Revised: March 5, 2026
Accepted: April 21, 2026
Published online: September 25, 2026
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With the alarming rise in the global prevalence of the disease, type 2 diabetes mellitus (T2DM) has recently become the leading cause of chronic kidney disease (CKD) worldwide. Proteinuria, the earliest and common indicator of diabetic kidney disease (DKD), not only increases the risk of progression of CKD to end-stage renal disease (ESRD) but also multiplies the risk of cardiovascular (CV) disease in patients with diabetes. Medications such as angiotensin-converting enzyme inhibitors (ACEis), angiotensin II receptor blockers (ARBs), sodium-glucose cotransporter-2 inhibitors (SGLT-2is), and mineralocorticoid receptor antagonists (MRAs) have been shown to reduce proteinuria and therefore possess disease-modifying properties in patients with DKD. Clinical trials have demon
Core Tip: Diabetic kidney disease (DKD) is a leading cause of morbidity and mortality in people with diabetes mellitus. Traditional disease-modifying treatments do not fully target the underlying mechanisms. The renin-angiotensin-aldosterone system is over activated and only partially suppressed by the renin-angiotensin-aldosterone system blockers like angiotensin- converting enzyme inhibitors or angiotensin II receptor blockers in the context of DKD. This article is based on the latest research evidence and discusses the relevant strategies for treating diabetic nephropathy patients.
- Citation: Jose A, Kamrul-Hasan ABM, Fernandez CJ, Pappachan JM. Efficacy of finerenone in reducing proteinuria in diabetic kidney disease on dapagliflozin and telmisartan: A disease-modifying approach. World J Nephrol 2026; 15(3): 120295
- URL: https://www.wjgnet.com/2220-6124/full/v15/i3/120295.htm
- DOI: https://dx.doi.org/10.5527/wjn.120295
Diabetes mellitus (DM) has become one of the most common chronic diseases worldwide, affecting 589 million adults in 2025, according to the latest estimates from the International Diabetes Federation[1]. Over 90% of these patients have type 2 DM (T2DM), and many of these individuals are either undiagnosed or not well-controlled metabolically. DM has recently emerged as one of the leading causes of chronic kidney disease (CKD), affecting one-third of people with renal disease and being a major reason for renal replacement therapy globally[2,3]. CKD in diabetic patients shows a wide range of clinical and biochemical abnormalities, collectively known as diabetic kidney disease (DKD), with microalbuminuria as the earliest sign. Prompt management of DM, alongside control of comorbidities like hypertension and dyslipidemia, along with lifestyle modifications, can greatly prevent DKD development[4]. Once microalbuminuria occurs, there is a significant risk of progression to overt proteinuria; therefore, more aggressive management is necessary to prevent rapid renal decline.
Recently, several disease-modifying treatments have been developed for DKD patients, including angiotensin-converting enzyme inhibitors (ACEis), angiotensin II receptor blockers (ARBs), sodium glucose cotransporter 2 inhibitors (SGLT-2is), and mineralocorticoid receptor antagonists (MRAs)[5]. In some cases, combining these medications may be required to optimize disease control and prevent progression. A recent retrospective observational study by Pasari et al[6] in the World Journal of Nephrology highlights the benefits of combining MRA (finerenone) with SGLT-2is (dapagliflozin). This article provides an up-to-date review of the current evidence for disease-modifying therapies in patients with DKD.
CKD is characterized by albuminuria, a low estimated glomerular filtration rate (eGFR), or both. Globally, DKD is now the leading cause of CKD, occurring in approximately 40% of people with type 2 diabetes and 30% of those with type 1 diabetes. The mechanisms of kidney damage in diabetes are multifactorial, including metabolic, hemodynamic, and inflammatory factors that contribute to fibrotic injury. Hyperglycemia induces afferent arteriolar dilatation, glomerular hyperfiltration, and intraglomerular hypertension. Intrarenal activation of the renin-angiotensin system triggers glomerular hyperfiltration via angiotensin II, constricting the efferent arteriole[7]. Angiotensin II stimulates intra-renal expression of proinflammatory and profibrotic mediators through barotrauma and direct cellular effects. The SGLT-2, expressed on the luminal surface of epithelial cells in the proximal convoluted tubule, is responsible for 90% of filtered glucose reabsorption. In hyperglycemia, a maladaptive increase in SGLT-2 expression and activity that worsens hyperglycemia by an increase in tubular glucose reabsorption[8].
