Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes
Open accessAbstract
BACKGROUND: Diabetes confers an increased risk of adverse cardiovascular and renal events. In the EMPA-REG OUTCOME trial, empagliflozin, a sodium-glucose cotransporter 2 inhibitor, reduced the risk of major adverse cardiovascular events in patients with type 2 diabetes at high risk for cardiovascular events. We wanted to determine the long-term renal effects of empagliflozin, an analysis that was a prespecified component of the secondary microvascular outcome of that trial. METHODS: We randomly assigned patients with type 2 diabetes and an estimated glomerular filtration rate of at least 30 ml per minute per 1.73 m(2) of body-surface area to receive either empagliflozin (at a dose of 10 mg or 25 mg) or placebo once daily. Prespecified renal outcomes included incident or worsening nephropathy (progression to macroalbuminuria, doubling of the serum creatinine level, initiation of renal-replacement therapy, or death from renal disease) and incident albuminuria. RESULTS: Incident or worsening nephropathy occurred in 525 of 4124 patients (12.7%) in the empagliflozin group and in 388 of 2061 (18.8%) in the placebo group (hazard ratio in the empagliflozin group, 0.61; 95% confidence interval, 0.53 to 0.70; P<0.001). Doubling of the serum creatinine level occurred in 70 of 4645 patients (1.5%) in the empagliflozin group and in 60 of 2323 (2.6%) in the placebo group, a significant relative risk reduction of 44%. Renal-replacement therapy was initiated in 13 of 4687 patients (0.3%) in the empagliflozin group and in 14 of 2333 patients (0.6%) in the placebo group, representing a 55% lower relative risk in the empagliflozin group. There was no significant between-group difference in the rate of incident albuminuria. The adverse-event profile of empagliflozin in patients with impaired kidney function at baseline was similar to that reported in the overall trial population. CONCLUSIONS: In patients with type 2 diabetes at high cardiovascular risk, empagliflozin was associated with slower progression of kidney disease and lower rates of clinically relevant renal events than was placebo when added to standard care. (Funded by the Boehringer Ingelheim and Eli Lilly and Company Diabetes Alliance; EMPA-REG OUTCOME ClinicalTrials.gov number, NCT01131676.).
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SGLT2i use in T2D reduces AKI risk by 25%.
“Additionally, the risk of AKI is actually reduced by 25% with SGLT2i use in persons with T2D.461”
From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [461]
The Safety and Adverse Events section reports fewer events consistent with acute renal failure, including AKI, in the empagliflozin group than in the placebo group. It does not report a 25% reduction in AKI risk, and this trial studied empagliflozin in people with T2D at high cardiovascular risk, not SGLT2 inhibitors as a class. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSGLT2is and GLP-1RAs have demonstrated benefits in preventing deleterious cardiorenal endpoints among individuals with type 2 diabetes.
“In recent years, sodium–glucose cotransporter 2 inhibitors (SGLT2is) and glucagon-like peptide-1 receptor antagonists (GLP-1RAs) have demonstrated benefits in preventing deleterious cardiorenal endpoints among individuals with type 2 diabetes, shifting disease management from a glucocentric approach to one that prioritises long-term cardiorenal health [5–7].”
From Racial and ethnic disparities in the uptake of SGLT2is and GLP-1RAs among Medicare beneficiaries with type 2 diabetes and heart failure, atherosclerotic cardiovascular disease and chronic kidney disease, 2013–2019 (2025) · cites this paper as [5]
The Renal Outcomes section reports fewer kidney events with empagliflozin than with placebo in patients with type 2 diabetes, and the Cardiovascular Outcomes section reports a lower risk of major adverse cardiovascular events. The paper concerns one SGLT2 inhibitor in patients at high cardiovascular risk; it does not establish benefits for GLP-1RAs or a shift in disease-management priorities. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSGLT2 inhibitors reduce renal tubular glucose reabsorption, weight, systemic blood pressure, intraglomerular pressure, and albuminuria and slow GFR loss through mechanisms that appear independent of glycemia.
“For example, SGLT2 inhibitors reduce renal tubular glucose reabsorption, weight, systemic blood pressure, intraglomerular pressure, and albuminuria and slow GFR loss through mechanisms that appear independent of glycemia (31,(89)(90)(91)(92).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2025 (2025) · cites this paper as [31]
The introduction (p. 324) says empagliflozin reduces renal glucose reabsorption and is associated with lower weight and blood pressure; it reports reduced intraglomerular pressure in patients with type 1 diabetes. The Renal Outcomes and Renal Function over Time sections report less progression to macroalbuminuria and slower long-term eGFR decline with empagliflozin in patients with type 2 diabetes. The paper does not establish that these renal effects occur independently of glycemia, and its findings on empagliflozin do not establish the full claim for SGLT2 inhibitors as a class. (LLM, conf=0.86)
Experimental — accuracy not yet measuredConcern that SGLT2 inhibitors may promote AKI through volume depletion has not been found to be true in randomized controlled trials of advanced kidney disease or high CVD risk with normal kidney function.
