The impact of dynamic kidney function prior to using sodium-glucose cotransporter-2 inhibitors in type 2 diabetes patients with low-risk renal disease progression.

Using GFR, Albuminuria, and Their Changes in Clinical Trials and Clinical Care

Background and Aims Dapagliflozin, a sodium–glucose co-transporter-2 inhibitor (SGLT2i), is indicated to treat chronic kidney disease (CKD). Clinical trials have shown that dapagliflozin significantly reduces albuminuria in patients with urine albumin-creatinine ratio (UACR) 200–5000 mg/g and has beneficial effects on estimated glomerular filtration rate (eGFR) decline and combined kidney outcomes. In the DAPA-CKD trial, dapagliflozin led to substantial reductions in the composite of sustained eGFR decline of ≥50%, end-stage kidney disease, and renal or cardiovascular death (hazard ratio [HR], 0.61; 95% confidence interval [CI]: 0.51, 0.72; p < 0.001), with similar reductions observed across UACR subgroups. Furthermore, compared with placebo, dapagliflozin reduced geometric mean UACR by 29.3% (95% CI: –33.1, –25.2; p < 0.0001), with no difference in relative UACR reduction by baseline UACR above or below 1000 mg/g. In the ZENITH-CKD study, over 12 weeks the combination of zibotentan (a novel endothelin A receptor antagonist) and dapagliflozin showed a robust reduction in UACR of 47.7% vs 28.3% for dapagliflozin alone, with this effect maintained in patients with UACR >700 mg/g. It is well known that renal disease progresses more quickly in patients with higher degree of albuminuria than in those with lower levels. We aimed to further characterize renal risk in patients with different levels of residual albuminuria despite standard of care treatment with renin–angiotensin system inhibitors (RASi) and SGLT2i. Methods We used a large USA claims database (Optum's de-identified Clinformatics® Data Mart Database [CDM]) to identify patients aged ≥18 years with CKD, defined as either two eGFR measurements ≤60 mL/min/1.73 m2 taken ≥90 days apart or a first eGFR ≤60 mL/min/1.73 m2 and a CKD diagnosis. Patients were indexed at the date of dapagliflozin 10 mg initiation between 30 April 2021 (date of approval for dapagliflozin in CKD) and March 2023. Patients with prior use of SGLT2i, immunosuppressive drugs, hydroxychloroquine, CKD stage 5 (based on eGFR <15 mL/min/1.73 m2 or dialysis), polycystic kidney disease, or type 1 or gestational diabetes were excluded. Patients were indexed on 1st January 2022 and grouped into two UACR groups: ≥700UACR group (≥700 mg/g) and <700UACR group (200–699 mg/g). Outcomes were UACR changes, eGFR slopes and CKD-associated hospitalizations within 1 year after dapagliflozin initiation. Hazard ratios were estimated using adjusted Cox survival regression. UACR follow-up analyses were restricted to patients with at least one follow-up measurement. Results In the 5908 patients with CKD, median UACRs at index in the ≥700UACR and <700UACR groups were 1414 mg/g and 102 mg/g, respectively. Patients in the ≥700UACR group vs <700UACR group had lower eGFR (40 vs 48 mL/min/1.73 m2), were younger (71 vs 74 years), and both groups had a high burden of comorbidities (heart failure: 38% vs 42%; type 2 diabetes: 74% vs 75%). RASi use was 81% and 74%, respectively. During follow-up, 22% of patients in the ≥700UACR group experienced a CKD-related hospitalization (25.1 events per 100 patient years) as compared to 19.5 events per 100 patient years in the <700UACR group (HR 1.38 [95% CI: 1.16, 1.64, p < 0.001]; Fig. panel A). The eGFR slope (95% Cl) of patients in the ≥700UACR group was –2.44 mL/min/1.73 m2 per year (–3.49, –1.65), compared with a flat eGFR trajectory in patients in the <700UACR group (0.39 [–0.11, 0.96]). In the ≥700UACR group with at least one follow-up measurement (n = 431), UACR lowered from 2077 mg/g to 1674 mg/g (–36.3%) within 1 month of dapagliflozin initiation but remained above 1200 mg/g throughout the 12-month follow-up period (Fig. panel B). Conclusions While treatment with RASi and SGLT2i are associated with reduced risk of renal outcomes in patients with CKD, awareness and management of residual albuminuria remains an area of unmet clinical need. The novel combination of zibotentan/dapagliflozin currently under investigation in the ZENITH High Proteinuria phase III trial (NCT06087835) seeks to address this need.

