Real-World Effects of Finerenone in Diabetics Kidney Disease: Data From Fine-Turk Study

Real-World Effects of Finerenone in Diabetics Kidney Disease: Data From Fine-Turk 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 Real-World Effects of Finerenone in Diabetics Kidney Disease: Data From Fine-Turk Study Serap Yadigar, Suat Akgür, Felemez Arslan, Mehmet Sezen, Büşra Özcan, and 78 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9043582/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Randomized trials have established the benefits of finerenone in type 2 diabetes with CKD; however, real-world evidence with high SGLT2 inhibitor uptake remains limited. Methods: FINE-TURK was a multicenter retrospective cohort study conducted at 56 nephrology centers in Turkey. Adults with type 2 diabetes and CKD initiating finerenone (January 2025 to June 2025) were assessed at baseline, month 1, and month 3. Primary endpoints were changes in estimated glomerular filtration rate (eGFR), serum potassium, and urinary albumin-to-creatinine ratio (UACR); hyperkalemia was defined as potassium >5.5 mEq/L. Results: Among 1,091 patients (60.6±11.5 years, 55% male), 87% received an SGLT2 inhibitor and 100% renin-angiotensin system blockade. Finerenone started at 10 mg in 85%. Paired analyses included 576 for eGFR, 648 for potassium, and 487 for UACR. Mean eGFR fell from 58.51±24.20 to 55.78±23.19 mL/min/1.73 m2 at month 1 and remained 55.78±23.13 at month 3 (both P<0.001 vs baseline). Mean potassium increased from 4.49±0.39 to 4.75±0.47 and 4.78±0.44 mEq/L (P<0.001). Median UACR declined from 690.6 (271.4-1538.0) mg/g to 468.0 (173.5-1195.5) at month 1 and 450.0 (154.5-1041.0) mg/g at month 3, corresponding to 32.2% and 34.8% reductions (P<0.001). Hyperkalemia occurred in 5.0% at both visits, commonly managed with potassium binders; hospitalizations were infrequent (2.8% and 3.1%), and no deaths occurred. Conclusions: In routine care with high SGLT2 inhibitor uptake, finerenone achieved a rapid reduction in albuminuria, with a modest early decline in eGFR, manageable potassium elevations, and low short-term event rates, supporting early use alongside standard therapy in contemporary clinical practice. Urology & Nephrology finerenone diabetic kidney disease chronic kidney disease albuminuria SGLT2 inhibitor hyperkalemia Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Introduction Chronic kidney disease (CKD) remains a major global health burden, and type 2 diabetes (T2D) is the leading cause of kidney failure worldwide 1 , 2 . Over the past decades 3 , renin-angiotensin system (RAS) inhibition has been the foundation of kidney protection in albuminuric diabetic CKD 4 – 6 , and sodium-glucose cotransporter 2 (SGLT2) inhibitors have further reduced cardiovascular events and slowed CKD progression 7 . Nevertheless, a substantial residual risk persists, and many patients continue to have clinically relevant albuminuria despite guideline-directed therapy 8 .Mineralocorticoid receptor overactivation contributes to inflammation and fibrosis in diabetic CKD. Although steroidal mineralocorticoid receptor antagonists can reduce albuminuria, their use is often limited by hyperkalemia and endocrine adverse effects 9 – 11 . Finerenone is a selective nonsteroidal mineralocorticoid receptor antagonist that provides anti-inflammatory and anti-fibrotic effects with fewer endocrine-related adverse events 12 – 15 . In the phase 3 FIDELIO-DKD and FIGARO-DKD trials, finerenone reduced the risk of kidney disease progression and cardiovascular events, with consistent cardiorenal benefits in the pooled FIDELITY analysis 16 . However, uptake of SGLT2 inhibitors was low in the pivotal trials, and contemporary real-world evidence, particularly from settings with widespread SGLT2 inhibitor use, remains limited. Because finerenone dosing and continuation decisions depend on early monitoring of eGFR and serum potassium, real-world trajectories in the first months after initiation are clinically important. The FINE TURK cohort was established to quantify early changes in eGFR, urinary albumin-to-creatinine ratio, and serum potassium at 1 and 3 months after initiation of finerenone in adults with T2D and CKD across multiple centers in Turkey and to describe hyperkalemia management, hospitalization events, and determinants of short-term responses. MATERIALS AND METHODS Study Design and Population This multicenter, retrospective cohort study evaluated the early efficacy and safety of finerenone in patients with type 2 diabetes mellitus and chronic kidney disease (CKD) receiving contemporary kidney-protective therapy. Data were collected from 56 nephrology centers across Türkiye between January 2025 and June 2025. The study was reported in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines and conducted in accordance with the Declaration of Helsinki. All participating centers obtained institutional review board approval, and informed consent was waived due to the retrospective nature of the study and the use of de-identified clinical data. We included adults aged ≥ 18 years with established type 2 diabetes mellitus and CKD who initiated finerenone for kidney protection during the study period. Patients were excluded if baseline or follow-up laboratory measurements were substantially incomplete. Of 1,168 patients screened, 77 were excluded due to insufficient data, yielding a final cohort of 1,091. Data Collection Standardized data collection protocols were implemented across all participating centers. Baseline demographic data included age, sex, body mass index, and comorbidities, including hypertension, cardiovascular disease, and diabetes duration. Concomitant medications were systematically recorded, including renin-angiotensin system (RAS) inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide 1 receptor agonists, diuretics, and lipid-lowering therapies. Laboratory measurements were obtained at baseline and approximately 1–3 months thereafter, in accordance with routine clinical practice protocols at each center. Measured parameters included serum creatinine, estimated glomerular filtration rate (eGFR, calculated using the CKD-EPI equation), serum potassium, and urinary albumin-to-creatinine ratio (UACR). Finerenone was initiated at 10 mg or 20 mg once daily according to clinical judgment, baseline eGFR, and serum potassium levels. Dose adjustments and discontinuation were managed by treating physicians according to clinical response and tolerability. Outcomes Primary endpoints were changes in eGFR (mL/min/1.73m²), serum potassium (mEq/L), and UACR (mg/g) from baseline to months 1–3. Secondary endpoints included the incidence and severity of hyperkalemia, management strategies employed, reasons for finerenone discontinuation and reinitiation, hospitalizations, and all-cause mortality. Statistical Analysis All continuous variables were assessed for normality using the Shapiro-Wilk test. As all primary variables and their changes from baseline were found to be non-normally distributed (Shapiro-Wilk p < 0.001 for all), non-parametric tests were used as the primary analytical approach, with parametric tests reported in parallel. Continuous variables are presented as median [interquartile range (IQR)] or mean ± standard deviation (SD) as appropriate, and categorical variables as counts and percentages. Changes from baseline to months 1–3 were evaluated using the Wilcoxon signed-rank test as the primary analysis and paired t-tests as a secondary analysis. Effect sizes were calculated using Cohen’s d. For albuminuria, which exhibited a highly right-skewed distribution, analyses were performed on both raw and natural log-transformed data to ensure robustness. Two-tailed p-values < 0.05 were considered statistically significant. As a sensitivity analysis, linear mixed models (LMMs) with random intercepts were fitted for all three primary endpoints to assess the robustness of the paired analyses and to account for within-patient correlation. The model specification was: Y = β ₀+β ₁(Time )+β ₂(Baseline ) + u + ε, where β₁ represents the fixed time effect (primary parameter of interest) and u the random intercept for patient i. Models were estimated using restricted maximum likelihood (REML). Analysis of covariance (ANCOVA) models were fitted to evaluate the predictive value of baseline parameters on follow-up values. Treatment responses were examined across predefined subgroups stratified by baseline eGFR category (≤ 30, 30–45, 45–60, > 60 mL/min/1.73m²) and baseline albuminuria category (microalbuminuria < 300 mg/g vs. macroalbuminuria ≥ 300 mg/g). Spearman's rank correlation coefficient was calculated to assess the relationship between baseline values and the magnitude of treatment response. All analyses were performed using Python 3.11 with SciPy, statsmodels, and scikit-learn. Results Study Population The final cohort comprised 1,091 patients (mean age 60.6 ± 11.5 years, 55.0% male) with type 2 diabetes and CKD. Hypertension was nearly universal (99.6%), and 37.8% had established cardiovascular disease with a mean diabetes duration of 12.4 ± 8.9 years. At baseline, median eGFR was 53.5 [IQR: 41.0–74.0] mL/min/1.73m², mean serum potassium was 4.48 ± 0.39 mEq/L, and median UACR was 781.6 [IQR: 336.1-1542.5] mg/g. All patients were receiving RAS blockade (64.4% at maximally tolerated doses), and notably, 87.0% of patients with available data were concurrently treated with SGLT2 inhibitors, reflecting contemporary practice patterns. Finerenone was initiated at 10 mg in 85.0% of patients and at 20 mg in 15.0%. Among those who initiated at 10 mg and had dose data available at month 3 (n = 460), 140 (30.4%) were uptitrated to 20 mg. Paired baseline and months 1–3 measurements were available for eGFR in 571 patients (52.4%), serum potassium in 646 (59.2%), and UACR in 474 (43.5%), reflecting routine clinical practice patterns across 56 centers. Primary Endpoints Finerenone initiation was associated with statistically significant changes in all three primary endpoints, consistent with the study hypothesis (Table 1 , Fig. 1 ). Table 1 Primary Endpoints—Changes from Baseline to Months 1–3 Endpoint n Baseline Month 1–3 Change % Change p-value 95% CI eGFR (mL/min/1.73m²) 571 53.5 [41.0–74.0] 51.0 [38.0–73.0] -2.34 ± 11.88 -3.8% < 0.001 [-3.32, -1.36] Serum K⁺ (mEq/L) 646 4.50 [4.20–4.80] 4.80 [4.50–5.10] + 0.30 ± 0.46 + 6.8% < 0.001 [0.27, 0.34] UACR (mg/g) 474 781.6 [336.1-1542.5] 468.2 [155.0-1042.0] -248.0 [-600.0, -53.5] -40.1% < 0.001 [-310.0, -205.0]† Log-UACR 474 6.53 ± 1.29 5.92 ± 1.45 -0.607 ± 0.78 -45.5% < 0.001 [-0.68, -0.54] Data presented as median [IQR] or mean ± SD. p-values are from Wilcoxon signed-rank tests. †95% CI for median change in UACR was calculated using bootstrapping (10,000 iterations). Among 571 patients with paired eGFR measurements, median eGFR declined from 53.5 [41.0–74.0] to 51.0 [38.0–73.0] mL/min/1.73m² (mean change − 2.34 ± 11.88 mL/min, 95% CI -3.32 to -1.36; Wilcoxon p < 0.001; Cohen’s d = -0.20). This modest 3.8% median relative decline is consistent with an adaptive hemodynamic dip commonly observed with mineralocorticoid receptor antagonism and does not reflect progressive kidney injury. Among 646 patients with paired potassium measurements, median serum potassium increased from 4.50 [4.20–4.80] to 4.80 [4.50–5.10] mEq/L (mean change + 0.30 ± 0.46 mEq/L, 95% CI 0.27 to 0.34; Wilcoxon p < 0.001; Cohen’s d = 0.66). Despite the statistically significant increase, mean potassium remained