“There was concern that sodium-glucose cotransporter 2 (SGLT2) inhibitors may promote AKI through volume depletion, particularly when combined with diuretics or other medications that reduce glomerular filtration; however, this has not been found to be true in randomized controlled trials of advanced kidney disease (29) or high CVD risk with normal kidney function (30)(31)(32).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [31]
The Safety and Adverse Events section reports fewer events consistent with acute renal failure, including AKI, with empagliflozin than with placebo, and similar rates of events consistent with volume depletion. The Results section says more than 99% of participants had established cardiovascular disease, but 25.5% had a baseline eGFR below 60; this was not exclusively a trial of people with normal kidney function. The paper also does not establish the claimed mechanism or report an AKI result specifically for patients taking diuretics. (LLM, conf=0.87)
Experimental — accuracy not yet measuredSGLT2 inhibitors reduce kidney tubular glucose reabsorption, weight, systemic blood pressure, intraglomerular pressure, and albuminuria and slow GFR loss through mechanisms that appear independent of glycemia.
“For example, SGLT2 inhibitors reduce kidney tubular glucose reabsorption, weight, systemic blood pressure, intraglomerular pressure, and albuminuria and slow GFR loss through mechanisms that appear independent of glycemia (31,(97)(98)(99)(100)(101).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [31]
The introduction (p. 324) says empagliflozin reduces renal glucose reabsorption, weight, blood pressure, and intraglomerular pressure; Renal Outcomes reports less progression to macroalbuminuria, and Renal Function over Time reports slower eGFR decline than with placebo. The Discussion says changes in hyperglycemia and other risk factors are unlikely to fully explain the renal benefit, but does not establish that the mechanisms are independent of glycemia. The evidence is for empagliflozin in the studied populations, rather than SGLT2 inhibitors as a class. (LLM, conf=0.86)
Experimental — accuracy not yet measured
While glucose-lowering effects of SGLT2 inhibitors are blunted with eGFR <45 mL/min/1.73m2, kidney and cardiovascular benefits were still seen at eGFR levels as low as 20 mL/min/1.73m2 even with no significant change in glucose.
“while the glucose-lowering effects of SGLT2 inhibitors are blunted with eGFR <45 mL/min/1.73m 2 , the kidney and cardiovascular benefits were still seen at eGFR levels as low as 20 mL/min/ 1.73 m 2 even with no significant change in glucose (4,29,31,107,123,127,129,130).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [31]
The Results report participants with baseline eGFR of 30–44 mL/min/1.73 m², and the Renal Outcomes section reports kidney benefits with empagliflozin; Figure 2 (p. 330) also reports a benefit for the composite of nephropathy or cardiovascular death. The cited passages do not establish benefits at eGFR as low as 20, blunted glucose lowering below 45, or benefits occurring without a significant change in glucose. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLarge clinical trials have shown benefits of newer glucose-lowering medications on cardiovascular and kidney outcomes in patients with CKD with type 2 diabetes.
“Large clinical trials have shown benefits of newer glucose-lowering medications on cardiovascular and kidney outcomes in patients with CKD with type 2 diabetes.5, 6, 7, 8, 9, 10, 11, 12, 13, 14”
From Disparities in SGLT2 Inhibitor or Glucagon-Like Peptide 1 Receptor Agonist Initiation Among Medicare-Insured Adults With CKD in the United States (2023) · cites this paper as [9]
The Renal Outcomes section reports fewer kidney events with empagliflozin than placebo, with consistent benefit across subgroups; the Discussion says this included patients with prevalent kidney disease. The Cardiovascular Outcomes section reports a cardiovascular benefit for the overall type 2 diabetes trial population, but does not establish that benefit specifically for patients with CKD. This paper also evaluates one medication, rather than newer glucose-lowering medications as a group. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAs in other SGLT2 inhibitor trials, there was an initial dip in estimated GFR followed by stabilization of kidney-function decline.
“As in other trials of SGLT2 inhibitors, there was an initial dip in the estimated GFR, followed by a stabilization of kidney-function decline.7,8,10”
From Dapagliflozin in Patients with Chronic Kidney Disease (2020) · cites this paper as [7]
SGLT2 inhibitors have not been found to promote AKI in randomized controlled trials of advanced kidney disease or high cardiovascular risk with normal kidney function.
“There was concern that sodium-glucose cotransporter 2 (SGLT2) inhibitors may promote AKI through volume depletion, particularly when combined with diuretics or other medications that reduce glomerular filtration; however, this has not been found to be true in randomized controlled trials of advanced kidney disease (29) or high CVD risk with normal kidney function (30)(31)(32).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2025 (2025) · cites this paper as [31]
Large-scale cardiovascular outcome trials of SGLT2 inhibitors have shown promising effects on a range of albuminuria and serum creatinine-based kidney outcomes in patients with, or at high risk of, atherosclerotic cardiovascular disease.
“Large-scale cardio vascular outcome trials [10][11][12][13][14][15] of SGLT2 inhibitors, which were originally designed to meet regulatory requirements and ensure cardiovascular safety, have shown promising effects on a range of albuminuria and serum creatinine-based kidney outcomes in patients with, or at high risk of, atherosclerotic cardiovascular disease.”
From SGLT2 inhibitors for the prevention of kidney failure in patients with type 2 diabetes: a systematic review and meta-analysis (2019) · cites this paper as [11]
In cardiovascular trials of SGLT2 inhibitors, exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes.