IntroductionA urine albumin–creatinine ratio (UACR) > 700 mg/g signifies severe kidney damage, and nephrology referral is recommended for intensified management. The impact of UACR ≥ 700 mg/g on outcomes and the efficacy of kidney protective therapies in patients have not been thoroughly examined.MethodsUsing claims healthcare data from the USA, we identified prevalent patients with chronic kidney disease and a UACR measurement on 1 January 2022, and grouped them by UACR level. We also identified new users of sodium–glucose cotransporter 2 inhibitors (SGLT2i) between 2021 and 2023. Outcomes included estimated glomerular filtration rate (eGFR) slopes and risks of adverse outcomes and mortality.ResultsOf the 46,626 patients with UACR ≥ 300 mg/g, 23,998 had UACR ≥ 700 mg/g. In the UACR ≥ 700 and UACR 300 to < 700 mg/g groups, mean age was 72 and 74 years, median eGFR was 42 and 50 mL/min/1.73 m2, median UACR was 1376 and 437 mg/g at baseline and eGFR slopes were − 5.5 and − 3.1 mL/min/1.73 m2 per year, respectively. Compared to the UACR < 10 mg/g group, adjusted hazard ratio of risk of cardiorenal hospitalizations was 5.83 (95% CI 5.55–6.12) and 3.53 (95% CI 3.34–3.73), atherosclerotic cardiovascular disease hospitalizations was 2.97 (95% CI 2.76–3.19) and 2.33 (95% CI 2.15–2.52), and all-cause death was 2.89 (95% CI 2.78–3.02) and 2.10 (95% CI 2.01–2.20) in the UACR ≥ 700 and UACR 300 to < 700 mg/g groups, respectively. Of the 5908 new users of SGLT2i with UACR ≥ 700 mg/g, UACR and eGFR slope improved as expected (to 720 mg/g and − 2.44 mL/min/1.73 m2 per year, respectively).ConclusionsA UACR ≥ 700 mg/g identifies patients at high risk of accelerated kidney function decline and adverse outcomes. While emerging therapies such as SGLT2i had the expected benefits, the persistence of residual proteinuria/albuminuria and associated risks highlight an unmet need for optimized and new treatment strategies.Supplementary InformationThe online version contains supplementary material available at 10.1007/s12325-025-03364-8.

Canagliflozin reduced kidney disease progression in participants with type 2 diabetes in the CANagliflozin cardioVascular Assessment Study (CANVAS) Program. This analysis explored potential mediators of the effects of canagliflozin on kidney outcomes. The percent mediating effect of 18 biomarkers indicative of disease was determined by comparing the hazard ratios for the effect of randomized treatment from an unadjusted model and from a model adjusting for the average post-randomization level of each biomarker. Multivariable analyses assessed the joint effects of biomarkers that mediated most strongly in univariable analyses. The kidney outcome was defined as a composite of 40% estimated glomerular filtration rate decline, end-stage kidney disease, or death due to kidney disease. Nine biomarkers (systolic blood pressure [8.9% of effect explained], urinary albumin:creatinine ratio [UACR; 23.9%], gamma glutamyltransferase [4.1%], hematocrit [51.1%], hemoglobin [41.3%], serum albumin [19.5%], erythrocytes [56.7%], serum urate [35.4%], and urine pH [7.5%]) individually mediated the effect of canagliflozin on the kidney outcome. In a parsimonious multivariable model, erythrocyte concentration, serum urate, and systolic blood pressure maximized cumulative mediation (115%). Mediating effects of UACR, but not other mediators, were highly dependent upon the baseline level of UACR: UACR mediated 42% and 7% of the effect in those with baseline UACR 30 mg/g or more and under 30 mg/g, respectively. The identified mediators support existing hypothesized mechanisms for the prevention of kidney outcomes with sodium glucose co-transporter 2 inhibitors. Thus, the disparity in mediating effects across baseline UACR subgroups suggests that the mechanism for kidney protection with canagliflozin may vary across patient subgroups.

