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Cited by 262Diabetes Treatment and ManagementChronic Kidney Disease and DiabetesDiabetes Management and Research

11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2025

Open access
American Diabetes Association Professional Practice Committee, ElSayed, Nuha A., McCoy, Rozalina G., Aleppo, Grazia, Balapattabi, Kirthikaa, Beverly, Elizabeth A., Briggs Early, Kathaleen, Bruemmer, Dennis +15 more·2025·Diabetes Care
DOI 10.2337/dc25-s011PMC PMC11635029
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Abstract

ADA Standards of Care chapter on chronic kidney disease and risk management in diabetes.

Integrity signals

Registry

Crossref · 10.2337/dc25-s011

Cites

139 of 139 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

161 of 204 cited sources checked · 48 supported · 14 flagged · accuracy not yet measured

  • Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Compared with placebo, empagliflozin reduced the risk of incident or worsening nephropathy (a composite of progression to UACR >300 mg/g creatinine, doubling of serum creatinine, ESKD, or death from ESKD) by 39%.

    “Specifically, compared with placebo, empagliflozin reduced the risk of incident or worsening nephropathy (a composite of progression to UACR >300 mg/g creatinine, doubling of serum creatinine, ESKD, or death from ESKD) by 39%”
    Quote in the paperSubstantial claim4 of 4 sources checked
    • cites [91] Neal, 2017, Canagliflozin and cardiovascular and renal events in type 2 diabetes, N Engl J Med source

      The Renal Outcomes section reports results for canagliflozin versus placebo, not empagliflozin. Its renal composite is a sustained 40% reduction in eGFR, renal-replacement therapy, or renal death (hazard ratio 0.60); it does not report the claimed nephropathy composite or 39% reduction. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [95] Marso, 2016, Liraglutide and cardiovascular outcomes in type 2 diabetes, N Engl J Med source

      The Results (Microvascular Outcomes; page unavailable) report a reduction in nephropathy events with liraglutide, not empagliflozin. The Discussion mentions empagliflozin only in a comparison of cardiovascular outcomes. Searches for empagliflozin nephropathy and the claimed 39% reduction found no passage addressing that result. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [98] Marso, 2016, Semaglutide and cardiovascular outcomes in patients with type 2 diabetes, N Engl J Med source

      The Results section reports a reduction in new or worsening nephropathy with semaglutide, not empagliflozin, versus placebo (hazard ratio 0.64, corresponding to 36% rather than 39%). The Discussion attributes the 39% reduction to nonfatal stroke, not nephropathy. The Other Outcomes section also defines a different nephropathy composite from the one claimed; page numbers are unavailable in our copy. (LLM, conf=0.88)

      Checked by a reasoning model — may be wrong.

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    • cites [111] Zinman, 2015, Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes, N Engl J Med source

      Study Outcomes (p. 3) defines cardiovascular outcomes and lists acute renal failure as a safety event, but does not define the claimed nephropathy composite. The discussion (p. 11) says renal function was maintained and acute renal failure was less frequent with empagliflozin; our copy does not report a 39% reduction in incident or worsening nephropathy (searched: nephropathy, 39%, and the composite’s components). (LLM, conf=0.76)

      Experimental — accuracy not yet measured
  • Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Empagliflozin reduced the risk of doubling of serum creatinine accompanied by eGFR ≤45 mL/min/1.73m2 by 44%.

    “and the risk of doubling of serum creatinine accompanied by eGFR #45 mL/min/1.73m 2 by 44%”
    Quote in the paperSubstantial claim4 of 4 sources checked
    • cites [91] Neal, 2017, Canagliflozin and cardiovascular and renal events in type 2 diabetes, N Engl J Med source

      The Renal Outcomes section reports results for canagliflozin, not empagliflozin. It reports a hazard ratio of 0.60 for a composite of sustained 40% eGFR reduction, renal-replacement therapy, or renal death—not a 44% reduction in creatinine doubling accompanied by eGFR ≤45. Page numbers are unavailable in our copy. (LLM, conf=0.88)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [95] Marso, 2016, Liraglutide and cardiovascular outcomes in type 2 diabetes, N Engl J Med source