“In cardiovascular trials of inhibitors of sodium-glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes.”
From Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy (2019) · cites this paper as [9]
In cardiovascular safety trials of SGLT2 inhibitors in type 2 diabetes, secondary kidney endpoints and cardiovascular events were consistently reduced.
“In clinical trials designed to demonstrate the CVD safety of SGLT2 inhibitors in type 2 diabetes mellitus (T2DM), consistent reductions in risks for secondary kidney disease end points (albuminuria and a composite of serum creatinine doubling or 40% estimated glomerular filtration rate decline, kidney failure, or death), along with reductions in CVD events, were observed.”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
EMPA-REG OUTCOME was the first cardiovascular outcome trial to demonstrate safety of an SGLT2 inhibitor and the first to show clear benefit of a glucose-lowering agent for major adverse cardiovascular events in type 2 diabetes with atherosclerotic cardiovascular disease.
“The first reported cardiovascular disease (CVD) outcome trial (CVOT) to demonstrate safety of an SGLT2 inhibitor, the EMPA-REG OUTCOME trial, was also the first to show clear benefit of a particular glucose-lowering agent for protection against major adverse cardiovascular events (MACE) in people with T2DM and ASCVD.”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
Empagliflozin reduced the risk for secondary kidney disease endpoints including albuminuria progression, serum creatinine doubling, kidney failure, and death.
“Empagliflozin also reduced the risk for secondary kidney disease end points (albuminuria progression, serum creatinine doubling, kidney failure, and death) (11).”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
Diuresis is an important mechanism for reducing blood pressure and risk for heart failure events.
“Diuresis is an important mechanism for reducing blood pressure and risk for HF events (11–16,35).”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
Reductions in hospitalizations for heart failure were seen in EMPA-REG OUTCOME, CANVAS, and DECLARE-TIMI 58, including patients with and without prevalent atherosclerotic cardiovascular disease and those with and without a history of heart failure.
“Reductions in hospitalizations for HF were seen in EMPA-REG OUTCOME, CANVAS, and DECLARE-TIMI 58, including patients with and without prevalent ASCVD and those with and without a history of HF.”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
EMPA-REG OUTCOME was the first cardiovascular outcome trial to demonstrate that empagliflozin reduced the risk for a secondary kidney disease outcome (severely increased albuminuria, doubling of serum creatinine accompanied by eGFR ≤45 mL/min/1.73 m2, initiation of kidney replacement therapy, or death from kidney disease) to 12.7% versus 18.8% in the placebo group (HR 0.61; 95% CI 0.53-0.70).
“EMPA-REG OUTCOME was the first CVOT to demonstrate that treatment with an SGLT2 inhibitor, empagliflozin, reduced the risk for a secondary kidney disease outcome (severely increased albuminuria, doubling of serum creatinine accompanied by eGFR ≤45 mL/min/1.73 m2, initiation of KRT, or death from kidney disease) to 12.7% versus 18.8% in the placebo group (HR, 0.61; 95% CI, 0.53–0.70) (11).”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
The effect on new-onset albuminuria was observed in CANVAS and DECLARE-TIMI-58, but not in the EMPA-REG OUTCOME trial.
“This effect was observed in CANVAS (12) and DECLARE-TIMI-58 (67), but not in the EMPA-REG OUTCOME trial (11).”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
After the first 4 weeks of treatment during which eGFR declined with empagliflozin, eGFR stabilized in the empagliflozin groups and declined steadily in the placebo group.
“Importantly, after the first 4 weeks of treatment during which eGFR declined with empagliflozin, eGFR stabilized in the empagliflozin groups and declined steadily in the placebo group.”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
In the cardiovascular outcome trials and CREDENCE, kidney-protective effects are consistent overall and in participants with different levels of glycemic control (HbA1c below 7% or above 9%) or eGFR strata (above 90, 60-90, or 30-60 mL/min/1.73 m2).
“In the CVOTs and CREDENCE, kidney-protective effects are consistent overall (Fig. 6) (69) and in participants with different levels of glycemic control (HbA1c <7% or >9%) or eGFR strata (>90, 60–90, or 30–60 mL/min/1.73 m2) (11,12,14,70).”
From SGLT2 inhibition for CKD and cardiovascular disease in type 2 diabetes: report of a scientific workshop sponsored by the National Kidney Foundation (2021) · cites this paper as [11]
Empagliflozin reduced progression of chronic kidney disease (12.7% versus 18.8%; 39% relative risk reduction).
“and progression of chronic kidney disease (12.7% versus 18.8%; 39% RRR)”
From Clinical management of stable coronary artery disease in patients with type 2 diabetes mellitus: a scientific statement from the American Heart Association (2020) · cites this paper as [220]
Recent cardiovascular outcomes trials demonstrate that SGLT2 inhibitors may reduce heart failure morbidity and mortality and slow decline in renal function.
“Recent cardiovascular outcomes trials demonstrate that therapies that inhibit sodium glucose cotransporter (SGLT)2 may reduce heart failure morbidity and mortality and slow decline in renal function (7,8,23,42,43).”