Finerenone—A New Frontier in Renin-Angiotensin-Aldosterone System Inhibition in Diabetic Kidney Disease

Background and Aims Chronic kidney disease (CKD) is a significant public health concern, accounting for 3.2% of annual United Kingdom (UK) health care spending, with increasing burdens expected due to rising comorbidities and an aging population. Sodium-glucose co-transporter-2 inhibitors (SGLT-2i) are an effective first-line therapeutic option that can slow disease progression to later more costly stages including kidney replacement therapy (KRT); however, uptake remains low with an estimated 17% of indicated UK patients receiving treatment. Notably, beyond the label indication, a urine albumin creatinine ratio (UACR) test is an additional barrier for access to SGLT-2is in the UK. The Kidney Disease: Improving Global Outcomes (KDIGO) 2024 Clinical Practice Guideline recommends use of SGLT-2is in alignment with the label population for patients with CKD and type 2 diabetes (T2D), and, for those without T2D, criteria include comorbidity history and UACR status. With a lack of alignment in recommendations between KDIGO, UK Kidney Association, and National Institute for Health and Care Excellence, this study aimed to evaluate the clinical and economic implications of both broad and restrictive SGLT-2i eligibility criteria based on UACR for patients with CKD in the UK to provide insights into the potential long-term benefits of broader eligibility for these therapies. Method The IMPACT CKD microsimulation model was used to simulate a population of patients with diagnosed CKD for 25 years across four scenarios. In order of increasingly restrictive SGLT-2i eligibility criteria for patients with CKD, scenarios considered: 1) use by all patients with CKD, 2) use by the KDIGO 2024 Guideline population, 3) full access for T2D, restricted access for non-T2D with UACR &amp;lt;200 mg/g (i.e., non-T2D UACR restriction), and 4) restricted access to those with CKD and UACR &amp;lt;200 mg/g (i.e., all-CKD UACR restriction). Other guideline-directed medical therapies for CKD (except SGLT-2i) were not increased beyond their current background use. Use of SGLT-2i was modelled to have an improvement in eGFR decline, reduction in cardiovascular and acute kidney events, and a one-time improvement in UACR. The model projected CKD and KRT prevalence, incidence of all-cause mortality, and costs associated with CKD, KRT, and total costs including SGLT-2i treatment with a per patient annual cost of £477.30 over the simulated 25 years. Results Results compare the cumulative 25-year burden of CKD in each of the restricted SGLT-2i eligibility criteria scenarios to the full CKD population scenario (Table 1). Increasingly restrictive SGLT-2i criteria were projected to decrease the cumulative number of CKD patients (non-KRT) from −0.4% in the KDIGO scenario, to −1.0% with non-T2D UACR restriction, and −1.3% in the most restrictive scenario (i.e., all-CKD UACR restriction) due to projected increases in cumulative all-cause mortality. The cumulative number of patients on dialysis were projected to increase by +8.8% in the KDIGO scenario, +24.4% with the non-T2D UACR restriction, and +31.4% with the all-CKD UACR restriction. Restrictive SGLT-2i criteria were projected to increase the CKD-related and KRT costs, respectively, by +1.9% and +6.0% in the KDIGO scenario, +1.6% and +16.6% with the non-T2D UACR restriction, and +2.8% and +21.2% with the all-CKD UACR restriction. Total costs (including SGLT-2i treatment costs) were projected to decrease with more restricted use. Similar cumulative net workdays were projected across all scenarios. Conclusion The results of the present analysis projected benefits for patients and healthcare systems with broad SGLT-2i eligibility criteria, aligning with National Health Service priorities to reduce the dialysis burden, manage CKD progression efficiently, and address inequities in access to care for non-diabetic CKD populations. Decisions to implement SGLT-2i criteria should consider the multidimensional impact of treating fewer patients, including increases in clinical and economic burden.

MON-299 KIDNEY OUTCOMES ASSOCIATED WITH INITIATION OF SODIUM GLUCOSE CO-TRANSPORTER 2 INHIBITION VERSUS OTHER GLUCOSE LOWERING DRUGS - AN ANALYSIS FROM THE CVD-REAL STUDY