Hyperglycemia causes dysregulated intracellular signaling, leading to the formation of advanced glycation end products (AGEs), reactive oxygen species (ROS), and activation of protein kinase C and the Janus kinase signal transducer and activator of transcription pathways. Oxidative stress, a hallmark of DKD, results from mitochondrial dysfunction, increased production of ROS, and impaired antioxidant defenses. Reactive oxygen species causes injury to the cell DNA, facilitates peroxidation of lipids, and alters the proteins, thereby causing inflammation and endothelial dysfunction[9]. Podocytes exposed to AGE exhibit increased nuclear factor κB-mediated upregulation of messenger RNA for various proinflammatory mediators. In podocytes and endothelial cells, AGEs bind to the receptor for AGE (RAGE), triggering inflammation and inducing the expression and activation of interleukins (IL) (IL-1β and IL-18). AGEs also increase the expression of serum amyloid A, a RAGE ligand, which perpetuates a feed-forward cycle of inflammatory gene expression. These intracellular signals leads to the continuous release of proinflammatory mediators and profibrotic factors, as well as immune cell recruitment, ultimately resulting in renal damage[10]. Figure 1 shows the pathobiology of DKD.
Patients with DM and proteinuria also have a higher prevalence of modifiable risk factors like hypertension and dyslipidemia which increases the CVD risk independently. These risk factors together increase the endothelial dysfunction thereby expediting the CVD risk. Hyperglycemia in uncontrolled diabetes activates the renin-angiotensin-aldosterone system (RAAS), leading to increased angiotensin II levels, which cause vasoconstriction and inflammation, resulting in proteinuria and atherosclerosis[11]. Proteinuria is an important prognostication factor of cardiovascular disease (CVD) in individuals with DM. Macroalbuminuria in the nephrotic-range increases the risk of CVD by four to five times compared to those without proteinuria[12]. In the CKD-ROUTE study[13], it was identified that both proteinuria and diabetes as independent factors and in unison increases cardiovascular events in patients having CKD stages 2-5. After accounting for potential confounders, individuals having urine protein creatinine ratio (UPCR ≥ 0.5) had a 4.09-times increased risk of cardiovascular events compared to those without either. The difference was observed over a time period of three years. In the Strong Heart study[14] it was observed that co-existing macroalbuminuria in patients with diabetes will make them prone for CVD with a four-to fivefold increased risk compared to those individuals with diabetes but without albu
The treatment of DKD focuses on achieving glycemic control and normalizing blood pressure, along with lifestyle modifications such as regular exercise and weight management. RAAS inhibitors protects the kidney by reducing intraglomerular pressure, glomerular hyperfiltration, and angiotensin II-induced oxidative stress, inflammation, and fibrosis. The benefits of ACE inhibitors and ARBs in DKD were established in 1993 with the landmark Collaborative Study Group trial (Captopril in T1DM)[16], followed by RENAAL (with Losartan, 2001)[17] and IDNT (with Irbesartan, 2001) trials[18].
SGLT-2is lower blood glucose by decreasing glucose reabsorption at the proximal tubule, resulting in glucosuria and restoring tubulo-glomerular feedback by increasing distal delivery of sodium chloride to the macula densa. The solute reabsorption at the macula densa generates adenosine as a by-product of ATP utilization. Adenosine acts in a paracrine manner to enhance afferent arteriolar vasoconstriction, suppress renin release from juxtaglomerular cells, and reduce efferent arteriolar constriction. The balance between increasing afferent and decreasing efferent arteriolar constriction in response to SGLT-2 inhibition may vary depending on diabetes type, age of the individual, and genetic polymorphisms in the SLC5A2 gene[8]. In patients with DKD from the CANagliflozin Treatment And Trial Analysis-Sulfonylurea (CANTATA-SU) trial, treatment with canagliflozin decreased circulating levels of IL-6, tumor necrosis factor (TNF) receptor-1, matrix metalloproteinase-7, and fibronectin-1[19]. Reductions in plasma TNF receptor-1 and TNF receptor-2 with canagliflozin were associated with better patient outcomes in the CANVAS trial[20]. The renal benefits of SGLT-2is were established in cardiovascular outcome trials like DAPA-CKD[21], EMPA-KIDNEY[22], EMPA-REG OUTCOME[23], and CREDENCE trials[24].