within the normal range at all time points. Among 474 patients with paired UACR measurements (excluding one patient with a follow-up value of zero for log-transformation), median UACR decreased from 781.6 [336.1-1542.5] to 468.2 [155.0-1042.0] mg/g, corresponding to a 40.1% median reduction (Wilcoxon p < 0.001). Log-transformed analysis confirmed a mean change of -0.607 ± 0.78 log units (95% CI -0.68 to -0.54; p < 0.001; Cohen’s d = -0.78), corresponding to a 45.5% reduction. This substantial and rapid reduction in albuminuria represents a clinically meaningful early response to finerenone therapy. Sensitivity Analysis Linear mixed model analysis confirmed the robustness of all primary findings (Fig. 2 ). The fixed time effects were near-identical to paired analyses: eGFR − 2.34 mL/min/1.73m² (SE 0.50, p < 0.001); potassium + 0.31 mEq/L (SE 0.02, p < 0.001); and log-UACR − 0.607 (SE 0.04, p < 0.001). Minimal random intercept variances across all three models indicated that, after accounting for baseline values, treatment effects were homogeneous across the patient population. The near-perfect concordance between two fundamentally different analytical approaches—one assuming independence (paired test) and the other modeling within-patient correlation (LMM)—provides strong evidence that the observed treatment effects are robust and not an artifact of the analytical method. Subgroup and Correlation Analyses Subgroup analyses demonstrated consistency of treatment response across diverse patient populations (Fig. 3 ). eGFR decline was observed across all baseline eGFR categories: ≤30 mL/min (n = 39, -0.85 ± 5.16 mL/min), 30–45 (n = 159, -1.23 ± 5.85), 45–60 (n = 149, -2.52 ± 8.35), and > 60 (n = 224, -3.27 ± 16.83). Albuminuria reduction was consistent regardless of baseline severity, with median reductions of -35.6% in microalbuminuria (n = 109) and − 40.3% in macroalbuminuria (n = 366). ANCOVA models showed that baseline eGFR explained 76.8% of the variance in follow-up eGFR (R²=0.768), baseline potassium explained 17.7% (R²=0.177), and baseline log-UACR explained 71.4% (R²=0.714). Crucially, the treatment effect remained statistically significant for all primary outcomes after adjusting for these baseline covariates (p < 0.001), indicating consistent efficacy regardless of initial values. Correlation analysis between baseline values and the magnitude of change revealed weak correlations for eGFR (Spearman ρ=-0.145, p = 0.001) and log-UACR (ρ=-0.034, p = 0.458), indicating that treatment effects are largely independent of baseline status (Fig. 4 ). A moderate negative correlation was observed for potassium (ρ=-0.419, p 5.5 mEq/L) occurred in 27 of 646 patients (4.2%), and severe hyperkalemia (K⁺ >6.0 mEq/L) in only 5 (0.8%). Among the 27 patients who developed hyperkalemia, the predominant management strategy was initiation of a potassium binder (40.7%, n = 11), finerenone discontinuation (33.3%, n = 9), and observation alone (18.5%, n = 5) (Fig. 5 , Panel A ). Finerenone was discontinued in 39 patients (3.6%) by month 3. The most common reasons were hyperkalemia (33.3%), other causes (28.2%), and financial reasons (20.5%) (Fig. 5 , Panel B ). Among the 27 patients with follow-up data after discontinuation, 8 (29.6%) were re-initiated on finerenone, predominantly after potassium normalization. During the follow-up period, 6 deaths (0.5%) were recorded. Causes of death included coronary artery disease, hemorrhagic stroke, decompensated heart failure, and gastrointestinal bleeding. None of the deaths were considered by the investigators to be directly attributable to finerenone therapy or hyperkalemia. DISCUSSION In this multicenter, retrospective, real-world cohort spanning 56 nephrology centers, initiation of finerenone in adults with type 2 diabetes and chronic kidney disease receiving contemporary kidney-protective therapy was associated with three consistent early trajectories at routine follow-up within 1 to 3 months. First, albuminuria declined rapidly and substantially. Second, kidney function showed a small early eGFR dip of limited magnitude. Third, serum potassium increased modestly, while clinically relevant hyperkalemia remained uncommon and was generally manageable in routine practice. The scale of FINE-TURK and the high prevalence of background sodium-glucose cotransporter 2 (SGLT2) inhibitor use provide an updated real-world complement to the pivotal finerenone program conducted in an era of comparatively low SGLT2 inhibitor uptake 16 – 18 . The most clinically salient signal was the magnitude of albuminuria reduction. Among patients with paired measurements, UACR decreased by approximately 40% within the first 1 to 3 months, with concordant findings on log-transformed analyses, supporting a robust early anti-albuminuric effect despite the inherent variability of spot UACR in routine care. This degree and timing of response are consistent with the early albuminuria-lowering observed in FIDELIO-DKD and FIGARO-DKD, reinforcing the biological plausibility that finerenone’s anti-inflammatory and anti-fibrotic effects translate into measurable short-term biomarker improvement in contemporary practice 10 , 12 – 14 , 17 , 18 . Although early UACR reduction has been linked to long-term cardiorenal benefit in clinical trials, the current observational design and short follow-up preclude inference regarding long-term endpoints; continued follow-up in this national cohort will be essential to determine whether early biomarker changes translate into sustained eGFR benefit and fewer clinical events 17 , 18 . Kidney function changes were modest. The early mean eGFR decline of approximately 2 to 3 mL/min/1.73 m² is consistent in direction with the hemodynamic dip commonly observed after initiation of several kidney-protective agents, including renin-angiotensin system (RAS) blockade and SGLT2 inhibition 6 , 19 . Importantly, sensitivity analyses using linear mixed models yielded estimates that closely match paired analyses, arguing against analytic artifact and supporting the robustness of the observed trajectory. Subgroup analyses suggested that this early eGFR change occurred across baseline eGFR categories, supporting the feasibility of finerenone use across a broad spectrum of kidney function within indicated ranges, while emphasizing the need for early monitoring in those at highest risk of acute declines. Hyperkalemia remains the principal safety concern with mineralocorticoid receptor antagonism 11 , 15 . In this cohort, serum potassium increased by approximately 0.30 mEq/L; however, hyperkalemia above 5.5 mEq/L occurred in only 4.2% of patients with paired potassium data, and severe hyperkalemia above 6.0 mEq/L was rare (0.8%). When hyperkalemia occurred, management most commonly involved initiation of a potassium binder, and discontinuation rates were low by month 3, with a notable proportion of patients later re-initiated after potassium normalization. Several factors may plausibly contribute to this favorable early potassium profile, including high concomitant use of SGLT2 inhibitors, contemporary diuretic utilization patterns, and common initiation at lower finerenone doses. Collectively, these findings support the feasibility of integrating finerenone into the modern therapeutic “stack” when early potassium surveillance and structured potassium-lowering strategies are applied 17 , 18 . An important practical implication is the generalizability of early finerenone-associated biomarker effects in contemporary care. The cohort reflects routine nephrology practice, with high uptake of background kidney-protective therapy, including near-universal RAS blockade and widespread use of SGLT2 inhibitors 4 – 7 . Early responses were broadly consistent across albuminuria and eGFR strata, and correlations between baseline values and magnitude of response were weak for eGFR and UACR, suggesting that early albuminuria lowering is not limited to a narrow phenotype. In contrast, a more pronounced association between baseline potassium and the change in potassium is consistent with regression toward the mean and underscores the continued importance of baseline potassium as a safety signal. This study has limitations inherent to retrospective observational designs. The absence of a control group limits causal inference and leaves residual confounding, including potential changes in concomitant medications, blood pressure, glycemic control, diet counseling, and laboratory timing that are not fully standardized across centers. Paired laboratory measurements were available in roughly half of the cohort, which may introduce selection bias; documenting baseline differences between patients with and without paired follow-up would strengthen interpretability. Outcomes were not adjudicated. While short-term mortality was low, deaths occurred during follow-up and attribution cannot be established in this design. Finally, the current report focuses on early biomarker trajectories rather than hard kidney or cardiovascular outcomes; longer follow-up is required to assess sustained eGFR slope, hospitalization patterns, and clinical endpoints. In summary, in a large national real-world cohort characterized by contemporary background therapy and high SGLT2 inhibitor use, finerenone initiation was associated with rapid and substantial albuminuria reduction, a small early eGFR dip, and a manageable potassium profile with low rates of severe hyperkalemia and low overall discontinuation. These findings support early integration of finerenone into combination kidney-protective therapy with appropriate laboratory monitoring and proactive hyperkalemia management 17 , 18 . References Liyanage T, Ninomiya T, Jha V et al (2015) Worldwide access to treatment for end-stage kidney disease: a systematic review. Lancet 385(9981):1975–1982 Wu P-P, Kor C-T, Hsieh M-C, Hsieh Y-P (2018) Association between end-stage renal disease and incident diabetes mellitus—A nationwide population-based cohort study. J Clin Med 7(10):343 Campbell RC, Ruggenenti P, Remuzzi G (2003) Proteinuria in diabetic nephropathy: treatment and evolution. Curr Diab Rep 3(6):497–504 Cardiology ACo C, ACo, Association AH (2017) ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults a report of the American College of Cardiology/American Heart Association Task Force on Clinical practice guidelines. Hypertension . 