From Evaluation of renal and cardiovascular protection mechanisms of SGLT2 inhibitors: model-based analysis of clinical data (2018) · cites this paper as [42]
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2018 ESC/ESH Guidelines for the management of arterial hypertension
Williams, B., Mancia, G., Spiering, W., Agabiti Rosei, E., Azizi, M., Burnier, M., Clement, D. L., Coca, A., de Simone, G., Dominiczak, A., et al. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehy339 · Cited by 10,286 · see citing works
Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes
Neal, B., Perkovic, V., Mahaffey, K. W., de Zeeuw, D., Fulcher, G., Erondu, N., Shaw, W., Law, G., Desai, M., & Matthews, D. R. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1611925 · Cited by 7,830 · see citing works
Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction
McMurray, J. J. V., Solomon, S. D., Inzucchi, S. E., Køber, L., Kosiborod, M. N., Martinez, F. A., Ponikowski, P., Sabatine, M. S., Anand, I. S., Bělohlávek, J., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1911303 · Cited by 7,140 · see citing works
Self-citationDapagliflozin and Cardiovascular Outcomes in Type 2 Diabetes
Wiviott, S. D., Raz, I., Bonaca, M. P., Mosenzon, O., Kato, E. T., Cahn, A., Silverman, M. G., Zelniker, T. A., Kuder, J. F., Murphy, S. A., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1812389 · Cited by 6,382 · see citing works
Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy
Perkovic, V., Jardine, M. J., Neal, B., Bompoint, S., Heerspink, H. J. L., Charytan, D. M., Edwards, R., Agarwal, R., Bakris, G., Bull, S., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1811744 · Cited by 6,189 · see citing works
Self-citationDapagliflozin in Patients with Chronic Kidney Disease
Heerspink, H. J. L., Stefánsson, B. V., Correa-Rotter, R., Chertow, G. M., Greene, T., Hou, F.-F., Mann, J. F. E., McMurray, J. J. V., Lindberg, M., Rossing, P., et al. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa2024816 · Cited by 5,618 · see citing works
Davies, M. J., D’Alessio, D. A., Fradkin, J., Kernan, W. N., Mathieu, C., Mingrone, G., Rossing, P., Tsapas, A., Wexler, D. J., & Buse, J. B. (2018) · Diabetes Care · doi:10.2337/dci18-0033 · Cited by 3,518 · see citing works
Diabetic Kidney Disease: Challenges, Progress, and Possibilities
Alicic, R. Z., Rooney, M. T., & Tuttle, K. R. (2017) · Clinical Journal of the American Society of Nephrology · doi:10.2215/cjn.11491116 · Cited by 2,898 · see citing works
Zelniker, T. A., Wiviott, S. D., Raz, I., Im, K., Goodrich, E. L., Bonaca, M. P., Mosenzon, O., Kato, E. T., Cahn, A., Furtado, R. H. M., et al. (2019) · The Lancet · doi:10.1016/s0140-6736(18)32590-x · Cited by 2,845 · see citing works
Williams, B., Mancia, G., Spiering, W., Agabiti Rosei, E., Azizi, M., Burnier, M., Clement, D. L., Coca, A., de Simone, G., Dominiczak, A., et al. (2018) · Journal of Hypertension · doi:10.1097/hjh.0000000000001940 · Cited by 2,885 · see citing works
Virani, S. S., Newby, L. K., Arnold, S. V., Bittner, V., Brewer, L. C., Demeter, S. H., Dixon, D. L., Fearon, W. F., Hess, B., Johnson, H. M., et al. (2023) · Circulation · doi:10.1161/cir.0000000000001168 · Cited by 1,598 · see citing works
Cardiovascular outcomes with ertugliflozin in type 2 diabetes
Cannon, C. P., Pratley, R., Dagogo-Jack, S., Mancuso, J., Huyck, S., Masiukiewicz, U., Charbonnel, B., Frederich, R., Gallo, S., Cosentino, F., et al. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa2004967 · Cited by 1,514 · see citing works
Davies, M. J., D’Alessio, D. A., Fradkin, J., Kernan, W. N., Mathieu, C., Mingrone, G., Rossing, P., Tsapas, A., Wexler, D. J., & Buse, J. B. (2018) · Diabetologia · doi:10.1007/s00125-018-4729-5 · Cited by 1,455 · see citing works
Katsarou, A., Gudbjörnsdottir, S., Rawshani, A., Dabelea, D., Bonifacio, E., Anderson, B. J., Jacobsen, L. M., Schatz, D. A., & Lernmark, Å. (2017) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2017.16 · Cited by 1,475 · see citing works
KDIGO 2020 Clinical practice guideline for diabetes management in chronic kidney disease
de Boer, I. H., Caramori, M. L., Chan, J. C. N., Heerspink, H. J. L., Hurst, C., Khunti, K., Liew, A., Michos, E. D., Navaneethan, S. D., Olowu, W. A., et al. (2020) · Kidney International · doi:10.1016/j.kint.2020.06.019 · Cited by 1,399 · see citing works