The mineralocorticoid receptor (MR) for aldosterone translocates to the nucleus upon ligand binding and functions as a transcription factor. In the tubular epithelium of the collecting duct, MR activation leads to sodium reabsorption and potassium secretion. In non-epithelial kidney cells, MR upregulates the expression of proinflammatory and profibrotic genes associated with DKD progression. Hyperglycemia promotes inappropriate MR activation, known as “MR overactivation”, in the kidney and heart, leading to oxidative stress through the upregulation of nicotinamide adenine dinucleotide phosphate oxidase, which increases the expression of proinflammatory and profibrotic mediators such as nuclear factor κB, IL-6, IL-1β, TNF-α, interferon-γ, monocyte chemoattractant protein-1, and connective tissue growth factor. MR also enhances plasminogen activator inhibitor–1 activity, promoting extracellular matrix accumulation and fibrosis[25]. There is a difference between the MR effects in the heart and the kidneys which is due to the variable 11βHSD2 tissue expression[26]. 11βHSD2 is located in the distal renal tubules, and aldosterone promotes sodium reabsorption and potassium excretion. This enzyme being absent in cardiomyocytes, podocytes, and macrophages, cortisol acts as the crucial MR ligand. Chronic ACEi/ARB use in patients with congestive heart failure, CKD, or hypertension causes aldosterone breakthrough which is postulated to be non-ACE dependent thereby reducing the cardiorenal protection offered by the medication[27]. This aldosterone breakthrough, further increases plasma aldosterone, exacerbates MR overactivation and leads to further reduction in eGFR[28]. Figure 2 shows the mechanisms involved in cardiorenal damage by MR overactivation.
Spironolactone-the trailblazer MR antagonist was analyzed in 2014, in a Cochrane Database systematic review of 27 studies with 1549 subjects. It was observed that proteinuria and blood pressure were reduced but the effects at the end of treatment on GFR was not consistent and had an increased probability of hyperkalemia. Spironolactone also increased the risk of gynecomastia[29]. The ill-effects on eGFR and hyperkalemia were mitigated to some extent by using non-steroidal MRA.
The discovery of nonsteroidal MRAs was initiated with the successful cloning of the MR in 1987[30]. The knowledge about the expression of MR provided a molecular basis for the invention of nonsteroidal MRAs, and was a milestone in the development history of aldosterone antagonists[31]. The third-generation MRAs, apararenone, esaxerenone, and finerenone, have greater selectivity and potency for inhibiting MR than steroidal MRAs (spironolactone-first generation; eplerenone-second-generation), with a lower risk of hyperkalemia[32]. Finerenone shows a balanced distribution between cardiac and renal tissues, unlike steroidal MRAs, which primarily concentrate in the kidneys. Finerenone reduces albuminuria in a dose-dependent manner[33].
ARTS-DN by Bakris et al[34] was a trailblazer study assessing finerenone’s safety and efficacy in DKD patients. It was a multicenter, randomized double-blind trial conducted in 821 patients who were having severely increased proteinuria and already on ACEi/ARB treatment. Primary endpoints were a change in the urine albumin-to-creatinine ratio (UACR) value and eGFR. Alteration in the serum potassium levels was a safety endpoint. In a span of 3 months, it was observed that finerenone significantly reduced UACR from baseline at all the doses of 7.5, 10, 15 and 20 mg (P values were 0.004, 0.001, 0.001, 0.001 respectively for each dose) with no increased risk of hyperkalemia when compared to placebo. The improvement in UACR was dose-dependent during the treatment with finerenone. Fu et al[35] in a meta-analysis observed that finerenone decreased proteinuria and CVD risk in individuals with CKD without causing significant reduction in the eGFR.