2018;71(6):E13-E115 Care D (2019) Standards of medical care in diabetes 2019. Diabetes Care 42(Suppl 1):S124–S138 Cravedi P, Ruggenenti P, Remuzzi G (2007) Intensified inhibition of renin-angiotensin system: a way to improve renal protection? Curr Hypertens Rep 9(5):430–436 Giglio RV, Patti AM, Rizvi AA et al (2023) Advances in the pharmacological management of diabetic nephropathy: a 2022 international update. Biomedicines 11(2):291 Sternlicht H, Bakris GL (2017) The kidney in hypertension. Med Clin 101(1):207–217 Ando K, Ohtsu H, Uchida S, Kaname S, Arakawa Y, Fujita T (2014) Anti-albuminuric effect of the aldosterone blocker eplerenone in non-diabetic hypertensive patients with albuminuria: a double-blind, randomised, placebo-controlled trial. lancet Diabetes Endocrinol 2(12):944–953 Blasi ER, Rocha R, Rudolph AE, Blomme EA, Polly ML, McMahon EG (2003) Aldosterone/salt induces renal inflammation and fibrosis in hypertensive rats. Kidney Int 63(5):1791–1800 Mehdi UF, Adams-Huet B, Raskin P, Vega GL, Toto RD (2009) Addition of angiotensin receptor blockade or mineralocorticoid antagonism to maximal angiotensin-converting enzyme inhibition in diabetic nephropathy. J Am Soc Nephrol 20(12):2641–2650 Bärfacker L, Kuhl A, Hillisch A et al (2012) Discovery of BAY 94-8862: a nonsteroidal antagonist of the mineralocorticoid receptor for the treatment of cardiorenal diseases. ChemMedChem 7(8):1385–1403 Grune J, Beyhoff N, Smeir E et al (2018) Selective mineralocorticoid receptor cofactor modulation as molecular basis for finerenone’s antifibrotic activity. Hypertension 71(4):599–608 Kolkhof P, Borden SA (2012) Molecular pharmacology of the mineralocorticoid receptor: prospects for novel therapeutics. Mol Cell Endocrinol 350(2):310–317 Pitt B, Zannad F, Remme WJ et al (1999) The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 341(10):709–717 Bakris GL, Agarwal R, Anker SD et al (2019) Design and baseline characteristics of the finerenone in reducing kidney failure and disease progression in diabetic kidney disease trial. Am J Nephrol 50(5):333–344 Agarwal R, Filippatos G, Pitt B et al (2022) Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis. Eur Heart J 43(6):474–484 Bakris GL, Agarwal R, Anker SD et al (2020) Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes. N Engl J Med 383(23):2219–2229 Cahn A, Melzer-Cohen C, Pollack R, Chodick G, Shalev V (2019) Acute renal outcomes with sodium‐glucose co‐transporter‐2 inhibitors: real‐world data analysis. Diabetes Obes Metabolism 21(2):340–348 Additional Declarations The authors declare no competing interests. Cite Share Download PDF Status: Posted Version 1 posted 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. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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-9043582","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":601459667,"identity":"0eccfa14-3e1c-48b3-97c8-a323d375cdbc","order_by":0,"name":"Serap Yadigar","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA9UlEQVRIiWNgGAWjYFAD9saGAwkVDAwGROvg4Tl88MGHMyRpkUhLNpzZRoQW+fbeh58L/tjk2zPkmEnzzjssb87efIDhR8U2nFoMzhw3lp7ZlmbZw3AGqGXbYcOdPccSGHvO3MatRSKNQZq34bABD2MPWAvjhhs5BsyMbbi1yM9/xvyb589/Ax5mHqCWOYftCWphuMHGJs3DdsCAh40N6P2Gw4kEtRicSWOzntmWbMBzhhkYyMfSkzecOZZwEJ9f5NuPMd8u+GNnwD7/ITAqa6xtNxxvPvjgRwUehwEBMxK7GUwewKseTUsdIcWjYBSMglEwAgEAnddZxN27jeYAAAAASUVORK5CYII=","orcid":"https://orcid.org/0000-0002-3156-4883","institution":"Kartal Dr Lütfi Kırdar City Hospital,Department of Nephrology, İstanbul/Turkey","correspondingAuthor":true,"prefix":"","firstName":"Serap","middleName":"","lastName":"Yadigar","suffix":""},{"id":604763842,"identity":"2847d886-44e5-4a53-b317-53781543bb00","order_by":1,"name":"Suat Akgür","email":"","orcid":"https://orcid.org/0000-0003-1745-6744","institution":"Bursa Çekirge State Hospital Nephrology Clinic, Bursa","correspondingAuthor":false,"prefix":"","firstName":"Suat","middleName":"","lastName":"Akgür","suffix":""},{"id":604766047,"identity":"7f05d8d4-6747-4745-8dc2-a1140b7489fe","order_by":2,"name":"Felemez Arslan","email":"","orcid":"","institution":"University of Health Sciences Türkiye, Bakırköy Dr. Sadi Konuk Training and Research Hospital, Clinic of Internal Medicine","correspondingAuthor":false,"prefix":"","firstName":"Felemez","middleName":"","lastName":"Arslan","suffix":""},{"id":604767936,"identity":"4e6e1936-54c4-4b7d-ae8e-cd93ca4ff1ac","order_by":3,"name":"Mehmet Sezen","email":"","orcid":"","institution":"Department of Nephrology Bursa City Hospital Bursa, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"","lastName":"Sezen","suffix":""},{"id":604768155,"identity":"38595ddb-99dc-4366-8efc-3daf124c4a7d","order_by":4,"name":"Büşra Özcan","email":"","orcid":"","institution":"Division of Endocrinology and Metabolism, Ankara Ataturk Sanatoryum Training and Research Hospital, Ankara, Turkey.","correspondingAuthor":false,"prefix":"","firstName":"Büşra","middleName":"","lastName":"Özcan","suffix":""},{"id":604768255,"identity":"f082b063-3995-437d-864f-72d5038b9685","order_by":5,"name":"Elif Yıldırım Ayaz","email":"","orcid":"","institution":"Department of Internal Medicine, Health Sciences University, Sultan 2. Abdülhamid Han Training and Research Hospital, Istanbul, Turkey.","correspondingAuthor":false,"prefix":"","firstName":"Elif","middleName":"Yıldırım","lastName":"Ayaz","suffix":""},{"id":604768256,"identity":"5992c533-17f4-443a-a16f-53a336dd3829","order_by":6,"name":"Betül Doğantekin","email":"","orcid":"","institution":"University of Health Sciences Sultan Abdulhamid Han Training and Research Hospital, Department of Internal Medicine, Kadıköy, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Betül","middleName":"","lastName":"Doğantekin","suffix":""},{"id":604768476,"identity":"da4c15fb-f704-4410-9679-b58cbfd162c8","order_by":7,"name":"İlker Atay","email":"","orcid":"","institution":"Division of Nephrology, Dokuz Eylül University School of Medicine, İzmir, Turkiye.","correspondingAuthor":false,"prefix":"","firstName":"İlker","middleName":"","lastName":"Atay","suffix":""},{"id":604769072,"identity":"278c4302-100e-43ea-9a4a-706e4bb53973","order_by":8,"name":"Serpil Müge Değer","email":"","orcid":"","institution":"Division of Nephrology, Dokuz Eylül University School of Medicine, İzmir, Turkiye.","correspondingAuthor":false,"prefix":"","firstName":"Serpil","middleName":"Müge","lastName":"Değer","suffix":""},{"id":604769137,"identity":"56356c3d-f7f5-4019-9fe3-4d30577505eb","order_by":9,"name":"Mustafa Demir","email":"","orcid":"","institution":"Health Sciences University Kayseri City Hospital Nephrology Clinic, Kayseri Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Mustafa","middleName":"","lastName":"Demir","suffix":""},{"id":604769213,"identity":"a661af06-05cd-4685-9c84-57538a9de325","order_by":10,"name":"Sümeyra Koyuncu","email":"","orcid":"","institution":"Health Sciences University Kayseri City Hospital Nephrology Clinic, Kayseri Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Sümeyra","middleName":"","lastName":"Koyuncu","suffix":""},{"id":604769231,"identity":"5e4934f8-0de6-4bf0-b006-4c7f91bbe79f","order_by":11,"name":"Üstün Yılmaz","email":"","orcid":"","institution":"Health Sciences University Antalya Training and Research Hospital Nephrology Clinic, Antalya, Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Üstün","middleName":"","lastName":"Yılmaz","suffix":""},{"id":604769410,"identity":"cf7a3be0-190e-4a65-a4fb-7c95e9c80eea","order_by":12,"name":"Ayça İnci","email":"","orcid":"","institution":"Akdeniz University Faculty of Medicine ,Department of Internal Medicine, Division of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Ayça","middleName":"","lastName":"İnci","suffix":""},{"id":604769632,"identity":"4a18b970-3ffc-434b-8785-814d98ef0db5","order_by":13,"name":"Hülya Çolak","email":"","orcid":"","institution":"Health Sciences University İzmir City Hospital Nephrology Clinic, İzmir, Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Hülya","middleName":"","lastName":"Çolak","suffix":""},{"id":604769761,"identity":"41db5e74-91c3-48e5-b302-3a2eb5eebc7d","order_by":14,"name":"Bülent Demirelli","email":"","orcid":"","institution":"Marmara University Asaf Ataseven Training and Research Hospital, Nephrology Clinic, İstanbul Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Bülent","middleName":"","lastName":"Demirelli","suffix":""},{"id":604771250,"identity":"0cd5f2a7-279d-4db9-9b46-e81b857c48a7","order_by":15,"name":"Serhan Tuğlular","email":"","orcid":"","institution":"Marmara University School of Medicine, Dept of Internal Medicine, Division of Nephrology, İstanbul Türkiye .","correspondingAuthor":false,"prefix":"","firstName":"Serhan","middleName":"","lastName":"Tuğlular","suffix":""},{"id":604772636,"identity":"f7aa7f4c-b602-460b-a24a-dc221366fd78","order_by":16,"name":"Ebru Gök Oğuz","email":"","orcid":"","institution":"Department of Nephrology, University of Health Sciences, Etlik City Hospital, Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Ebru","middleName":"Gök","lastName":"Oğuz","suffix":""},{"id":604773271,"identity":"2b4657b4-f4e0-4527-a794-6b499f099880","order_by":17,"name":"Mehmet Deniz Aylı","email":"","orcid":"","institution":"Depertment of Nephrology, University of Health Sciences, Etlik City Hospital, Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"Deniz","lastName":"Aylı","suffix":""},{"id":604773394,"identity":"3dd7aca2-5c9b-4bb7-b335-5a716e3dad06","order_by":18,"name":"Ezgi Avanaz","email":"","orcid":"","institution":"Health Sciences University, Antalya City Hospital Department of Nephrology Antalya, Turkiye.","correspondingAuthor":false,"prefix":"","firstName":"Ezgi","middleName":"","lastName":"Avanaz","suffix":""},{"id":604773451,"identity":"747bc98f-90aa-4432-af83-819f5827e408","order_by":19,"name":"Fatih Yılmaz","email":"","orcid":"","institution":"Health Sciences University, Antalya City Hospital Department of Nephrology Antalya,Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Fatih","middleName":"","lastName":"Yılmaz","suffix":""},{"id":604773552,"identity":"79326cad-57ee-45ef-b08e-f778bf1039a9","order_by":20,"name":"Beyza Doğan","email":"","orcid":"","institution":"Health Sciences University Konya City Hospital Nephrology Clinic, Konya Turkiye. Department of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Beyza","middleName":"","lastName":"Doğan","suffix":""},{"id":604773673,"identity":"7a5879fe-a239-4a25-990d-18ec005792c2","order_by":21,"name":"Süleyman Karaköse","email":"","orcid":"","institution":"Health Sciences University Konya City Hospital Nephrology Clinic, KonyaTürkiye","correspondingAuthor":false,"prefix":"","firstName":"Süleyman","middleName":"","lastName":"Karaköse","suffix":""},{"id":604777574,"identity":"9654965f-f371-4947-9d0c-c22a6286bbb5","order_by":22,"name":"Mine Şebnem Karakan","email":"","orcid":"","institution":"Department of Nephrology, Yıldırım Beyazıt Univesity, Ankara, Turkiye","correspondingAuthor":false,"prefix":"","firstName":"Mine","middleName":"Şebnem","lastName":"Karakan","suffix":""},{"id":604777575,"identity":"63dd078d-fba7-4489-8da1-48aa14e458c1","order_by":23,"name":"Bahar Gürlek Demirci","email":"","orcid":"","institution":"Department of Nephrology, Yıldırım Beyazıt Univesity, Ankara, Turkiye","correspondingAuthor":false,"prefix":"","firstName":"Bahar","middleName":"Gürlek","lastName":"Demirci","suffix":""},{"id":604777748,"identity":"930c3940-b73c-47e7-a638-b463120f8cc2","order_by":24,"name":"Kültigin Türkmen","email":"","orcid":"","institution":"Necmettin Erbakan University Faculty of Medicine Department of Internal Medicine Division of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Kültigin","middleName":"","lastName":"Türkmen","suffix":""},{"id":604777993,"identity":"a6d41610-0103-473d-bc6a-f97320478a84","order_by":25,"name":"İsmail Baloğlu","email":"","orcid":"","institution":"Necmettin Erbakan University, Medical School,","correspondingAuthor":false,"prefix":"","firstName":"İsmail","middleName":"","lastName":"Baloğlu","suffix":""},{"id":604778564,"identity":"18a668f7-1665-4bcd-b225-849486c89642","order_by":26,"name":"Mehmet Batmazoğlu","email":"","orcid":"","institution":"Department of Nephrology, Denizli State Hospital Denizli, Turkiye.","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"","lastName":"Batmazoğlu","suffix":""},{"id":604778565,"identity":"9f598e77-fc82-41a0-a708-3a496c37d830","order_by":27,"name":"Mehmet Mert","email":"","orcid":"","institution":"Denizli Özel Sağlık Hastanesi","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"","lastName":"Mert","suffix":""},{"id":604778634,"identity":"370ed1de-2948-4218-a0a3-24054de37185","order_by":28,"name":"Emre