Aims/IntroductionThe slope of estimated glomerular filtration rate (eGFR) decline (eGFR slope) in early‐stage type 2 diabetes patients might predict the future risk of end‐stage renal disease. Type 2 diabetes patients who show rapid progressive eGFR decline are termed rapid decliners. Several studies of rapid decliners have investigated the efficacy of sodium–glucose cotransporter 2 inhibitors (SGLT2i) in patients with advanced renal dysfunction; however, no studies, to our knowledge, have focused on patients with preserved renal function. Therefore, we investigated the efficacy of SGLT2i in rapid decliners with preserved renal function.Materials and MethodsThis study enrolled type 2 diabetes patients with baseline eGFR ≥60 mL/min/1.73 m2 who had been treated with SGLT2i for ≥3 years. Among these individuals, we defined those with annual eGFR declines ≥5 mL/min/1.73 m2 per year before SGLT2i administration as rapid decliners. The primary end‐point was the change in eGFR slope after SGLT2i administration.ResultsAmong 165 patients treated with SGLT2i for ≥3 years, 21 patients were rapid decliners with preserved renal function. The mean age and eGFR at SGLT2i administration were 58.6 years and 87.1 mL/min/1.73 m2, respectively. The mean annual eGFR slope improved significantly in those administered SGLT2i compared with the control group (−1.00 and −4.36 mL/min/1.73 m2 per year, respectively; P < 0.001). Notably, the steeper the eGFR slope before starting SGLT2i administration, the larger the improvement of eGFR slope, which was independent of the reduction of albuminuria.ConclusionsEarly intervention with SGLT2i may have renoprotective effects in type 2 diabetes patients with rapid decline and preserved renal function.

Background and Aims The chronic kidney disease associated with type II diabetes mellitus is often linked to a high risk of deterioration in kidney function. In this context, the glucagon-like peptide-1 receptor agonist (GLP-1RAs) semaglutide has been shown to have a nephroprotective effect which specifically results in reduced proteinuria. Most trials performed to date have failed to show significant effects when applying very robust criteria to evaluate this nephroprotective effect (such as creatinine doubling time or need for dialysis), although very long follow-up times would be required to demonstrate this effect. Of note, the estimated glomerular filtration rate (eGFR) slope may help determine the nephroprotective effect without requiring such long follow-ups. However, the effect of on the eGFR slope in patients with chronic kidney disease (CKD), especially those in stages 3 and 4, has not yet been adequately evaluated. Method Our objective was to determine the effect of adding subcutaneous semaglutide to the treatment of 156 type II diabetic patients with CKD, a high risk of progression, and a negative eGFR slope prior to starting the intervention. Of these patients, 72% had stage 3 or 4 CKD and they were followed for an average of 3 years. Results The mean eGFR slope was −4.24 mL/min/m2 1.73 m2/year prior to semaglutide but after the start of treatment, and with a mean follow-up of 3 years, an improvement in the slope to −0.34 mL/min/m2 1.73 m2/year (p = 0.005) was observed. The additional use of semaglutide in patients already treated with sodium-glucose cotransporter 2 inhibitors (SGLT2is) was especially positive with on eGFR slope (−4.52 vs +0.22 mL/min/1.73 m2/year, p=0.0001). This benefit was also observed in patients with an eGFR of less than 60 mL/min/1.73 m2, semaglutide had an even more favourable effect on the slope +1.06 mL/min/1.73 m2/year (p = 0.001). The patients who benefited the most were those with albuminuria of less than 1,000 mg/g creatinine. Conclusion In our real-life study in a population at risk for rapid deterioration of renal function, the administration of subcutaneous semaglutide conferred an improvement in the eGFR slope in the medium and long term, with this difference being especially relevant when its treatment was added to patients treated with SGLT2is.

New Glucose-Lowering Agents for Diabetic Kidney Disease.

Pitfalls in Using Estimated Glomerular Filtration Rate Slope as a Surrogate for the Effect of Drugs on the Risk of Serious Adverse Renal Outcomes in Clinical Trials of Patients With Heart Failure.