Table 1 shows the landmark clinical trials on finerenone, FIDELIO-DKD, and FIGARO-DKD, which demonstrated reductions in primary composite renal and cardiovascular outcomes, respectively[36,37]. The renal benefits of SGLT-2is in trials were observed regardless of MRA use, and the benefits of finerenone in the FIDELIO and FIGARO studies were noted irrespective of SGLT-2is use. The serious hyperkalemia risk associated with MRA was significantly lowered by the concurrent use of SGLT-2is.
| Trial name | No of Subjects (T2DM on maximally tolerated ACEi/ARB) | Follow up | Renal outcomes (kidney failure, more than 40 percentage decrease in eGFR from baseline, or renal death) | CV outcome (cardiovascular death, nonfatal MI, nonfatal stroke, or heart failure hospitalization) | Reduction of UACR from baseline to month 4 |
| FIDELIO-DKD[20] | 5734 | 2.6 years | 17.8 percentage with finerenone vs 21.1 percentage with placebo (HR = 0.82, 95%CI: 0.73-0.93; P = 0.001) | 13.0 percentage with finerenone vs 14.8 percentage with placebo (HR = 0.86, 95%CI: 0.75-0.99; P = 0.03) | 31% greater reduction than placebo [ratio of least-squares mean change from baseline (finerenone vs placebo), 0.69; 95%CI: 0.66-0.71] |
| FIGARO-DKD[21] | 7437 | 3.4 years | 9.5 percentage with finerenone vs 10.8 percentage with placebo (HR = 0.87, 95%CI: 0.76-1.01; P = 0.07) | 12.4 percentage with finerenone vs 14.2 percentage with placebo (HR = 0.87, 95%CI: 0.76-0.98; P = 0.03) | 32% greater reduction with finerenone than with placebo (ratio of the least-squares mean change from baseline, 0.68; 95%CI: 0.65-0.70) |
In the FIDELIO-DKD trial, hyperkalemia-related treatment discontinuation occurred in 2.3% of patients on finerenone compared to 0.9% of patients on placebo, but there was no significant difference between the groups for renal adverse events. In the FIDELITY SGLT-2is subgroup analysis of 706 individuals, finerenone was shown to provide additional renal benefits among patients using SGLT-2is at baseline, with an annual eGFR decline of -1.92 mL/minute/1.73 m2 with finerenone vs -3.45 mL/minute/1.73 m2 with placebo, without added adverse effects or hyperkalemia[38]. The pooled analysis of the FIDELIO-DKD and FIGARO-DKD FIDELITY studies concluded that, compared with placebo, finerenone significantly reduced composite kidney and CV outcomes[39]. FINE-ONE trial[40] conducted in 242 adolescents with T1DM for 6 months showed a 25% reduction of UACR compared to placebo (95%CI: 0.65-0.87; P = 0.0001).
The efficacy and safety of the newer steroidal MRAs like finerenone, apararenone, and esaxerenone in patients with DKD were assessed in a meta-analysis which showed a reduction in UACR and systolic blood pressure among those treated with the steroidal MRAs without significant adverse effects. Finerenone was observed to reduce the decline of eGFR from baseline and the incidence of heart failure. Apararenone showed superiority compared to finerenone in decreasing UACR. Finerenone when compared to esaxerenone was more effective in reducing the decline in eGFR from baseline. Esaxerenone and apararenone were better in controlling systolic blood pressure when indirectly compared with finerenone. Esaxerenone and finerenone were comparable in renoprotection[41].