Aydın","email":"","orcid":"","institution":"Department of Nephrology, Faculty of Medicine, Dicle University, Diyarbakır.","correspondingAuthor":false,"prefix":"","firstName":"Emre","middleName":"","lastName":"Aydın","suffix":""},{"id":604781578,"identity":"7ea69478-540b-4b21-866b-47685fb9e8eb","order_by":29,"name":"Fatma Yılmaz Aydın","email":"","orcid":"","institution":"Department of Internal Medicine, Faculty of Medicine, Dicle University, Diyarbakır.","correspondingAuthor":false,"prefix":"","firstName":"Fatma","middleName":"Yılmaz","lastName":"Aydın","suffix":""},{"id":604782239,"identity":"c95e5d20-d590-4948-a217-b207040e85a0","order_by":30,"name":"Ergün Parmaksız","email":"","orcid":"","institution":"Kartal Dr Lutfi Kirdar City Hospital, Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Ergün","middleName":"","lastName":"Parmaksız","suffix":""},{"id":604782327,"identity":"9258d98b-ac3a-425c-9b66-bc2e1176885b","order_by":31,"name":"Pınar Özdemir","email":"","orcid":"","institution":"Kartal Dr Lutfi Kirdar City Hospital, Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Pınar","middleName":"","lastName":"Özdemir","suffix":""},{"id":604782391,"identity":"6cc26950-4458-49e0-bb2c-b940b2f6df2c","order_by":32,"name":"Bartu Ediz","email":"","orcid":"","institution":"Kartal Dr Lutfi Kirdar City Hospital, Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Bartu","middleName":"","lastName":"Ediz","suffix":""},{"id":604783146,"identity":"6f3b9952-f4ab-45bb-8b0e-3f9def285b1f","order_by":33,"name":"Zeki Aydın","email":"","orcid":"","institution":"Department of Nephrology, University of Health Sciences, Darıca Farabi Training and Research Hospital, Kocaeli, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Zeki","middleName":"","lastName":"Aydın","suffix":""},{"id":604783170,"identity":"00a873c3-70e4-4d24-9c7d-55ef62520d00","order_by":34,"name":"Mehmet Emin Demir","email":"","orcid":"","institution":"Atılım University, School of Medicine, Medicana International Ankara Hospital, Department of Nephrology, Internal Medicine and Organ Transplantation, Ankara, Türkiye.","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"Emin","lastName":"Demir","suffix":""},{"id":605174006,"identity":"22890ceb-ec0e-4e8a-9b69-d82850403511","order_by":35,"name":"Siren Sezer","email":"","orcid":"","institution":"Atılım University, School of Medicine, Medicana International Ankara Hospital, Department of Nephrology, Internal Medicine and Organ Transplantation, Ankara, Türkiye.","correspondingAuthor":false,"prefix":"","firstName":"Siren","middleName":"","lastName":"Sezer","suffix":""},{"id":604793078,"identity":"c9d5dcaa-e4d7-4410-a811-8bd463a0e558","order_by":36,"name":"Suat Ünver","email":"","orcid":"","institution":"Acıbadem Hospital, Department of Internal Medicine and Nephrology, Istanbul, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Suat","middleName":"","lastName":"Ünver","suffix":""},{"id":604795619,"identity":"e8bee951-ce70-4c09-979a-06678d758460","order_by":37,"name":"Öznur Baykal","email":"","orcid":"","institution":"Basaksehir Cam and Sakura City Hospital, Department of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Öznur","middleName":"","lastName":"Baykal","suffix":""},{"id":604796606,"identity":"89fb1aa9-000c-4641-9e6b-32faea161226","order_by":38,"name":"Beril Akman","email":"","orcid":"","institution":"Acıbadem Hospital, Department of Internal Medicine and Nephrology, Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Beril","middleName":"","lastName":"Akman","suffix":""},{"id":604796607,"identity":"cf216130-2653-4b5d-a2d1-ac3ce9c3d3df","order_by":39,"name":"Atila Altuntaş","email":"","orcid":"","institution":"Suleyman Demirel University Faculty of Medicine, Department of Internal Medicine, Division of Nephrology.","correspondingAuthor":false,"prefix":"","firstName":"Atila","middleName":"","lastName":"Altuntaş","suffix":""},{"id":604796875,"identity":"7e1fd68a-3817-4f30-b108-c876d70c10e6","order_by":40,"name":"Mahmud İslam","email":"","orcid":"","institution":"Sakarya university, school of medicine; Department of nephrology.","correspondingAuthor":false,"prefix":"","firstName":"Mahmud","middleName":"","lastName":"İslam","suffix":""},{"id":604796876,"identity":"f10c1ad2-33c5-427b-9503-24333c2f6213","order_by":41,"name":"Fatma Sibel Yücel Koçak","email":"","orcid":"","institution":"Department of Nephrology, Health Sciences University, Bakirkoy Dr. Sadi Konuk Training and Research Hospital, Istanbul, Turkey.","correspondingAuthor":false,"prefix":"","firstName":"Fatma","middleName":"Sibel Yücel","lastName":"Koçak","suffix":""},{"id":604796933,"identity":"3dbeb8e7-24c8-4deb-a54e-b0b535aabebe","order_by":42,"name":"Meral Mert","email":"","orcid":"","institution":"Health Sciences University Bakırköy Dr. Sadi Konuk Training and Research Hospital Endocrinology Clinic, İstanbul, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Meral","middleName":"","lastName":"Mert","suffix":""},{"id":604797125,"identity":"8695ded5-c654-4127-a745-760b19600e23","order_by":43,"name":"Belda Dursun","email":"","orcid":"","institution":"Pamukkale University, Medical School, Nephrology Department","correspondingAuthor":false,"prefix":"","firstName":"Belda","middleName":"","lastName":"Dursun","suffix":""},{"id":604797222,"identity":"2f48d42e-1b96-4b5f-980d-e9a5c49076a1","order_by":44,"name":"Necmi Eren","email":"","orcid":"","institution":"Kocaeli University Faculty of Medicine, Department of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Necmi","middleName":"","lastName":"Eren","suffix":""},{"id":604797284,"identity":"2b731bd9-f6a3-47b6-973c-c0bd2ce2df25","order_by":45,"name":"Simge Bardak Demir","email":"","orcid":"","institution":"Ankara Yildirim Beyazit University Yenimahalle Education and Research Hospital, Department of Nephrology, Ankara","correspondingAuthor":false,"prefix":"","firstName":"Simge","middleName":"Bardak","lastName":"Demir","suffix":""},{"id":604797373,"identity":"a853e3d1-8085-4d27-825d-047eb504ee8e","order_by":46,"name":"Alper Tuna Güven","email":"","orcid":"","institution":"Başkent University Faculty of Medicine Deparment of Internal Medicine, Division of General Internal Medicine, Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Alper","middleName":"Tuna","lastName":"Güven","suffix":""},{"id":604797455,"identity":"1e603d5a-ed11-402b-9d15-7098c6210a77","order_by":47,"name":"Ayşe Bilgiç","email":"","orcid":"","institution":"Ankara Medical Park Hospital, Department of Nephrology,Ankara","correspondingAuthor":false,"prefix":"","firstName":"Ayşe","middleName":"","lastName":"Bilgiç","suffix":""},{"id":604797654,"identity":"54c83a09-d319-41a5-a35c-ee109cc813e0","order_by":48,"name":"Arda Erdut","email":"","orcid":"","institution":"Hacettepe University Faculty of Medicine, Department of Internal Medicine, Division of Nephrology Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Arda","middleName":"","lastName":"Erdut","suffix":""},{"id":604799743,"identity":"16bbb967-a5a9-46c7-bcad-31fbbcff1e84","order_by":49,"name":"Gülşah Keskin","email":"","orcid":"","institution":"University of Health Sciences, Haydarpaşa Numune Training and Research Hospital, Division of Endocrinology and Metabolism","correspondingAuthor":false,"prefix":"","firstName":"Gülşah","middleName":"","lastName":"Keskin","suffix":""},{"id":605284054,"identity":"0172f931-2017-454c-993d-ba4a8943be9e","order_by":50,"name":"Ahmet Ziya Şahin","email":"","orcid":"","institution":"Adana Faculty of Medicine, Department of Nephrology, University of Health Sciences, Adana, Turkey.","correspondingAuthor":false,"prefix":"","firstName":"Ahmet","middleName":"Ziya","lastName":"Şahin","suffix":""},{"id":605284055,"identity":"d50a774a-7fb5-458d-a36c-89f2b3221e25","order_by":51,"name":"Mehmet Horoz","email":"","orcid":"","institution":"Adana Faculty of Medicine, Department of Nephrology, University of Health Sciences, Adana, Turkey.","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"","lastName":"Horoz","suffix":""},{"id":605284056,"identity":"3cca337e-9760-4637-b92a-3f6c61eef43d","order_by":52,"name":"Merve Tekinyıldız","email":"","orcid":"","institution":"Ankara Training and Research Hospital, Department of Internal Medicine, Division of Nephrology Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Merve","middleName":"","lastName":"Tekinyıldız","suffix":""},{"id":605284421,"identity":"790f023b-fec5-4ea1-a8e5-b9d3f276b162","order_by":53,"name":"Murat Durunay","email":"","orcid":"","institution":"Ankara Training and Research Hospital, Department of Internal Medicine, Division of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Murat","middleName":"","lastName":"Durunay","suffix":""},{"id":605284422,"identity":"f7941522-6e15-413e-8e97-bbc394405f75","order_by":54,"name":"Serkan Feyyaz Yalın","email":"","orcid":"","institution":"Kartal Dr Lutfi Kirdar City Hospital, Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Serkan","middleName":"Feyyaz","lastName":"Yalın","suffix":""},{"id":605290835,"identity":"7bd7cd92-e886-47e4-ba32-9b3e4a9cdf97","order_by":55,"name":"Murat Altunok","email":"","orcid":"","institution":"Department of Nephrology, Trabzon Kanuni Training and Research Hospital, Yomra, Trabzon","correspondingAuthor":false,"prefix":"","firstName":"Murat","middleName":"","lastName":"Altunok","suffix":""},{"id":605290836,"identity":"7320cc71-7b1e-46ab-a6df-b319a5e483f8","order_by":56,"name":"Funda Sarı","email":"","orcid":"","institution":"Akdeniz University Faculty of Medicine, Department of Internal Medicine","correspondingAuthor":false,"prefix":"","firstName":"Funda","middleName":"","lastName":"Sarı","suffix":""},{"id":605290837,"identity":"e3295e42-5726-47ac-8bca-019282c6e1bf","order_by":57,"name":"Ramazan Sarı","email":"","orcid":"","institution":"Akdeniz University Faculty of Medicine, Department of Internal Medicine Division of Endocrinology and Metabolism","correspondingAuthor":false,"prefix":"","firstName":"Ramazan","middleName":"","lastName":"Sarı","suffix":""},{"id":605291366,"identity":"ca3b13c1-c524-4eb3-9062-ec1f02dcc7b0","order_by":58,"name":"Dilek Torun","email":"","orcid":"","institution":"Baskent University School of Medicine Adana Dr Turgut Noyan Teaching and Research Center Department of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Dilek","middleName":"","lastName":"Torun","suffix":""},{"id":605293933,"identity":"1cb28fe8-0681-4cc4-81e6-7a42bedaf959","order_by":59,"name":"Serdar Kahvecioğlu","email":"","orcid":"","institution":"Health Sciences University, Bursa Yuksek Ihtisas Training and Research Hospital Nephrology Clinic, Bursa, Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Serdar","middleName":"","lastName":"Kahvecioğlu","suffix":""},{"id":605293934,"identity":"8519e04b-2a30-4019-8037-b5e9993bd556","order_by":60,"name":"Serap Yalçınkaya","email":"","orcid":"","institution":"Health Sciences University, Bursa Yuksek Ihtisas Training and Research Hospital Nephrology Clinic, Bursa, Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Serap","middleName":"","lastName":"Yalçınkaya","suffix":""},{"id":605293935,"identity":"5fb93296-a04e-4cb5-adc2-3af62da1d1cc","order_by":61,"name":"Tülin Akagün","email":"","orcid":"","institution":"Giresun University Faculty of Medicine, Nephrology Clinic","correspondingAuthor":false,"prefix":"","firstName":"Tülin","middleName":"","lastName":"Akagün","suffix":""},{"id":605293936,"identity":"ed438aa6-4f25-4fed-b78c-74894ebd8a53","order_by":62,"name":"Hüseyin Çelik","email":"","orcid":"","institution":"Bursa Acıbadem Hospital,Department of Nephrology, Bursa