interest.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthical approval\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eInformed consent was waived due to the non-interventional design of the study and retrospective nature of data collection.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was funded by grants from the Xiamen Municipal Bureau of Science and Technology (Grant No. 3502Z20244ZD1061).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Availability\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll data generated or analyzed in this study are included in this published article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe are grateful for the subjects in our hospital. We also thank all colleagues who collected all medical information and clinical data.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor Contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eB.X., Y.L. and T.G. designed and conducted the study, acquired and analyzed data, and wrote the manuscript. J.F., X.G., W.Z, and T.Y. acquired and analyzed data. All authors read and approved the final manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eWebster AC, Nagler EV, Morton RL, Masson P. Chronic Kidney Disease. Lancet. 2017;389(10075):1238-1252. \u003c/li\u003e\n\u003cli\u003eBarrera-Chimal J, Girerd S, Jaisser F. Mineralocorticoid receptor antagonists and kidney diseases: pathophysiological basis. Kidney Int. 2019;96(2):302-319.\u003c/li\u003e\n\u003cli\u003eEpstein M. Aldosterone and Mineralocorticoid Receptor Signaling as Determinants of Cardiovascular and Renal Injury: From Hans Selye to the Present. Am J Nephrol. 2021;52(3):209-216.\u003c/li\u003e\n\u003cli\u003ePatel V, Joharapurkar A, Jain M. Role of mineralocorticoid receptor antagonists in kidney diseases. Drug Dev Res. 2021;82(3):341-363.\u003c/li\u003e\n\u003cli\u003eBarrera-Chimal J, Lima-Posada I, Bakris GL, Jaisser F. Mineralocorticoid receptor antagonists in diabetic kidney disease - mechanistic and therapeutic effects. Nat Rev Nephrol. 2022;18(1):56-70.\u003c/li\u003e\n\u003cli\u003eLainscak M, Pelliccia F, Rosano G, et al. Safety profile of mineralocorticoid receptor antagonists: Spironolactone and eplerenone. Int J Cardiol. 2015;200:25-29.\u003c/li\u003e\n\u003cli\u003eQuach K, Lvtvyn L, Baigent C, et al. The Safety and Efficacy of Mineralocorticoid Receptor Antagonists in Patients Who Require Dialysis: A Systematic Review and Meta-analysis. Am J Kidney Dis. 2016;68(4):591-598.\u003c/li\u003e\n\u003cli\u003eHasegawa T, Nishiwaki H, Ota E, Levack WM, Noma H. Aldosterone antagonists for people with chronic kidney disease requiring dialysis. Cochrane Database Syst Rev. 2021;2(2):CD013109.\u003c/li\u003e\n\u003cli\u003eBakris GL, Filippatos GS, Farmakis D, Epstein M, and Pitt B. (2021). Aldosterone Antagonists and CVD. Washington, DC: American College of Cardiology. Available at: https://www.acc.org/latest-in-cardiology/articles/2021/07/19/13/42/aldosterone-antagonists-and-cvd (Accessed July 19, 2021).\u003c/li\u003e\n\u003cli\u003ePitt B, Kober L, Ponikowski P, et al. Safety and tolerability of the novel non-steroidal mineralocorticoid receptor antagonist BAY 94-8862 in patients with chronic heart failure and mild or moderate chronic kidney disease: a randomized, double-blind trial. Eur Heart J. 2013;34(31):2453-2463.\u003c/li\u003e\n\u003cli\u003eGeorgianos PI, Agarwal R. Mineralocorticoid Receptor Antagonism in Chronic Kidney Disease. Kidney Int Rep. 2021;6(9):2281-2291.\u003c/li\u003e\n\u003cli\u003eGrune J, Beyhoff N, Smeir E, et al. Selective Mineralocorticoid Receptor Cofactor Modulation as Molecular Basis for Finerenone\u0026apos;s Antifibrotic Activity. Hypertension. 2018;71(4):599-608.\u003c/li\u003e\n\u003cli\u003eBakris GL, Agarwal R, Chan JC, et al. Effect of Finerenone on Albuminuria in Patients With Diabetic Nephropathy: A Randomized Clinical Trial. JAMA. 2015;314(9):884-894.\u003c/li\u003e\n\u003cli\u003eBakris GL, Agarwal R, Anker SD, et al. Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes. N Engl J Med. 2020;383(23):2219-2229.