In the EX-DKD study, a multicenter (22 sites), open-label, prospective study in 113 individuals, esaxerenone reduced BP and improved albuminuria regardless of the severity of albuminuria without significant hyperkalemia or eGFR reduction[42]. A pooled subanalysis of five multicenter, prospective, open-label, single-arm studies on esaxerenone in hypertensive patients with T2DM with and without concomitant SGLT2i indicated that esaxerenone significantly lowered blood pressure in hypertensive patients with T2DM, regardless of SGLT2i use. Esaxerenone was also observed to reduce the UACR (in the initial 12 weeks). It also improved the NT-proBNP levels in the patients. The incidence of serum potassium ≥ 5.5 mEq/L was numerically lower among those who were simultaneously receiving SGLT2i[43]. Esaxe
A meta-analysis of 8 RCTs which was conducted in 14450 individuals with CKD and T2D, non-steroidal MRAs showed a greater reduction in urinary albumin-to-creatinine ratio, eGFR and systolic blood pressure but with an increased risk of hyperkalemia when compared to placebo. Esaxerenone showed no significant difference when compared with finerenone in UACR reduction [weighted mean difference (WMD) = 0.24, 95%CI: -0.016-0.496, P = 0.869]; and apararenone and esaxerenone showed greater decrease in systolic blood pressure (WMD = 1.37, 95%CI: 0.456-2.284, P = 0.010; WMD = 3.11, 95%CI: 0.544-5.676 P = 0.021) when compared with finerenone. Esaxerenone, was studied in Japanese patients for a period of 3 years. The study was conducted in individuals with T2DM, DKD, and hypertension who were already on RAAS inhibitors. It showed that the reduction in UACR was observed independent of the concomitant use of SGLT2is and GLP-1 receptor agonists or initial UACR prior to treatment[45]. A dose-response, parallel-group, randomized, double-blind, placebo-controlled, multicenter, phase 2, 24-week study and an open-label, uncontrolled, 28-week extension study comparing apararenone with placebo was conducted and it was observed that as a percentage of baseline, mean UACR was decreased to 62.9%, 50.8%, and 46.5% in the 2.5 mg, 5 mg, and 10 mg apararenone groups, respectively, at week 24 (placebo: 113.7% at week 24; all P < 0.001 vs placebo) and the 52-week administration was safe and tolerable. A decline in eGFR was noticed along with hyperkalemia, however they were not clinically or statistically significant[46]. While starting non-steroidal MRA like finerenone or esaxerenone an acute drop in eGFR is frequently observed. This initial decline named as “hemodynamic” or “pseudo-worsening” of renal function usually occurs within the first 4 months of treatment. This is postulated to result from changes in intraglomerular pressure. Similar early reduction in eGFR is seen with ACE inhibitors, ARBs, or SGLT2 inhibitors[47]. If the eGFR decline exceeds 40%, down-titrating the dose may be considered. KDIGO guidelines recommend baseline assessment and regular monitoring of serum creatinine and potassium when using MRAs[48]. In the FINEARTS-HF trial, a decline of eGFR occurred in 23% of patients after starting finerenone compared to 13.4% in the placebo group. After the initial decline, eGFR stabilizes or follows a slower decline than placebo demonstrating a net renal protective effect[49]. Table 2 summarizes a comparison of third-generation non-steroidal mineralocorticoid receptor antagonists.
| Characteristic features | Finerenone | Esaxerenone | Apararenone (MT-3995) |
| Primary clinical indication | Diabetic kidney disease (2021-Food and Drug Administration of the United States, 2022-European Medicines Agency) | Hypertension; diabetic nephropathy (Japan)[45] | Diabetic nephropathy (investigational)[46] |
| Relative potency in MR antagonism to Spironolactone | Similar. Specific affinity for MR receptor | Higher | Lesser |
| Half-life (t1/2). Active metabolites | 2-3 hours. None | 30 hours. Not clinically relevant | 275-285 hours |
| Tissue distribution (rodent studies)[41] | Balanced (heart = kidney) | Balanced (heart = kidney) | Balanced (heart = kidney) |
| BP lowering effect | Modest | Potent | Potent |
| Hyperkalemia risk | Less compared to steroidal MRA. Can start when blood potassium ≤ 4.8 - > 5.0 mmol/L | higher rate compared with eplerenone (ESAX-HTN)[44] | Minor risk |
| Blood-brain barrier | Does not cross | Crosses | Likely crosses |
| Dose schedule | eGFR ≥ 60 mL/minute/1.73 m2: 20 mg/day; eGFR 25-59 mL/minute/1.73 m2: 10 mg/day; eGFR < 25 mL/minute/ | 1.25-2.5 mg/day | 2.5, 5, 10 mg/day |
The MRAs increase sodium excretion and decrease potassium excretion in the kidney, causing hyperkalemia which is mitigated by non-steroidal MRA[50]. Both finerenone and esaxerenone have a moderate risk of hyperkalemia when used in patients with CKD and T2DM. The risk is similar in both the medications and is reduced when used along with SGLT2i[51]. Finerenone is approved for DKD but not for the treatment of hypertension. Esaxerenone is primarily indicated for the treatment of hypertension.