Turkey","correspondingAuthor":false,"prefix":"","firstName":"Hüseyin","middleName":"","lastName":"Çelik","suffix":""},{"id":605293937,"identity":"85c9a136-59ca-4372-a60a-bfbdf6081b5d","order_by":63,"name":"Sinan Kazan","email":"","orcid":"","institution":"Afyonkarahisar Health Sciences Univeristy, Department of Nephrology, Afyonkarahisar Turkey","correspondingAuthor":false,"prefix":"","firstName":"Sinan","middleName":"","lastName":"Kazan","suffix":""},{"id":605293938,"identity":"41d52385-0dc8-49b0-b1c5-ec3a4df8090f","order_by":64,"name":"İlyas Öztürk","email":"","orcid":"","institution":"Kahramanmaras Necip Fazil City Hospital, Department of Nephrology","correspondingAuthor":false,"prefix":"","firstName":"İlyas","middleName":"","lastName":"Öztürk","suffix":""},{"id":605294828,"identity":"7ce45183-7167-49f0-8692-3cb9c7d4e175","order_by":65,"name":"Mehmet Polat","email":"","orcid":"","institution":"Republic of Türkiye Ministry of Health Karabük Training and Research Hospital,Department of Nephrology,","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"","lastName":"Polat","suffix":""},{"id":605294829,"identity":"ecdf7334-d8b7-46ff-83d7-48e95043055e","order_by":66,"name":"Mehmet Fethullah Aydın","email":"","orcid":"","institution":"Department of Nephrology, Balıkesir Atatürk City Hospital, Balıkesir, Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Mehmet","middleName":"Fethullah","lastName":"Aydın","suffix":""},{"id":605294830,"identity":"21b51163-1444-409d-affa-806ced585172","order_by":67,"name":"Meral Meşe","email":"","orcid":"","institution":"Kartal Dr Lutfi Kirdar City Hospital, Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Meral","middleName":"","lastName":"Meşe","suffix":""},{"id":605294831,"identity":"5b10958c-9530-4a2c-a44f-d675400a739c","order_by":68,"name":"Melike Hazal Yavuz Umut","email":"","orcid":"","institution":"Kartal Dr Lutfi Kirdar City Hospital, Nephrology","correspondingAuthor":false,"prefix":"","firstName":"Melike","middleName":"Hazal Yavuz","lastName":"Umut","suffix":""},{"id":605294832,"identity":"38caf909-5b72-4953-903c-4be2af968f14","order_by":69,"name":"Asil Demirezen","email":"","orcid":"","institution":"Gazi University Faculty of Medicine, Department of Nephrology Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Asil","middleName":"","lastName":"Demirezen","suffix":""},{"id":605294833,"identity":"f4ee800f-c490-420a-966b-78da42c02dd3","order_by":70,"name":"Ülver Derici","email":"","orcid":"","institution":"Gazi University Faculty of Medicine, Department of Nephrology ,Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Ülver","middleName":"","lastName":"Derici","suffix":""},{"id":605297240,"identity":"ed723e41-c792-42b3-941e-2116992e81b4","order_by":71,"name":"Eda Altun","email":"","orcid":"","institution":"Kocaeli City Hospital, Department of Nephrology, Kocaeli, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Eda","middleName":"","lastName":"Altun","suffix":""},{"id":605297241,"identity":"684ed2ad-3b68-47b1-91d1-b0d0949e1b07","order_by":72,"name":"Serkan Bakırdöğen","email":"","orcid":"","institution":"Canakkale Onsekiz Mart University School of Medicine Department of Internal Medicine Division of Nephrology, Canakkale, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Serkan","middleName":"","lastName":"Bakırdöğen","suffix":""},{"id":605297242,"identity":"6e0d15a5-5d1b-4c42-8d49-acbb45f82ac3","order_by":73,"name":"Ekrem Kara","email":"","orcid":"","institution":"Recep Tayyip Erdogan University, Faculty of Medicine, Department of Internal Medicine, Division of Nephrology, Rize ,Turkey","correspondingAuthor":false,"prefix":"","firstName":"Ekrem","middleName":"","lastName":"Kara","suffix":""},{"id":605301733,"identity":"94be0527-1ee6-44f7-b0f1-cc14eb6b6ff6","order_by":74,"name":"Cüneyt Akgöl","email":"","orcid":"","institution":"Burdur State Hospital, Nephrology, Burdur Turkey","correspondingAuthor":false,"prefix":"","firstName":"Cüneyt","middleName":"","lastName":"Akgöl","suffix":""},{"id":605301734,"identity":"d7de57ec-3783-4e41-9a2e-6f6845016f3f","order_by":75,"name":"Mahmut Başar Aykent","email":"","orcid":"","institution":"Ministry of Health Şişli Hamidiye Etfal Training and Research Hospital, Department of Nephrology, Istanbul, Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Mahmut","middleName":"Başar","lastName":"Aykent","suffix":""},{"id":605301735,"identity":"0f0dd284-86fb-4ae2-9a92-b09cac4c105b","order_by":76,"name":"Ali İlter","email":"","orcid":"","institution":"Nephrology Clinic, Kütahya Evliya Çelebi Education and Research Hospital,Kütahya, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Ali","middleName":"","lastName":"İlter","suffix":""},{"id":605301736,"identity":"15dc2807-ee4c-46e1-bdb7-0e5399fd4928","order_by":77,"name":"Ahmet Ekmekçi","email":"","orcid":"","institution":"Department of Cardiology, Faculty of Medicine, Bahçeşehir University, Istanbul 34353, Türkiye Memmorial Göztepe Hospital","correspondingAuthor":false,"prefix":"","firstName":"Ahmet","middleName":"","lastName":"Ekmekçi","suffix":""},{"id":605301737,"identity":"03f97477-78b5-4d43-bf93-f158b9198f68","order_by":78,"name":"Sena Ulu","email":"","orcid":"","institution":"Department of Nephrology, Health Sciences University, Sultan Abdülhamid Han Training and Research Hospital, Istanbul, Turkey.","correspondingAuthor":false,"prefix":"","firstName":"Sena","middleName":"","lastName":"Ulu","suffix":""},{"id":605301738,"identity":"1f2fdeff-1148-485f-8377-8aa5312c839d","order_by":79,"name":"Bilge Özlü Başer","email":"","orcid":"","institution":"Mimar Sinan Fine Arts University Department of Statistics","correspondingAuthor":false,"prefix":"","firstName":"Bilge","middleName":"Özlü","lastName":"Başer","suffix":""},{"id":605301739,"identity":"91463d13-12b8-4694-973e-cd5903f049ba","order_by":80,"name":"Mustafa Arıcı","email":"","orcid":"","institution":"Hacettepe University Faculty of Medicine, Department of Internal Medicine, Division of Nephrology Ankara, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Mustafa","middleName":"","lastName":"Arıcı","suffix":""},{"id":605301740,"identity":"baf93754-af91-47a7-bcf9-3b4c0de193c6","order_by":81,"name":"Elif Arı Bakır","email":"","orcid":"","institution":"Department of Nephrology, University of Health Sciences, Kartal Dr Lutfi Kirdar City Hospital, İstanbul, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Elif","middleName":"Arı","lastName":"Bakır","suffix":""},{"id":605301741,"identity":"0ed8f9be-a259-4613-8f20-4b0f3370b69b","order_by":82,"name":"Erkan Şengül","email":"","orcid":"","institution":"Department of Nephrology, University of Health Sciences, Kocaeli City Hospital, Kocaeli, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Erkan","middleName":"","lastName":"Şengül","suffix":""}],"badges":[],"createdAt":"2026-03-05 19:06:57","currentVersionCode":1,"declarations":{"humanSubjects":true,"vertebrateSubjects":false,"conflictsOfInterestStatement":false,"humanSubjectEthicalGuidelines":true,"humanSubjectConsent":true,"humanSubjectClinicalTrial":false,"humanSubjectCaseReport":false,"vertebrateSubjectEthicalGuidelines":false},"doi":"10.21203/rs.3.rs-9043582/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9043582/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":104874261,"identity":"0aa2de41-524c-4262-a2f1-2991745081b1","added_by":"auto","created_at":"2026-03-18 08:29:40","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":106712,"visible":true,"origin":"","legend":"\u003cp\u003ePrimary Outcomes—Changes in eGFR, Serum Potassium, and Albuminuria from Baseline to Months 1-3. Paired changes in primary endpoints from baseline to months 1-3. Panel A displays eGFR changes (n=571) with individual patient trajectories (gray lines) and mean ± SE (red). Mean eGFR declined by 2.34 mL/min/1.73m² (p\u0026lt;0.001). Panel B shows serum potassium changes (n=646) with a mean increase of 0.30 mEq/L (p\u0026lt;0.001); the dashed line indicates the hyperkalemia threshold (5.5 mEq/L). Panel C displays albuminuria changes on a log scale (n=474), with a 40.1% median reduction (p\u0026lt;0.001).\u003c/p\u003e","description":"","filename":"627ccdba1c294930b6648f1dc6bae5ef.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9043582/v1/eb1297ea6fe8b24785ac16d8.jpeg"},{"id":104874227,"identity":"90f14827-80d0-4088-8147-c2c9b2781bd2","added_by":"auto","created_at":"2026-03-18 08:29:35","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":103651,"visible":true,"origin":"","legend":"\u003cp\u003eLinear Mixed Model Results—Individual Trajectories and Model Predictions. LMM results for all three primary endpoints, displaying individual patient trajectories (gray lines), observed mean ± SE (colored markers), and LMM-predicted population trajectory (dashed red line). The near-perfect concordance between LMM predictions and observed means demonstrates the robustness of primary findings.\u003c/p\u003e","description":"","filename":"b0b51de504364e8481156301cc32dee9.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9043582/v1/9b108880ad1ec0e29e3ff76a.jpeg"},{"id":104874294,"identity":"974f6327-2d99-40cf-a609-e224c6e7e99b","added_by":"auto","created_at":"2026-03-18 08:29:51","extension":"jpeg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":90534,"visible":true,"origin":"","legend":"\u003cp\u003eSubgroup Consistency—Treatment Response Across Patient Populations. Consistency of treatment response across predefined subgroups. Panel A shows eGFR decline stratified by baseline eGFR category. Panel B displays albuminuria reduction by baseline category (microalbuminuria \u0026lt;300 mg/g, n=109; macroalbuminuria ≥300 mg/g, n=366).\u003c/p\u003e","description":"","filename":"c7004e83ac754474a61b14a4d47e65f3.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9043582/v1/c60b2728768691f60f5d254e.jpeg"},{"id":104874224,"identity":"53886ce2-56ec-4f2e-a601-f5cefe566aed","added_by":"auto","created_at":"2026-03-18 08:29:33","extension":"jpeg","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":90534,"visible":true,"origin":"","legend":"\u003cp\u003eCorrelation Analysis—Baseline Independence of Treatment Response. Relationship between baseline values and magnitude of treatment response using Spearman’s rank correlation. Panel A: baseline eGFR vs. eGFR change (ρ=-0.145, p=0.001). Panel B: baseline K⁺ vs. K⁺ change (ρ=-0.419, p\u0026lt;0.001). Panel C: baseline log-UACR vs. log-UACR change (ρ=-0.034, p=0.458).\u003c/p\u003e","description":"","filename":"c7004e83ac754474a61b14a4d47e65f3.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9043582/v1/e0255262136ab49c5374fff9.jpeg"},{"id":104874225,"identity":"0705b903-90a1-4c0e-9262-7ac597a8feee","added_by":"auto","created_at":"2026-03-18 08:29:34","extension":"jpeg","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":97351,"visible":true,"origin":"","legend":"\u003cp\u003eHyperkalemia Management and Finerenone Discontinuation. Panel A shows management strategies for 27 patients who developed hyperkalemia (K⁺ \u0026gt;5.5 mEq/L). Panel B displays reasons for finerenone discontinuation among 39 patients.\u003c/p\u003e","description":"","filename":"e6376ca4de37404895bf739a1dbb63dc.