Background and Aims Diabetes Mellitus type 2 (DM2) leads to chronic kidney disease in a 30-40% of diabetic patients and it is the major cause of end stage renal disease (ESRD). The clinical course of diabetic kidney disease is very heterogeneous and there is a lack of agreement between clinical parameters and renal histology. Besides, lesions of non-diabetic kidney disease (NDRD) can coexist with lesions of diabetic nephropathy (DN) in two-thirds of kidney biopsies in patients with diabetes. There is not a specific treatment against diabetic kidney disease, treatment based in the blockade of renin-angiotensin-aldosterone system has demonstrated a delay of kidney function decline but the diabetic kidney disease is still the main cause of renal replacement by dialysis. Recently, a new class of oral glucose -lowering drugs, sodium-glucose cotransporter 2 (SGLT2) inhibitors, have shown beneficial effects into cardiovascular protection and chronic kidney disease in diabetic patients but it is not clear the beneficial effect in DN. The aim of this study is to evaluate the role of SGLT2 inhibitors in diabetic patients with DN biopsy-confirmed and compare with a group of diabetic patients with NDRD (DN and superimposed non diabetic renal disease lesions, NDRD). Method This is a retrospective study with DM2 patients and kidney biopsy performed. Patient demographic characteristics were recorded and diagnosis of Hypertension, duration of DM2, presence or absence of diabetic retinopathy (DR), macrovascular disease and treatment with renin–angiotensin– aldosterone system blockers (RAASB), oral hypoglycaemic agents, insulin, and aldosterone antagonists. Histological lesions were recorded according to the pathologic classification of DN. Renal function was based on estimated filtration rate CKD-EPI (eGFR mil/min/m2), the urine albumin-creatinine ratio (UACR mg/gr) and the 24 h proteinuria (g/24 h). Diabetic patients were classified according to the kidney biopsies in DN and NDRD. The follow up was assessed at the time of sodium-glucose cotransporter 2 (SGLT2) inhibitors started, 6, 12 and 24 months. Results A total of 64 DM2 patients with kidney biopsy were included in the study. Basal characteristics are summarized in Table 1. DN was diagnosed in 47% and NDRD in 53% of DM2 patients. DM2 patients with NDRD were older (64 ± 10 vs 70 ± 10, p = 0.017), and with more macrovascular disease than patients with DN, 6 (20%) vs 15 (44%), p = 0.04. Instead, DM2 patients with DN showed higher uACR levels than NDRD (2355 ± 2540 vs 706 ± 730, p = 0.02). A 40% of DM2 patients with DN were classified in nodular sclerosis class III of glomerular classification of DN. Interstitial fibrosis and tubular atrophy score were higher in DN versus NDRD patients, (interstitial fibrosis 12 (40%) vs 3 (9%), p = 0.006, tubular atrophy 10 (33%) vs 3 (9%), p = 0.02, Table 2. At the end of follow up, 20% of DM2 patients developed ESRD. According SGLT2 inhibitors treatment, a higher proportion of ESRD and death were observed in DM2 patients without SGLT2 inhibitors than patients with SGLT2 inhibitors, ESRD 11 (39%) vs 2 (6%), p = 0.001, death 9 (32%) vs 4 (11%), p = 0.03. Serum creatinine levels were lower in DM2 patients with SGLT2 inhibitors (118 ± 63.7 vs 203 ± 80.7, p = 0.001), but no differences was observed in uACR between groups. A significant reduction in serum creatinine levels with better eGFR were observed in both groups (DN and NDRD) under SGLT2 inhibitors comparing to group without SGLT2 inhibitors, serum creatinine levels 124 ± 78 vs 236 ± 83, p = 0.008, 107 ± 40 vs 201 ± 110, p = 0.02, and eGFR mil/min/m2 60.9 ± 27.5 vs 25.1 ± 7.2, p = 0.004, 62.6 ± 21.2 vs 33.7 ± 16.2, p = 0.005, Table 3. Conclusion A higher proportion of DM2 showed NDRD lesions in kidney biopsy. Treatment with SGLT2 inhibitors reduced progression of chronic renal disease in DN and NDRD DM2 patients. A reduced progression to ESRD and death were also observed in NDRD DM2 patients with SGLT2 treatment.