Recent studies highlight Bardoxolone methyl's effectiveness in treating DKD[52]. It acts as an antioxidant and inflammation modulator, showing promise in reducing inflammation and oxidative stress associated with DKD. Pirfenidone, is an oral antifibrotic, antioxidant which inhibits the transforming growth factor-beta pathway and AMP; is used in idiopathic pulmonary fibrosis. It has been evaluated for patients with decreasing renal function[53]. Nintedanib, known for its anti-fibrotic effects across various organs, may be capable of slowing DKD progression[54].
Endothelin receptor antagonist atrasentan in a randomized, double-blind, placebo-controlled trial in individuals with T2DM, CKD and macroalbuminuria showed significant albuminuria reduction[55] but with fluid retention and edema as significant adverse effects. The SONAR phase II trial showed that 12 weeks of atrasentan treatment, reduced albuminuria correlating with Proprotein Convertase Subtilisin/Kexin type-9 reduction[56]. Selonsertib inhibits Apoptosis Signal-Regulating Kinase 1 , which is activated by ROS and triggers downstream apoptosis and fibrosis and showed reduced albuminuria in pre-clinical models[57].
SGLT-2is reduced glomerular hyperfiltration by changing intraglomerular hemodynamics, while finerenone helps lower renal inflammation and fibrosis, offering complementary benefits in preventing DKD progression when used together. In addition to reducing proteinuria, this drug combination also supports regression of cardiac and renal fibrosis. Addi
The CONFIDENCE trial showed the beneficial effects of early combination therapy on albuminuria in DKD[59]. In this trial, 818 participants with CKD, eGFR between 30 and 90 mL/minute/1.73 m2 of body surface area, with UACR between 100 and 5000 mg/g, and T2DM who were already on a RAAS inhibitor were studied. The individuals were assigned in 1:1:1 ratio as to receive various combinations. Finerenone or empagliflozin or empagliflozin with finerenone matching placebo. At the end of 6 months, the reduction in UACR with combination therapy was 29% greater than with finerenone alone and 32% greater than with empagliflozin alone. The combination of empagliflozin with finerenone also caused a greater reduction in systolic blood pressure than either therapy alone. The incidence of symptomatic hypotension was low and the blood pressure changes were reversible with drug discontinuation[59].
Pasari et al[6] showed that among individuals with T2DM already receiving maximum tolerable doses of telmisartan and dapagliflozin, when finerenone was added at a dose of 10 mg daily; a reduction in proteinuria in 66.7% of the sub
A similar observation was noticed in FIDELITY pooled analysis which combined data from the FIDELIO-DKD and FIGARO-DKD trials showing that finerenone significantly reduced the UACR and provided greater renal benefits for patients with higher baseline albuminuria. A similar pattern was observed in a realworld DKD cohort by Song et al of 48 patients on finerenone (with background RAAS inhibitors ± SGLT2i ± GLP1 agonists) which showed, baseline median UACR of 364 mg/g, with a greater reduction of albuminuria in the macroalbuminuria subgroup[60-63]. However, the study’s small sample size warrants confirmation of the reproducibility of beneficial effects in further prospective trials; also, the effect of finerenone’s dose-dependent reduction in proteinuria needs evaluation in further studies with 20 mg finerenone dose.
Triple medication combination therapy (ACEi/ARBs + SGLT-2is + MRAs) could become the cornerstone of future DKD treatment. In the FIDELITY subgroup analysis, adding GLP-1 agonists showed additional benefits and may lead to quadruple therapy for DKD. Finerenone, which is more expensive than ACEi/ARB, will require cost-effectiveness assessments. Patients starting finerenone should be informed about the risk of hyperkalemia and monitored for blood pressure changes. More research is needed on the optimal sequence of therapies (e.g., SGLT-2is before or after finerenone) and their effectiveness in non-diabetic proteinuric kidney diseases, as well as the cardiac benefits. In the current era of person-centric and precision medicine, genomics, proteomics, and metabolomics need to be considered. Polymorphisms in genes such as ACE, AGTR1, and SLC12A3 highlight individual variations in susceptibility to DKD. Proteomics provides insights into inflammation, oxidative stress, and endothelial dysfunction in the pathogenesis of DKD and identifies potential targets for therapeutic interventions. The potential for new biomarkers to predict response to finerenone therapy should be assessed. Further research is necessary to fully understand how finerenone affects patient-centered outcomes beyond traditional clinical endpoints.
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