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9043582/v1/efbc9664087566b89d5a6d65.jpeg"},{"id":104874298,"identity":"b0c3b2bf-ce8c-4509-8287-22cb4a3a068c","added_by":"auto","created_at":"2026-03-18 08:29:56","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1451704,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9043582/v1/b48cff0f-8175-4930-ab29-22151dd3c86c.pdf"}],"financialInterests":"The authors declare no competing interests.","formattedTitle":"\u003cp\u003e\u003cstrong\u003eReal-World Effects of Finerenone in Diabetics Kidney\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDisease: Data From Fine-Turk Study\u003c/strong\u003e\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eChronic kidney disease (CKD) remains a major global health burden, and type 2 diabetes (T2D) is the leading cause of kidney failure worldwide \u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e. Over the past decades \u003csup\u003e\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u003c/sup\u003e, renin-angiotensin system (RAS) inhibition has been the foundation of kidney protection in albuminuric diabetic CKD \u003csup\u003e\u003cspan additionalcitationids=\"CR5\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e, and sodium-glucose cotransporter 2 (SGLT2) inhibitors have further reduced cardiovascular events and slowed CKD progression \u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e. Nevertheless, a substantial residual risk persists, and many patients continue to have clinically relevant albuminuria despite guideline-directed therapy \u003csup\u003e\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e.Mineralocorticoid receptor overactivation contributes to inflammation and fibrosis in diabetic CKD. Although steroidal mineralocorticoid receptor antagonists can reduce albuminuria, their use is often limited by hyperkalemia and endocrine adverse effects \u003csup\u003e\u003cspan additionalcitationids=\"CR10\" citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u003c/sup\u003e. Finerenone is a selective nonsteroidal mineralocorticoid receptor antagonist that provides anti-inflammatory and anti-fibrotic effects with fewer endocrine-related adverse events \u003csup\u003e\u003cspan additionalcitationids=\"CR13 CR14\" citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u003c/sup\u003e. In the phase 3 FIDELIO-DKD and FIGARO-DKD trials, finerenone reduced the risk of kidney disease progression and cardiovascular events, with consistent cardiorenal benefits in the pooled FIDELITY analysis \u003csup\u003e\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e\u003c/sup\u003e. However, uptake of SGLT2 inhibitors was low in the pivotal trials, and contemporary real-world evidence, particularly from settings with widespread SGLT2 inhibitor use, remains limited.\u003c/p\u003e \u003cp\u003eBecause finerenone dosing and continuation decisions depend on early monitoring of eGFR and serum potassium, real-world trajectories in the first months after initiation are clinically important. The FINE TURK cohort was established to quantify early changes in eGFR, urinary albumin-to-creatinine ratio, and serum potassium at 1 and 3 months after initiation of finerenone in adults with T2D and CKD across multiple centers in Turkey and to describe hyperkalemia management, hospitalization events, and determinants of short-term responses.\u003c/p\u003e"},{"header":"MATERIALS AND METHODS","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy Design and Population\u003c/h2\u003e \u003cp\u003eThis multicenter, retrospective cohort study evaluated the early efficacy and safety of finerenone in patients with type 2 diabetes mellitus and chronic kidney disease (CKD) receiving contemporary kidney-protective therapy. Data were collected from 56 nephrology centers across T\u0026uuml;rkiye between January 2025 and June 2025. The study was reported in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines and conducted in accordance with the Declaration of Helsinki. All participating centers obtained institutional review board approval, and informed consent was waived due to the retrospective nature of the study and the use of de-identified clinical data.\u003c/p\u003e \u003cp\u003eWe included adults aged\u0026thinsp;\u0026ge;\u0026thinsp;18 years with established type 2 diabetes mellitus and CKD who initiated finerenone for kidney protection during the study period. Patients were excluded if baseline or follow-up laboratory measurements were substantially incomplete. Of 1,168 patients screened, 77 were excluded due to insufficient data, yielding a final cohort of 1,091.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eData Collection\u003c/h3\u003e\n\u003cp\u003eStandardized data collection protocols were implemented across all participating centers. Baseline demographic data included age, sex, body mass index, and comorbidities, including hypertension, cardiovascular disease, and diabetes duration. Concomitant medications were systematically recorded, including renin-angiotensin system (RAS) inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide 1 receptor agonists, diuretics, and lipid-lowering therapies. Laboratory measurements were obtained at baseline and approximately 1\u0026ndash;3 months thereafter, in accordance with routine clinical practice protocols at each center. Measured parameters included serum creatinine, estimated glomerular filtration rate (eGFR, calculated using the CKD-EPI equation), serum potassium, and urinary albumin-to-creatinine ratio (UACR). Finerenone was initiated at 10 mg or 20 mg once daily according to clinical judgment, baseline eGFR, and serum potassium levels. Dose adjustments and discontinuation were managed by treating physicians according to clinical response and tolerability.\u003c/p\u003e\n\u003ch3\u003eOutcomes\u003c/h3\u003e\n\u003cp\u003ePrimary endpoints were changes in eGFR (mL/min/1.73m\u0026sup2;), serum potassium (mEq/L), and UACR (mg/g) from baseline to months 1\u0026ndash;3. Secondary endpoints included the incidence and severity of hyperkalemia, management strategies employed, reasons for finerenone discontinuation and reinitiation, hospitalizations, and all-cause mortality.\u003c/p\u003e \u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003eStatistical Analysis\u003c/h2\u003e \u003cp\u003eAll continuous variables were assessed for normality using the Shapiro-Wilk test. As all primary variables and their changes from baseline were found to be non-normally distributed (Shapiro-Wilk p\u0026thinsp;\u0026lt;\u0026thinsp;0.001 for all), non-parametric tests were used as the primary analytical approach, with parametric tests reported in parallel. Continuous variables are presented as median [interquartile range (IQR)] or mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation (SD) as appropriate, and categorical variables as counts and percentages.\u003c/p\u003e \u003cp\u003eChanges from baseline to months 1\u0026ndash;3 were evaluated using the Wilcoxon signed-rank test as the primary analysis and paired t-tests as a secondary analysis. Effect sizes were calculated using Cohen\u0026rsquo;s d. For albuminuria, which exhibited a highly right-skewed distribution, analyses were performed on both raw and natural log-transformed data to ensure robustness. Two-tailed p-values\u0026thinsp;\u0026lt;\u0026thinsp;0.05 were considered statistically significant.\u003c/p\u003e \u003cp\u003eAs a sensitivity analysis, linear mixed models (LMMs) with random intercepts were fitted for all three primary endpoints to assess the robustness of the paired analyses and to account for within-patient correlation. The model specification was: Y\u0026thinsp;=\u0026thinsp;β ₀+β ₁(Time )+β ₂(Baseline )\u0026thinsp;+\u0026thinsp;u\u0026thinsp;+\u0026thinsp;ε, where β₁ represents the fixed time effect (primary parameter of interest) and u the random intercept for patient i. Models were estimated using restricted maximum likelihood (REML). Analysis of covariance (ANCOVA) models were fitted to evaluate the predictive value of baseline parameters on follow-up values. Treatment responses were examined across predefined subgroups stratified by baseline eGFR category (\u0026le;\u0026thinsp;30, 30\u0026ndash;45, 45\u0026ndash;60, \u0026gt;\u0026thinsp;60 mL/min/1.73m\u0026sup2;) and baseline albuminuria category (microalbuminuria\u0026thinsp;\u0026lt;\u0026thinsp;300 mg/g vs. macroalbuminuria\u0026thinsp;\u0026ge;\u0026thinsp;300 mg/g). Spearman's rank correlation coefficient was calculated to assess the relationship between baseline values and the magnitude of treatment response. All analyses were performed using Python 3.11 with SciPy, statsmodels, and scikit-learn.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eStudy Population\u003c/h2\u003e \u003cp\u003eThe final cohort comprised 1,091 patients (mean age 60.6\u0026thinsp;\u0026plusmn;\u0026thinsp;11.5 years, 55.0% male) with type 2 diabetes and CKD. Hypertension was nearly universal (99.6%), and 37.8% had established cardiovascular disease with a mean diabetes duration of 12.4\u0026thinsp;\u0026plusmn;\u0026thinsp;8.9 years. At baseline, median eGFR was 53.5 [IQR: 41.0\u0026ndash;74.0] mL/min/1.73m\u0026sup2;, mean serum potassium was 4.48\u0026thinsp;\u0026plusmn;\u0026thinsp;0.39 mEq/L, and median UACR was 781.6 [IQR: 336.1-1542.5] mg/g. All patients were receiving RAS blockade (64.4% at maximally tolerated doses), and notably, 87.0% of patients with available data were concurrently treated with SGLT2 inhibitors, reflecting contemporary practice patterns. Finerenone was initiated at 10 mg in 85.0% of patients and at 20 mg in 15.0%. Among those who initiated at 10 mg and had dose data available at month 3 (n\u0026thinsp;=\u0026thinsp;460), 140 (30.4%) were uptitrated to 20 mg. Paired baseline and months 1\u0026ndash;3 measurements were available for eGFR in 571 patients (52.4%), serum potassium in 646 (59.2%), and UACR in 474 (43.5%), reflecting routine clinical practice patterns across 56 centers.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003ePrimary Endpoints\u003c/h3\u003e\n\u003cp\u003eFinerenone initiation was associated with statistically significant changes in all three primary endpoints, consistent with the study hypothesis (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\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\u003ePrimary Endpoints\u0026mdash;Changes from Baseline to Months 1\u0026ndash;3\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"8\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c8\" colnum=\"8\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEndpoint\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003en\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eBaseline\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eMonth 1\u0026ndash;3\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eChange\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003e% Change\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e \u003cp\u003ep-value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c8\"\u003e \u003cp\u003e95% CI\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eeGFR\u003c/b\u003e (mL/min/1.73m\u0026sup2;)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e571\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e53.5 [41.0\u0026ndash;74.0]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e51.0 [38.0\u0026ndash;73.0]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-2.34\u0026thinsp;\u0026plusmn;\u0026thinsp;11.88\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e-3.8%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e[-3.32, -1.36]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eSerum K⁺\u003c/b\u003e (mEq/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e646\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e4.50 [4.20\u0026ndash;4.80]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e4.80 [4.50\u0026ndash;5.10]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e+\u0026thinsp;0.30\u0026thinsp;\u0026plusmn;\u0026thinsp;0.46\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e+\u0026thinsp;6.8%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e[0.27, 0.34]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eUACR\u003c/b\u003e (mg/g)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e474\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e781.6 [336.1-1542.