\u003c/li\u003e\n\u003cli\u003eZhang H, Xie J, Hao C, et al. Finerenone in Patients with Chronic Kidney Disease and Type 2 Diabetes: The FIDELIO-DKD Subgroup from China. Kidney Dis (Basel). 2023;9(6):498-506.\u003c/li\u003e\n\u003cli\u003ePitt B, Filippatos G, Agarwal R, et al. Cardiovascular Events with Finerenone in Kidney Disease and Type 2 Diabetes. N Engl J Med. 2021;385(24):2252-2263.\u003c/li\u003e\n\u003cli\u003eAgarwal R, Filippatos G, Pitt B, et al. Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis [published correction appears in Eur Heart J. 2022 May 21;43(20):1989. doi: 10.1093/eurheartj/ehab886]. Eur Heart J. 2022;43(6):474-484.\u003c/li\u003e\n\u003cli\u003eGhosal S, Sinha B. Finerenone in type 2 diabetes and renal outcomes: A random-effects model meta-analysis. Front Endocrinol (Lausanne). 2023;14:1114894.\u003c/li\u003e\n\u003cli\u003eZhang MZ, Bao W, Zheng QY, Wang YH, Sun LY. Efficacy and Safety of Finerenone in Chronic Kidney Disease: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. Front Pharmacol. 2022;13:819327.\u003c/li\u003e\n\u003cli\u003eTsuboi N, Kawamura T, Okonogi H, Ishii T, Hosoya T. The long-term antiproteinuric effect of eplerenone, a selective aldosterone blocker, in patients with non-diabetic chronic kidney disease. J Renin Angiotensin Aldosterone Syst. 2012;13(1):113-117.\u003c/li\u003e\n\u003cli\u003eZhou L, Li W. Effectiveness and safety of finerenone in Chinese CKD patients without diabetes: a retrospective, real-world study. Int Urol Nephrol. 2024;56(12):3877-3885.\u003c/li\u003e\n\u003cli\u003eWang X. WCN24-933 Effectiveness and safety of Finerenone in Chinese CKD patients without diabetes mellitus: A real-world retrospective study. Kidney International Reports. 2024;9(4, Supplement):S56-S7.\u003c/li\u003e\n\u003cli\u003eLevey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604-612. \u003c/li\u003e\n\u003cli\u003eNeuen BL, Weldegiorgis M, Herrington WG, Ohkuma T, Smith M, Woodward M. Changes in GFR and Albuminuria in Routine Clinical Practice and the Risk of Kidney Disease Progression. Am J Kidney Dis. 2021;78(3):350-360.e1.\u003c/li\u003e\n\u003cli\u003eLevey AS, Gansevoort RT, Coresh J, et al. Change in Albuminuria and GFR as End Points for Clinical Trials in Early Stages of CKD: A Scientific Workshop Sponsored by the National Kidney Foundation in Collaboration With the US Food and Drug Administration and European Medicines Agency. Am J Kidney Dis. 2020;75(1):84-104.\u003c/li\u003e\n\u003cli\u003eAgarwal R, Tu W, Farjat AE, et al. Impact of Finerenone-Induced Albuminuria Reduction on Chronic Kidney Disease Outcomes in Type 2 Diabetes : A Mediation Analysis. Ann Intern Med. 2023;176(12):1606-1616.\u003c/li\u003e\n\u003cli\u003eAklilu AM. Diagnosis of Chronic Kidney Disease and Assessing Glomerular Filtration Rate. Med Clin North Am. 2023;107(4):641-658.\u003c/li\u003e\n\u003cli\u003eBao W, Zhang M, Li N, Yao Z, Sun L. Efficacy and safety of finerenone in chronic kidney disease associated with type 2 diabetes: a systematic review and meta-analysis of randomized clinical trials. Eur J Clin Pharmacol. 2022;78(12):1877-1887.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-nephrology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bnep","sideBox":"Learn more about [BMC Nephrology](http://bmcnephrol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bnep/default.aspx","title":"BMC Nephrology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Finerenone, chronic kidney disease, non-diabetic","lastPublishedDoi":"10.21203/rs.3.rs-5729879/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-5729879/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eFinerenone, a novel non-steroidal mineralocorticoid receptor antagonist, has shown promising efficacy and safety profiles in the management of chronic kidney disease (CKD) associated with type 2 diabetes mellitus (T2DM). However, the effectiveness and safety of finerenone on non-diabetic CKD patients require further investigation.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eThis retrospective, real-world study involved non-diabetic CKD patients from April 2023 to June 2024. Participants received finerenone alongside standard CKD treatment. Primary clinical results included changes in the urinary albumin-to-creatinine ratio (UACR), estimated glomerular filtration rate (eGFR), and serum potassium (sK\u003csup\u003e+\u003c/sup\u003e) levels. The data were collected initially and during follow-ups at 1, 3, 6, and 12 months.