Self-citationHeerspink, H. J. L., Perkins, B. A., Fitchett, D. H., Husain, M., & Cherney, D. Z. I. (2016) · Circulation · doi:10.1161/circulationaha.116.021887 · Cited by 1,376 · see citing works
Self-citationKDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease
Rossing, P., Caramori, M. L., Chan, J. C. N., Heerspink, H. J. L., Hurst, C., Khunti, K., Liew, A., Michos, E. D., Navaneethan, S. D., Olowu, W. A., et al. (2022) · Kidney International · doi:10.1016/j.kint.2022.06.008 · Cited by 1,373 · see citing works
Self-citationLiraglutide and renal outcomes in type 2 diabetes
Mann, J. F. E., Ørsted, D. D., Brown-Frandsen, K., Marso, S. P., Poulter, N. R., Rasmussen, S., Tornøe, K., Zinman, B., & Buse, J. B. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1616011 · Cited by 1,253 · see citing works
Self-citationMcGuire, D. K., Shih, W. J., Cosentino, F., Charbonnel, B., Cherney, D. Z. I., Dagogo-Jack, S., Pratley, R., Greenberg, M., Wang, S., Huyck, S., et al. (2021) · JAMA Cardiology · doi:10.1001/jamacardio.2020.4511 · Cited by 1,235 · see citing works
Glomerular hyperfiltration in diabetes: mechanisms, clinical significance, and treatment
Tonneijck, L., Muskiet, M. H. A., Smits, M. M., van Bommel, E. J., Heerspink, H. J. L., van Raalte, D. H., & Joles, J. A. (2017) · Journal of the American Society of Nephrology · doi:10.1681/asn.2016060666 · Cited by 887 · see citing works
Neuen, B. L., Young, T., Heerspink, H. J. L., Neal, B., Perkovic, V., Billot, L., Mahaffey, K. W., Charytan, D. M., Wheeler, D. C., Arnott, C., et al. (2019) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(19)30256-6 · Cited by 893 · see citing works
Zelniker, T. A., Wiviott, S. D., Raz, I., Im, K., Goodrich, E. L., Furtado, R. H. M., Bonaca, M. P., Mosenzon, O., Kato, E. T., Cahn, A., et al. (2019) · Circulation · doi:10.1161/circulationaha.118.038868 · Cited by 781 · see citing works
Inzucchi, S. E., Zinman, B., Fitchett, D., Wanner, C., Ferrannini, E., Schumacher, M., Schmoor, C., Ohneberg, K., Johansen, O. E., George, J. T., et al. (2018) · Diabetes Care · doi:10.2337/dc17-1096 · Cited by 740 · see citing works
Self-citationMosenzon, O., Wiviott, S. D., Cahn, A., Rozenberg, A., Yanuv, I., Goodrich, E. L., Murphy, S. A., Heerspink, H. J. L., Zelniker, T. A., Dwyer, J. P., et al. (2019) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(19)30180-9 · Cited by 684 · see citing works
Tuttle, K. R., Lakshmanan, M. C., Rayner, B., Busch, R. S., Zimmermann, A. G., Woodward, D. B., & Botros, F. T. (2018) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(18)30104-9 · Cited by 648 · see citing works
Perkovic, V., de Zeeuw, D., Mahaffey, K. W., Fulcher, G., Erondu, N., Shaw, W., Barrett, T. D., Weidner-Wells, M., Deng, H., Matthews, D. R., et al. (2018) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(18)30141-4 · Cited by 637 · see citing works
Dunlay, S. M., Givertz, M. M., Aguilar, D., Allen, L. A., Chan, M., Desai, A. S., Deswal, A., Dickson, V. V., Kosiborod, M. N., Lekavich, C. L., et al. (2019) · Circulation · doi:10.1161/cir.0000000000000691 · Cited by 639 · see citing works
Vallon, V., & Thomson, S. C. (2017) · Diabetologia · doi:10.1007/s00125-016-4157-3 · Cited by 635 · see citing works
Joseph, J. J., Deedwania, P., Acharya, T., Aguilar, D., Bhatt, D. L., Chyun, D. A., Di Palo, K. E., Golden, S. H., Sperling, L. S., & on behalf of the American Heart Association Diabetes Committee of the Council on Lifestyle and Cardiometabolic Health; Council on Arteriosclerosis, T. A. V. B. C. O. C. C. A. C. O. H. (2022) · Circulation · doi:10.1161/cir.0000000000001040 · Cited by 660 · see citing works
Rabi, D. M., McBrien, K. A., Sapir-Pichhadze, R., Nakhla, M., Ahmed, S. B., Dumanski, S. M., Butalia, S., Leung, A. A., Harris, K. C., Cloutier, L., et al. (2020) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2020.02.086 · Cited by 583 · see citing works
Virani, S. S., Newby, L. K., Arnold, S. V., Bittner, V., Brewer, L. C., Demeter, S. H., Dixon, D. L., Fearon, W. F., Hess, B., Johnson, H. M., et al. (2023) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2023.04.003 · Cited by 596 · see citing works
Wheeler, D. C., Stefánsson, B. V., Jongs, N., Chertow, G. M., Greene, T., Hou, F. F., McMurray, J. J. V., Correa-Rotter, R., Rossing, P., Toto, R. D., et al. (2021) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(20)30369-7 · Cited by 556 · see citing works