Background and Aims Fabry disease is a rare X-linked congenital metabolic disorder caused by mutations in the alpha-galactosidase A (GLA) gene. These mutations lead to the accumulation of globotriaosylceramide (Gb3), a substrate of α-galactosidase A, within various tissues, including the kidneys. Renal involvement is a major complication in patients with Fabry disease (FD). Although enzyme replacement therapy (ERT) and chaperone therapy can slow the progression of kidney dysfunction, some patients eventually develop end-stage kidney disease. Sodium-glucose cotransporter 2 (SGLT2) inhibitors, initially developed as therapeutic agents for diabetes mellitus, have recently been explored for their potential in treating non-diabetic chronic kidney diseases (CKD). While several studies have demonstrated the renal protective effects of SGLT2 inhibitors in various CKD, their efficacy in FD remains unclear. The present study aims to evaluate the renal protective effects of SGLT2 inhibitors in patients with Fabry disease by analyzing data from our institutional database. Method As of December 2024, the database included 34 patients. Patients who had not received SGLT2 inhibitors were excluded, resulting leaving 10 patients for analysis. To assess the renal protective effects of SGLT2 inhibitors, we analyzed the estimated glomerular filtration rate (eGFR) slopes over two periods: one year before and one year after initiating SGLT2 inhibitor therapy. The eGFR slopes were calculated using two methods: an ordinary least-squares linear regression and a linear mixed-effects model. The eGFR slopes derived from the ordinary least-squares linear regression model were compared using the Wilcoxon signed-rank test. For the linear mixed-effects model, covariates were adjusted across three models: Model 1: included age and sex; Model 2: included the variables in Model 1 plus ERT and chaperone therapy; Model 3: further adjusted for the use of angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and angiotensin receptor-neprilysin inhibitors. Results Of the patients included in the analysis, 70.0% (n = 7) were men. At baseline, the mean age was 40.6 ± 17.6 years, and the mean eGFR was 87.9 ± 33.5 mL/min/1.73 m2, 70.0% (n = 7) received renin-angiotensin system inhibitors, and 90% (n = 9) received ERT (agalsidase-alpha, n = 6; agalsidase-beta, n = 3). No patient received chaperone therapy. Using the ordinary least-squares linear regression model, the eGFR slope significantly improved following SGLT2 inhibitor therapy, changing from -4.4 (interquartile range [IQR]: −10.6, 0.6) to 1.3 (IQR: −4.2, 9.7) mL/min/1.73 m²/year, P = 0.037). Similarly, the linear mixed-effects model showed significant improvement, with eGFR slope changing from −6.6 (95% confidence interval [CI]: -11.5, −1.7) to 1.0 (95% CI: −4.0, 6.0) mL/min/1.73 m²/year (P = 0.013). The improvement in eGFR slope remained statistically significant after adjusting for covariates (Model 1, from −3.9 (95% CI: −9.0, 1.2) to 4.1 (95% CI: −1.0, 9.3), P = 0.010; Model 2, from −4.8 (95% CI: −10.0, 0.4) to 2.4 (95% CI: −2.9, 7.8), P = 0.023; Model 3, from −2.5 (95% CI: −8.3, 3.2) to 6.0 (95% CI: 0.1, 12.0), P = 0.022). Conclusion SGLT2 inhibitors may mitigate kidney function decline in patients with FD, highlighting their potential as a novel therapeutic strategy for managing kidney disease in this population.

Background:Many studies have shown the effects of SGLT2 inhibitors on type 2 diabetes, but the effects in patients with type 2 diabetes with chronic kidney disease remains unclear. This study aims to evaluate the effects of SGLT2 inhibitors on renal outcomes in patients with type 2 diabetes mellitus with chronic kidney disease.Methods:We conducted systematic searches of PubMed, Embase, and Cochrane Central Register of Controlled Trials up to April 30, 2020 and included randomized controlled trials of SGLT2 inhibitors in adult type 2 diabetes mellitus (T2DM) patients with chronic kidney disease (CKD) reporting estimated glomerular filtration rate (eGFR) and/or urine albumin/creatinine ratio (UACR) changes and/or acute kidney injury or failure (AKI). Random effects models were adopted to measure the pooled outcomes.Results:Nine studies with 8826 participants were included. SGLT2 inhibitors were not associated with a significant change in eGFR (mean difference (MD), −0.75 ml/minutes per 1.73 m2, 95% CI −1.61 to 0.10, P = .09) in type 2 diabetic patients with CKD. UACR reduction after SGLT2 inhibitors was significant in type 2 diabetic patients with CKD (MD −24.27 mg/g, 95% CI −44.46 to −4.09, P = .02). SGLT2 inhibitors associated with AKI in the patients were significant (OR 0.80, 95% CI [0.66 to 0.98], P = .03).Conclusion:SGLT2 inhibitors had no significant effect on kidney function (eGFR measured) in the pooled analysis. And SGLT2 inhibitors effectively reduced UACR in T2DM with CKD. Besides, SGLT2 inhibitors could reduce the incidence of AKI.

n/a.