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e468.2 [155.0-1042.0]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-248.0 [-600.0, -53.5]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e-40.1%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e[-310.0, -205.0]\u0026dagger;\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eLog-UACR\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e474\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e6.53\u0026thinsp;\u0026plusmn;\u0026thinsp;1.29\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e5.92\u0026thinsp;\u0026plusmn;\u0026thinsp;1.45\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-0.607\u0026thinsp;\u0026plusmn;\u0026thinsp;0.78\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e-45.5%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e[-0.68, -0.54]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cem\u003eData presented as median [IQR] or mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD. p-values are from Wilcoxon signed-rank tests. \u0026dagger;95% CI for median change in UACR was calculated using bootstrapping (10,000 iterations).\u003c/em\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eAmong 571 patients with paired eGFR measurements, median eGFR declined from 53.5 [41.0\u0026ndash;74.0] to 51.0 [38.0\u0026ndash;73.0] mL/min/1.73m\u0026sup2; (mean change\u0026thinsp;\u0026minus;\u0026thinsp;2.34\u0026thinsp;\u0026plusmn;\u0026thinsp;11.88 mL/min, 95% CI -3.32 to -1.36; Wilcoxon p\u0026thinsp;\u0026lt;\u0026thinsp;0.001; Cohen\u0026rsquo;s d = -0.20). This modest 3.8% median relative decline is consistent with an adaptive hemodynamic dip commonly observed with mineralocorticoid receptor antagonism and does not reflect progressive kidney injury.\u003c/p\u003e \u003cp\u003eAmong 646 patients with paired potassium measurements, median serum potassium increased from 4.50 [4.20\u0026ndash;4.80] to 4.80 [4.50\u0026ndash;5.10] mEq/L (mean change\u0026thinsp;+\u0026thinsp;0.30\u0026thinsp;\u0026plusmn;\u0026thinsp;0.46 mEq/L, 95% CI 0.27 to 0.34; Wilcoxon p\u0026thinsp;\u0026lt;\u0026thinsp;0.001; Cohen\u0026rsquo;s d\u0026thinsp;=\u0026thinsp;0.66). Despite the statistically significant increase, mean potassium remained within the normal range at all time points.\u003c/p\u003e \u003cp\u003eAmong 474 patients with paired UACR measurements (excluding one patient with a follow-up value of zero for log-transformation), median UACR decreased from 781.6 [336.1-1542.5] to 468.2 [155.0-1042.0] mg/g, corresponding to a 40.1% median reduction (Wilcoxon p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). Log-transformed analysis confirmed a mean change of -0.607\u0026thinsp;\u0026plusmn;\u0026thinsp;0.78 log units (95% CI -0.68 to -0.54; p\u0026thinsp;\u0026lt;\u0026thinsp;0.001; Cohen\u0026rsquo;s d = -0.78), corresponding to a 45.5% reduction. This substantial and rapid reduction in albuminuria represents a clinically meaningful early response to finerenone therapy.\u003c/p\u003e\n\u003ch3\u003eSensitivity Analysis\u003c/h3\u003e\n\u003cp\u003eLinear mixed model analysis confirmed the robustness of all primary findings (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The fixed time effects were near-identical to paired analyses: eGFR\u0026thinsp;\u0026minus;\u0026thinsp;2.34 mL/min/1.73m\u0026sup2; (SE 0.50, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001); potassium\u0026thinsp;+\u0026thinsp;0.31 mEq/L (SE 0.02, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001); and log-UACR\u0026thinsp;\u0026minus;\u0026thinsp;0.607 (SE 0.04, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). Minimal random intercept variances across all three models indicated that, after accounting for baseline values, treatment effects were homogeneous across the patient population. The near-perfect concordance between two fundamentally different analytical approaches\u0026mdash;one assuming independence (paired test) and the other modeling within-patient correlation (LMM)\u0026mdash;provides strong evidence that the observed treatment effects are robust and not an artifact of the analytical method.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cdiv id=\"Sec11\" class=\"Section2\"\u003e \u003ch2\u003eSubgroup and Correlation Analyses\u003c/h2\u003e \u003cp\u003eSubgroup analyses demonstrated consistency of treatment response across diverse patient populations (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). eGFR decline was observed across all baseline eGFR categories: \u0026le;30 mL/min (n\u0026thinsp;=\u0026thinsp;39, -0.85\u0026thinsp;\u0026plusmn;\u0026thinsp;5.16 mL/min), 30\u0026ndash;45 (n\u0026thinsp;=\u0026thinsp;159, -1.23\u0026thinsp;\u0026plusmn;\u0026thinsp;5.85), 45\u0026ndash;60 (n\u0026thinsp;=\u0026thinsp;149, -2.52\u0026thinsp;\u0026plusmn;\u0026thinsp;8.35), and \u0026gt;\u0026thinsp;60 (n\u0026thinsp;=\u0026thinsp;224, -3.27\u0026thinsp;\u0026plusmn;\u0026thinsp;16.83). Albuminuria reduction was consistent regardless of baseline severity, with median reductions of -35.6% in microalbuminuria (n\u0026thinsp;=\u0026thinsp;109) and \u0026minus;\u0026thinsp;40.3% in macroalbuminuria (n\u0026thinsp;=\u0026thinsp;366).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eANCOVA models showed that baseline eGFR explained 76.8% of the variance in follow-up eGFR (R\u0026sup2;=0.768), baseline potassium explained 17.7% (R\u0026sup2;=0.177), and baseline log-UACR explained 71.4% (R\u0026sup2;=0.714). Crucially, the treatment effect remained statistically significant for all primary outcomes after adjusting for these baseline covariates (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001), indicating consistent efficacy regardless of initial values.\u003c/p\u003e \u003cp\u003eCorrelation analysis between baseline values and the magnitude of change revealed weak correlations for eGFR (Spearman ρ=-0.145, p\u0026thinsp;=\u0026thinsp;0.001) and log-UACR (ρ=-0.034, p\u0026thinsp;=\u0026thinsp;0.458), indicating that treatment effects are largely independent of baseline status (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003e). A moderate negative correlation was observed for potassium (ρ=-0.419, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001), consistent with regression toward the mean. These findings collectively support the generalizability of finerenone therapy across diverse patient populations.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec12\" class=\"Section2\"\u003e \u003ch2\u003eSafety Profile\u003c/h2\u003e \u003cp\u003eHyperkalemia (K⁺ \u0026gt;5.5 mEq/L) occurred in 27 of 646 patients (4.2%), and severe hyperkalemia (K⁺ \u0026gt;6.0 mEq/L) in only 5 (0.8%). Among the 27 patients who developed hyperkalemia, the predominant management strategy was initiation of a potassium binder (40.7%, n\u0026thinsp;=\u0026thinsp;11), finerenone discontinuation (33.3%, n\u0026thinsp;=\u0026thinsp;9), and observation alone (18.5%, n\u0026thinsp;=\u0026thinsp;5) (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003e, \u003cb\u003ePanel A\u003c/b\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eFinerenone was discontinued in 39 patients (3.6%) by month 3. The most common reasons were hyperkalemia (33.3%), other causes (28.2%), and financial reasons (20.5%) (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003e, \u003cb\u003ePanel B\u003c/b\u003e). Among the 27 patients with follow-up data after discontinuation, 8 (29.6%) were re-initiated on finerenone, predominantly after potassium normalization.\u003c/p\u003e \u003cp\u003eDuring the follow-up period, 6 deaths (0.5%) were recorded. Causes of death included coronary artery disease, hemorrhagic stroke, decompensated heart failure, and gastrointestinal bleeding. None of the deaths were considered by the investigators to be directly attributable to finerenone therapy or hyperkalemia.\u003c/p\u003e \u003c/div\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eIn this multicenter, retrospective, real-world cohort spanning 56 nephrology centers, initiation of finerenone in adults with type 2 diabetes and chronic kidney disease receiving contemporary kidney-protective therapy was associated with three consistent early trajectories at routine follow-up within 1 to 3 months. First, albuminuria declined rapidly and substantially. Second, kidney function showed a small early eGFR dip of limited magnitude. Third, serum potassium increased modestly, while clinically relevant hyperkalemia remained uncommon and was generally manageable in routine practice. The scale of FINE-TURK and the high prevalence of background sodium-glucose cotransporter 2 (SGLT2) inhibitor use provide an updated real-world complement to the pivotal finerenone program conducted in an era of comparatively low SGLT2 inhibitor uptake \u003csup\u003e\u003cspan additionalcitationids=\"CR17\" citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eThe most clinically salient signal was the magnitude of albuminuria reduction. Among patients with paired measurements, UACR decreased by approximately 40% within the first 1 to 3 months, with concordant findings on log-transformed analyses, supporting a robust early anti-albuminuric effect despite the inherent variability of spot UACR in routine care. This degree and timing of response are consistent with the early albuminuria-lowering observed in FIDELIO-DKD and FIGARO-DKD, reinforcing the biological plausibility that finerenone\u0026rsquo;s anti-inflammatory and anti-fibrotic effects translate into measurable short-term biomarker improvement in contemporary practice \u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e,\u003cspan additionalcitationids=\"CR13\" citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e,\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e,\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e. Although early UACR reduction has been linked to long-term cardiorenal benefit in clinical trials, the current observational design and short follow-up preclude inference regarding long-term endpoints; continued follow-up in this national cohort will be essential to determine whether early biomarker changes translate into sustained eGFR benefit and fewer clinical events \u003csup\u003e\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e,\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eKidney function changes were modest. The early mean eGFR decline of approximately 2 to 3 mL/min/1.73 m\u0026sup2; is consistent in direction with the hemodynamic dip commonly observed after initiation of several kidney-protective agents, including renin-angiotensin system (RAS) blockade and SGLT2 inhibition \u003csup\u003e\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e,\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e\u003c/sup\u003e. Importantly, sensitivity analyses using linear mixed models yielded estimates that closely match paired analyses, arguing against analytic artifact and supporting the robustness of the observed trajectory. Subgroup analyses suggested that this early eGFR change occurred across baseline eGFR categories, supporting the feasibility of finerenone use across a broad spectrum of kidney function within indicated ranges, while emphasizing the need for early monitoring in those at highest risk of acute declines.