Hypoxia signaling in human health and diseases: implications and prospects for therapeutics
Luo, Z., Tian, M., Yang, G., Tan, Q., Chen, Y., Li, G., Zhang, Q., Li, Y., Wan, P., & Wu, J. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01080-1 · Cited by 499 · see citing works
Blonde, L., Umpierrez, G. E., Reddy, S. S., McGill, J. B., Berga, S. L., Bush, M., Chandrasekaran, S., DeFronzo, R. A., Einhorn, D., Galindo, R. J., et al. (2022) · Endocrine Practice · doi:10.1016/j.eprac.2022.08.002 · Cited by 507 · see citing works
Das, S. R., Everett, B. M., Birtcher, K. K., Brown, J. M., Januzzi, J. L., Kalyani, R. R., Kosiborod, M., Magwire, M., Morris, P. B., Neumiller, J. J., et al. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.05.037 · Cited by 466 · see citing works
Wanner, C., Lachin, J. M., Inzucchi, S. E., Fitchett, D., Mattheus, M., George, J., Woerle, H. J., Broedl, U. C., von Eynatten, M., & Zinman, B. (2018) · Circulation · doi:10.1161/circulationaha.117.028268 · Cited by 469 · see citing works
Self-citationThe tubular hypothesis of nephron filtration and diabetic kidney disease
Vallon, V., & Thomson, S. C. (2020) · Nature Reviews Nephrology · doi:10.1038/s41581-020-0256-y · Cited by 465 · see citing works
Heerspink, H. J. L., Perco, P., Mulder, S., Leierer, J., Hansen, M. K., Heinzel, A., & Mayer, G. (2019) · Diabetologia · doi:10.1007/s00125-019-4859-4 · Cited by 457 · see citing works
McMurray, J. J. V., DeMets, D. L., Inzucchi, S. E., Køber, L., Kosiborod, M. N., Langkilde, A. M., Martinez, F. A., Bengtsson, O., Ponikowski, P., Sabatine, M. S., et al. (2019) · European Journal of Heart Failure · doi:10.1002/ejhf.1432 · Cited by 433 · see citing works
Self-citationWheeler, D. C., Toto, R. D., Stefánsson, B. V., Jongs, N., Chertow, G. M., Greene, T., Hou, F. F., McMurray, J. J. V., Pecoits-Filho, R., Correa-Rotter, R., et al. (2021) · Kidney International · doi:10.1016/j.kint.2021.03.033 · Cited by 420 · see citing works
11. Microvascular Complications and Foot Care: <i>Standards of Medical Care in Diabetes—2021</i>
American Diabetes Association (2021) · Diabetes Care · doi:10.2337/dc21-s011 · Cited by 395 · see citing works
Renoprotective effects of sodium-glucose cotransporter-2 inhibitors
Heerspink, H. J. L., Kosiborod, M., Inzucchi, S. E., & Cherney, D. Z. I. (2018) · Kidney International · doi:10.1016/j.kint.2017.12.027 · Cited by 393 · see citing works
Self-citationThe cardio-renal-metabolic connection: a review of the evidence
Marassi, M., & Fadini, G. P. (2023) · Cardiovascular Diabetology · doi:10.1186/s12933-023-01937-x · Cited by 386 · see citing works
Cherney, D. Z. I., Zinman, B., Inzucchi, S. E., Koitka-Weber, A., Mattheus, M., von Eynatten, M., & Wanner, C. (2017) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(17)30182-1 · Cited by 383 · see citing works
Self-citationDanne, T., Garg, S., Peters, A. L., Buse, J. B., Mathieu, C., Pettus, J. H., Alexander, C. M., Battelino, T., Ampudia-Blasco, F. J., Bode, B. W., et al. (2019) · Diabetes Care · doi:10.2337/dc18-2316 · Cited by 379 · see citing works
van Bommel, E. J. M., Muskiet, M. H. A., van Baar, M. J. B., Tonneijck, L., Smits, M. M., Emanuel, A. L., Bozovic, A., Danser, A. H. J., Geurts, F., Hoorn, E. J., et al. (2020) · Kidney International · doi:10.1016/j.kint.2019.09.013 · Cited by 363 · see citing works
Canagliflozin slows progression of renal function decline independently of glycemic effects
Heerspink, H. J. L., Desai, M., Jardine, M., Balis, D., Meininger, G., & Perkovic, V. (2017) · Journal of the American Society of Nephrology · doi:10.1681/asn.2016030278 · Cited by 361 · see citing works
Development of SGLT1 and SGLT2 inhibitors
Rieg, T., & Vallon, V. (2018) · Diabetologia · doi:10.1007/s00125-018-4654-7 · Cited by 377 · see citing works
Toyama, T., Neuen, B. L., Jun, M., Ohkuma, T., Neal, B., Jardine, M. J., Heerspink, H. L., Wong, M. G., Ninomiya, T., Wada, T., et al. (2019) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.13648 · Cited by 330 · see citing works
Das, S. R., Everett, B. M., Birtcher, K. K., Brown, J. M., Cefalu, W. T., Januzzi, J. L., Kalyani, R. R., Kosiborod, M., Magwire, M. L., Morris, P. B., et al. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.09.020 · Cited by 300 · see citing works
SGLT2 Inhibitors: A Review of Their Antidiabetic and Cardioprotective Effects
Tentolouris, A., Vlachakis, P., Tzeravini, E., Eleftheriadou, I., & Tentolouris, N. (2019) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph16162965 · Cited by 300 · see citing works