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eIn total, 37 non-diabetic CKD patients were included in the population; 21 individuals (56.8%) were male, and the mean age was 48.84\u0026thinsp;\u0026plusmn;\u0026thinsp;14.69 years. During the follow-up, there was a notable decrease in UACR, with a median reduction of 664.95 mg/g (IQR, 196.60-1226.70, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.002). The baseline average eGFR was 70.80\u0026thinsp;\u0026plusmn;\u0026thinsp;27.97 mL/min/1.73m\u003csup\u003e2\u003c/sup\u003e, with no notable alterations observed during the follow-up (\u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026gt;\u0026thinsp;0.05). In terms of safety analysis, the sK\u0026thinsp;+\u0026thinsp;levels were within the 3.5\u0026ndash;5.5 mmol/L range, with no significant difference from the baseline (\u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026gt;\u0026thinsp;0.05). No patients discontinued treatment or were hospitalized because of hyperkalemia.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eReal-world practice indicates that finerenone is effective and safe for non-diabetic CKD patients, but further large-scale, prospective studies are needed to confirm these findings.\u003c/p\u003e","manuscriptTitle":"Efficacy and safety of finerenone in non-diabetic CKD patients: a single-center, real-world, retrospective study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-01-01 09:44:59","doi":"10.21203/rs.3.rs-5729879/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-02-04T06:41:34+00:00","index":"","fulltext":""},{"type":"reviewerAgreed","content":"297323867066410155305278204698008273784","date":"2025-01-30T07:14:44+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"238165170868370268331254308248416059011","date":"2025-01-26T23:51:39+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-01-25T18:20:44+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"172981240575410261776845959532484274714","date":"2025-01-25T17:52:53+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"209507305673146549149620889452680026007","date":"2025-01-25T08:38:48+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"298758261172789976630766315748515306751","date":"2025-01-24T16:00:28+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-01-22T12:14:49+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"253685226944940274616618913987870288288","date":"2025-01-22T11:40:18+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-01-09T04:10:17+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2024-12-31T09:05:44+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2024-12-30T14:56:21+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2024-12-30T14:54:28+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Nephrology","date":"2024-12-29T12:19:00+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-nephrology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bnep","sideBox":"Learn more about [BMC Nephrology](http://bmcnephrol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bnep/default.aspx","title":"BMC Nephrology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"28ada555-3a42-4da5-992d-03eb96c69437","owner":[],"postedDate":"January 1st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2025-07-07T16:06:26+00:00","versionOfRecord":{"articleIdentity":"rs-5729879","link":"https://doi.org/10.1186/s12882-025-04241-w","journal":{"identity":"bmc-nephrology","isVorOnly":false,"title":"BMC Nephrology"},"publishedOn":"2025-07-01 15:57:16","publishedOnDateReadable":"July 1st, 2025"},"versionCreatedAt":"2025-01-01 09:44:59","video":"","vorDoi":"10.1186/s12882-025-04241-w","vorDoiUrl":"https://doi.org/10.1186/s12882-025-04241-w","workflowStages":[]},"version":"v1","identity":"rs-5729879","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-5729879","identity":"rs-5729879","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}