\u003c/p\u003e \u003cp\u003eHyperkalemia remains the principal safety concern with mineralocorticoid receptor antagonism \u003csup\u003e\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e,\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u003c/sup\u003e. In this cohort, serum potassium increased by approximately 0.30 mEq/L; however, hyperkalemia above 5.5 mEq/L occurred in only 4.2% of patients with paired potassium data, and severe hyperkalemia above 6.0 mEq/L was rare (0.8%). When hyperkalemia occurred, management most commonly involved initiation of a potassium binder, and discontinuation rates were low by month 3, with a notable proportion of patients later re-initiated after potassium normalization. Several factors may plausibly contribute to this favorable early potassium profile, including high concomitant use of SGLT2 inhibitors, contemporary diuretic utilization patterns, and common initiation at lower finerenone doses. Collectively, these findings support the feasibility of integrating finerenone into the modern therapeutic \u0026ldquo;stack\u0026rdquo; when early potassium surveillance and structured potassium-lowering strategies are applied \u003csup\u003e\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e,\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eAn important practical implication is the generalizability of early finerenone-associated biomarker effects in contemporary care. The cohort reflects routine nephrology practice, with high uptake of background kidney-protective therapy, including near-universal RAS blockade and widespread use of SGLT2 inhibitors \u003csup\u003e\u003cspan additionalcitationids=\"CR5 CR6\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e. Early responses were broadly consistent across albuminuria and eGFR strata, and correlations between baseline values and magnitude of response were weak for eGFR and UACR, suggesting that early albuminuria lowering is not limited to a narrow phenotype. In contrast, a more pronounced association between baseline potassium and the change in potassium is consistent with regression toward the mean and underscores the continued importance of baseline potassium as a safety signal.\u003c/p\u003e \u003cp\u003eThis study has limitations inherent to retrospective observational designs. The absence of a control group limits causal inference and leaves residual confounding, including potential changes in concomitant medications, blood pressure, glycemic control, diet counseling, and laboratory timing that are not fully standardized across centers. Paired laboratory measurements were available in roughly half of the cohort, which may introduce selection bias; documenting baseline differences between patients with and without paired follow-up would strengthen interpretability. Outcomes were not adjudicated. While short-term mortality was low, deaths occurred during follow-up and attribution cannot be established in this design. Finally, the current report focuses on early biomarker trajectories rather than hard kidney or cardiovascular outcomes; longer follow-up is required to assess sustained eGFR slope, hospitalization patterns, and clinical endpoints.\u003c/p\u003e \u003cp\u003eIn summary, in a large national real-world cohort characterized by contemporary background therapy and high SGLT2 inhibitor use, finerenone initiation was associated with rapid and substantial albuminuria reduction, a small early eGFR dip, and a manageable potassium profile with low rates of severe hyperkalemia and low overall discontinuation. These findings support early integration of finerenone into combination kidney-protective therapy with appropriate laboratory monitoring and proactive hyperkalemia management \u003csup\u003e\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e,\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eLiyanage T, Ninomiya T, Jha V et al (2015) Worldwide access to treatment for end-stage kidney disease: a systematic review. Lancet 385(9981):1975\u0026ndash;1982\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWu P-P, Kor C-T, Hsieh M-C, Hsieh Y-P (2018) Association between end-stage renal disease and incident diabetes mellitus\u0026mdash;A nationwide population-based cohort study. J Clin Med 7(10):343\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCampbell RC, Ruggenenti P, Remuzzi G (2003) Proteinuria in diabetic nephropathy: treatment and evolution. Curr Diab Rep 3(6):497\u0026ndash;504\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCardiology ACo C, ACo, Association AH (2017) ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults a report of the American College of Cardiology/American Heart Association Task Force on Clinical practice guidelines. \u003cem\u003eHypertension\u003c/em\u003e. 2018;71(6):E13-E115\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCare D (2019) Standards of medical care in diabetes 2019. Diabetes Care 42(Suppl 1):S124\u0026ndash;S138\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCravedi P, Ruggenenti P, Remuzzi G (2007) Intensified inhibition of renin-angiotensin system: a way to improve renal protection? Curr Hypertens Rep 9(5):430\u0026ndash;436\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGiglio RV, Patti AM, Rizvi AA et al (2023) Advances in the pharmacological management of diabetic nephropathy: a 2022 international update. Biomedicines 11(2):291\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSternlicht H, Bakris GL (2017) The kidney in hypertension. Med Clin 101(1):207\u0026ndash;217\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAndo K, Ohtsu H, Uchida S, Kaname S, Arakawa Y, Fujita T (2014) Anti-albuminuric effect of the aldosterone blocker eplerenone in non-diabetic hypertensive patients with albuminuria: a double-blind, randomised, placebo-controlled trial. lancet Diabetes Endocrinol 2(12):944\u0026ndash;953\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBlasi ER, Rocha R, Rudolph AE, Blomme EA, Polly ML, McMahon EG (2003) Aldosterone/salt induces renal inflammation and fibrosis in hypertensive rats. Kidney Int 63(5):1791\u0026ndash;1800\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMehdi UF, Adams-Huet B, Raskin P, Vega GL, Toto RD (2009) Addition of angiotensin receptor blockade or mineralocorticoid antagonism to maximal angiotensin-converting enzyme inhibition in diabetic nephropathy. J Am Soc Nephrol 20(12):2641\u0026ndash;2650\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eB\u0026auml;rfacker L, Kuhl A, Hillisch A et al (2012) Discovery of BAY 94-8862: a nonsteroidal antagonist of the mineralocorticoid receptor for the treatment of cardiorenal diseases. ChemMedChem 7(8):1385\u0026ndash;1403\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGrune J, Beyhoff N, Smeir E et al (2018) Selective mineralocorticoid receptor cofactor modulation as molecular basis for finerenone\u0026rsquo;s antifibrotic activity. Hypertension 71(4):599\u0026ndash;608\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKolkhof P, Borden SA (2012) Molecular pharmacology of the mineralocorticoid receptor: prospects for novel therapeutics. Mol Cell Endocrinol 350(2):310\u0026ndash;317\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePitt B, Zannad F, Remme WJ et al (1999) The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 341(10):709\u0026ndash;717\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBakris GL, Agarwal R, Anker SD et al (2019) Design and baseline characteristics of the finerenone in reducing kidney failure and disease progression in diabetic kidney disease trial. Am J Nephrol 50(5):333\u0026ndash;344\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAgarwal R, Filippatos G, Pitt B et al (2022) Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis. Eur Heart J 43(6):474\u0026ndash;484\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBakris GL, Agarwal R, Anker SD et al (2020) Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes. N Engl J Med 383(23):2219\u0026ndash;2229\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCahn A, Melzer-Cohen C, Pollack R, Chodick G, Shalev V (2019) Acute renal outcomes with sodium‐glucose co‐transporter‐2 inhibitors: real‐world data analysis. Diabetes Obes Metabolism 21(2):340\u0026ndash;348\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"Dr Lütfi Kırdar Kartal Eğitim ve Araştırma Hastanesi","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"finerenone, diabetic kidney disease, chronic kidney disease, albuminuria, SGLT2 inhibitor, hyperkalemia","lastPublishedDoi":"10.21203/rs.3.rs-9043582/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9043582/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground: Randomized trials have established the benefits of finerenone in type 2 diabetes with CKD; however, real-world evidence with high SGLT2 inhibitor uptake remains limited.\u003c/p\u003e\n\u003cp\u003eMethods: FINE-TURK was a multicenter retrospective cohort study conducted at 56 nephrology centers in Turkey. Adults with type 2 diabetes and CKD initiating finerenone (January 2025 to June 2025) were assessed at baseline, month 1, and month 3. Primary endpoints were changes in estimated glomerular filtration rate (eGFR), serum potassium, and urinary albumin-to-creatinine ratio (UACR); hyperkalemia was defined as potassium \u0026gt;5.5 mEq/L.\u003c/p\u003e\n\u003cp\u003eResults: Among 1,091 patients (60.6±11.5 years, 55% male), 87% received an SGLT2 inhibitor and 100% renin-angiotensin system blockade. Finerenone started at 10 mg in 85%. Paired analyses included 576 for eGFR, 648 for potassium, and 487 for UACR. Mean eGFR fell from 58.51±24.20 to 55.78±23.19 mL/min/1.73 m2 at month 1 and remained 55.78±23.13 at month 3 (both P\u0026lt;0.001 vs baseline). Mean potassium increased from 4.49±0.39 to 4.75±0.47 and 4.78±0.44 mEq/L (P\u0026lt;0.001). Median UACR declined from 690.6 (271.4-1538.0) mg/g to 468.0 (173.5-1195.5) at month 1 and 450.0 (154.5-1041.0) mg/g at month 3, corresponding to 32.2% and 34.8% reductions (P\u0026lt;0.001). Hyperkalemia occurred in 5.0% at both visits, commonly managed with potassium binders; hospitalizations were infrequent (2.8% and 3.1%), and no deaths occurred.\u003c/p\u003e\n\u003cp\u003eConclusions: In routine care with high SGLT2 inhibitor uptake, finerenone achieved a rapid reduction in albuminuria, with a modest early decline in eGFR, manageable potassium elevations, and low short-term event rates, supporting early use alongside standard therapy in contemporary clinical practice.\u003c/p\u003e","manuscriptTitle":"Real-World Effects of Finerenone in Diabetics Kidney\nDisease: Data From Fine-Turk Study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-03-18 08:28:06","doi":"10.21203/rs.3.rs-9043582/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"981ee188-de2e-4e92-9878-87ba760c8ac2","owner":[],"postedDate":"March 18th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":64420678,"name":"Urology \u0026 Nephrology"}],"tags":[],"updatedAt":"2026-03-18T08:28:07+00:00","versionOfRecord":[],"versionCreatedAt":"2026-03-18 08:28:06","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9043582","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9043582","identity":"rs-9043582","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}