Arnold, S. V., Bhatt, D. L., Barsness, G. W., Beatty, A. L., Deedwania, P. C., Inzucchi, S. E., Kosiborod, M., Leiter, L. A., Lipska, K. J., Newman, J. D., et al. (2020) · Circulation · doi:10.1161/cir.0000000000000766 · Cited by 304 · see citing works
Self-citationNocturnal Hypertension: New Technology and Evidence
Kario, K. (2018) · Hypertension · doi:10.1161/hypertensionaha.118.10971 · Cited by 298 · see citing works
11. Chronic Kidney Disease and Risk Management: <i>Standards of Medical Care in Diabetes—2022</i>
American Diabetes Association Professional Practice Committee (2022) · Diabetes Care · doi:10.2337/dc22-s011 · Cited by 344 · see citing works
Mahaffey, K. W., Jardine, M. J., Bompoint, S., Cannon, C. P., Neal, B., Heerspink, H. J. L., Charytan, D. M., Edwards, R., Agarwal, R., Bakris, G., et al. (2019) · Circulation · doi:10.1161/circulationaha.119.042007 · Cited by 291 · see citing works
Self-citationKidokoro, K., Cherney, D. Z. I., Bozovic, A., Nagasu, H., Satoh, M., Kanda, E., Sasaki, T., & Kashihara, N. (2019) · Circulation · doi:10.1161/circulationaha.118.037418 · Cited by 283 · see citing works
Cherney, D. Z. I., Dekkers, C. C. J., Barbour, S. J., Cattran, D., Abdul Gafor, A. H., Greasley, P. J., Laverman, G. D., Lim, S. K., Di Tanna, G. L., Reich, H. N., et al. (2020) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(20)30162-5 · Cited by 283 · see citing works
Ketoacidosis associated with SGLT2 inhibitor treatment: analysis of FAERS data
Blau, J. E., Tella, S. H., Taylor, S. I., & Rother, K. I. (2017) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.2924 · Cited by 271 · see citing works
Effects of the SGLT-2 inhibitor dapagliflozin on glomerular and tubular injury markers
Dekkers, C. C. J., Petrykiv, S., Laverman, G. D., Cherney, D. Z., Gansevoort, R. T., & Heerspink, H. J. L. (2018) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.13301 · Cited by 263 · see citing works
11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2025
American Diabetes Association Professional Practice Committee, ElSayed, N. A., McCoy, R. G., Aleppo, G., Balapattabi, K., Beverly, E. A., Briggs Early, K., Bruemmer, D., Echouffo-Tcheugui, J. B., Ekhlaspour, L., et al. (2025) · Diabetes Care · doi:10.2337/dc25-s011 · Cited by 262 · see citing works
Neuen, B. L., Ohkuma, T., Neal, B., Matthews, D. R., de Zeeuw, D., Mahaffey, K. W., Fulcher, G., Desai, M., Li, Q., Deng, H., et al. (2018) · Circulation · doi:10.1161/circulationaha.118.035901 · Cited by 257 · see citing works
Kario, K., Okada, K., Kato, M., Nishizawa, M., Yoshida, T., Asano, T., Uchiyama, K., Niijima, Y., Katsuya, T., Urata, H., et al. (2019) · Circulation · doi:10.1161/circulationaha.118.037076 · Cited by 251 · see citing works
Cherney, D. Z. I., Cooper, M. E., Tikkanen, I., Pfarr, E., Johansen, O. E., Woerle, H. J., Broedl, U. C., & Lund, S. S. (2018) · Kidney International · doi:10.1016/j.kint.2017.06.017 · Cited by 243 · see citing works
Self-citationJardine, M. J., Mahaffey, K. W., Neal, B., Agarwal, R., Bakris, G. L., Brenner, B. M., Bull, S., Cannon, C. P., Charytan, D. M., de Zeeuw, D., et al. (2017) · American Journal of Nephrology · doi:10.1159/000484633 · Cited by 234 · see citing works
Self-citationSGLT2 Inhibitor–Induced Sympathoinhibition
Herat, L. Y., Magno, A. L., Rudnicka, C., Hricova, J., Carnagarin, R., Ward, N. C., Arcambal, A., Kiuchi, M. G., Head, G. A., Schlaich, M. P., et al. (2020) · JACC: Basic to Translational Science · doi:10.1016/j.jacbts.2019.11.007 · Cited by 233 · see citing works
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Self-citationCardiac and Renal Effects of Sodium-Glucose Co-Transporter 2 Inhibitors in Diabetes
Zelniker, T. A., & Braunwald, E. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.06.040 · Cited by 236 · see citing works
Molecular mechanisms of renal aging
Schmitt, R., & Melk, A. (2017) · Kidney International · doi:10.1016/j.kint.2017.02.036 · Cited by 235 · see citing works
Unraveling the Role of Inflammation in the Pathogenesis of Diabetic Kidney Disease
Matoba, K., Takeda, Y., Nagai, Y., Kawanami, D., Utsunomiya, K., & Nishimura, R. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20143393 · Cited by 223 · see citing works
Role of the sympathetic nervous system in regulation of the sodium glucose cotransporter 2
Matthews, V. B., Elliot, R. H., Rudnicka, C., Hricova, J., Herat, L., & Schlaich, M. P. (2017) · Journal of Hypertension · doi:10.1097/hjh.0000000000001434 · Cited by 222 · see citing works
Halden, T. A. S., Kvitne, K. E., Midtvedt, K., Rajakumar, L., Robertsen, I., Brox, J., Bollerslev, J., Hartmann, A., Åsberg, A., & Jenssen, T. (2019) · Diabetes Care · doi:10.2337/dc19-0093 · Cited by 231 · see citing works
McMurray, J. J. V., DeMets, D. L., Inzucchi, S. E., Køber, L., Kosiborod, M. N., Langkilde, A. M., Martinez, F. A., Bengtsson, O., Ponikowski, P., Sabatine, M. S., et al. (2019) · European Journal of Heart Failure · doi:10.1002/ejhf.1548 · Cited by 222 · see citing works
Self-citationCortinovis, M., Perico, N., Ruggenenti, P., Remuzzi, A., & Remuzzi, G. (2022) · Nature Reviews Nephrology · doi:10.1038/s41581-022-00559-y · Cited by 214 · see citing works
Wanner, C., Heerspink, H. J. L., Zinman, B., Inzucchi, S. E., Koitka-Weber, A., Mattheus, M., Hantel, S., Woerle, H.-J., Broedl, U. C., von Eynatten, M., et al. (2018) · Journal of the American Society of Nephrology · doi:10.1681/asn.2018010103 · Cited by 209 · see citing works
Self-citationOnishi, A., Fu, Y., Patel, R., Darshi, M., Crespo-Masip, M., Huang, W., Song, P., Freeman, B., Kim, Y. C., Soleimani, M., et al. (2020) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00264.2020 · Cited by 206 · see citing works
Effects of dapagliflozin in stage 4 chronic kidney disease
Chertow, G. M., Vart, P., Jongs, N., Toto, R. D., Gorriz, J. L., Hou, F. F., McMurray, J. J. V., Correa-Rotter, R., Rossing, P., Sjöström, C. D., et al. (2021) · Journal of the American Society of Nephrology · doi:10.1681/asn.2021020167 · Cited by 201 · see citing works
Fioretto, P., Del Prato, S., Buse, J. B., Goldenberg, R., Giorgino, F., Reyner, D., Langkilde, A. M., Sjöström, C. D., Sartipy, P., & On Behalf of the DERIVE Study Investigators (2018) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.13413 · Cited by 195 · see citing works
Rangaswami, J., Bhalla, V., de Boer, I. H., Staruschenko, A., Sharp, J. A., Singh, R. R., Lo, K. B., Tuttle, K., Vaduganathan, M., Ventura, H., et al. (2020) · Circulation · doi:10.1161/cir.0000000000000920 · Cited by 192 · see citing works
A new class of drugs for heart failure: SGLT2 inhibitors reduce sympathetic overactivity
Sano, M. (2018) · Journal of Cardiology · doi:10.1016/j.jjcc.2017.12.004 · Cited by 188 · see citing works
Combination therapy with <scp>GLP</scp> ‐1 receptor agonist and <scp>SGLT2</scp> inhibitor
DeFronzo, R. A. (2017) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.12982 · Cited by 192 · see citing works
Acute kidney injury in patients on SGLT2 inhibitors: a propensity-matched analysis
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- Authors
- Wanner, C., Inzucchi, S. E., Lachin, J. M., Fitchett, D., von Eynatten, M., Mattheus, M., Johansen, O. E., Woerle, H. J., Broedl, U. C., & Zinman, B.
- Affiliations
- Mount Sinai Hospital (CA)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2016-07-28
- Volume
- 375
- Issue
- 4
- Pages
- 323-334
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2424539745
- Semantic Scholar
- 508b0daf6c74ba96dda7ddbaf04b0b4b7f8d97f5
- Cited by
- 3,655
- References
- 39
- Citations by year
- 2026: 179 · 2025: 241 · 2024: 289 · 2023: 347 · 2022: 415 · 2021: 425 · 2020: 457 · 2019: 395 · 2018: 418 · 2017: 362 · 2016: 117 · 2015: 3 · 2014: 3
- FWCI
- 433.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Bank (Australian Catholic University) (submittedVersion)
- Florence Research (University of Florence) (submittedVersion)
- Lirias (submittedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Keywords
- empagliflozin, SGLT2 inhibitors, type 2 diabetes, kidney disease progression, kidney disease, albuminuria, macroalbuminuria, serum creatinine doubling, renal replacement therapy, renal outcomes, EMPA-REG OUTCOME trial, impaired kidney function, cardiovascular risk, drug safety, adverse events, microvascular outcomes, hospitalization
- MeSH terms
- Aged, Albuminuria, Benzhydryl Compounds, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Female, Glomerular Filtration Rate, Glucosides, Humans, Hypoglycemic Agents, Kidney, Male, Middle Aged, Risk Factors, Proportional Hazards Models, Disease Progression, Kaplan-Meier Estimate, Microvessels, Intention to Treat Analysis
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