      The Methods > Outcomes passage defines doubling of serum creatinine with eGFR ≤45 mL/min/1.73 m² as part of this liraglutide trial’s nephropathy outcome. Results > Microvascular Outcomes reports a composite nephropathy benefit for liraglutide, not a 44% reduction in that specific outcome with empagliflozin. A search for empagliflozin renal outcomes found no passage reporting the claimed result. (LLM, conf=0.78)

      Experimental — accuracy not yet measured
    • cites [98] Marso, 2016, Semaglutide and cardiovascular outcomes in patients with type 2 diabetes, N Engl J Med source

      The Other Outcomes section defines doubling of serum creatinine with kidney function below 45 as one component of new or worsening nephropathy. But the trial studied semaglutide, not empagliflozin; the Primary Outcome section reports a 36% lower risk for the composite nephropathy outcome, not a 44% reduction for that component. (LLM, conf=0.88)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [111] Zinman, 2015, Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes, N Engl J Med source

      The discussion (p. 11) says renal function was maintained with empagliflozin and that acute renal failure was less frequent than with placebo. Our copy does not report a 44% reduction in doubling of serum creatinine accompanied by eGFR ≤45 mL/min/1.73 m²; searches for that endpoint and figure found no matching result. (LLM, conf=0.77)

      Experimental — accuracy not yet measured
  • Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Metformin is contraindicated in individuals with an eGFR <30 mL/min/1.73m2.

    “1) metformin is contraindicated in individuals with an eGFR <30 mL/min/1.73m 2”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [104] Lalau, 2018, Metformin treatment in patients with type 2 diabetes and chronic kidney disease stages 3A, 3B, or 4, Diabetes Care source

      The paper’s Conclusions recommend considering metformin initiation in severe CKD when the dose is adjusted to eGFR. Its figure defines CKD stage 4 as an eGFR of 15–29 mL/min/1.73 m², directly at odds with an unqualified claim that metformin is contraindicated below 30. The paper does not establish what a particular regulator’s labeling says for that range. (LLM, conf=0.84)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [105] Chu, 2020, Hospitalization for lactic acidosis among patients with reduced kidney function treated with metformin or sulfonylureas, Diabetes Care source
  • Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Semaglutide reduced the risk of new or worsening nephropathy (a composite of persistent UACR >300 mg/g creatinine, doubling of serum creatinine, or ESKD) by 36%.

    “and semaglutide reduced the risk of new or worsening nephropathy (a composite of persistent UACR >300 mg/g creatinine, doubling of serum creatinine, or ESKD) by 36% (each P < 0.01).”
    Quote in the paperSubstantial claim4 of 4 sources checked
    • cites [91] Neal, 2017, Canagliflozin and cardiovascular and renal events in type 2 diabetes, N Engl J Med source

      The Renal Outcomes section reports results for canagliflozin versus placebo, not semaglutide. It reports a hazard ratio of 0.73 for albuminuria progression and 0.60 for a differently defined composite renal outcome; it does not report the claimed 36% reduction in new or worsening nephropathy. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [95] Marso, 2016, Liraglutide and cardiovascular outcomes in type 2 diabetes, N Engl J Med source

      The Methods (Procedures; page unavailable) say this trial compared liraglutide with placebo, not semaglutide. The Results (Microvascular Outcomes; page unavailable) report a nephropathy hazard ratio of 0.78, corresponding to a 22% lower risk, not 36%. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [98] Marso, 2016, Semaglutide and cardiovascular outcomes in patients with type 2 diabetes, N Engl J Med source

      The A Primary Outcome section reports a nephropathy hazard ratio of 0.64 (P = 0.005), supporting the 36% risk reduction. But the Other Outcomes table note defines the composite more narrowly than the claim: doubling of serum creatinine also required creatinine clearance below 45 ml/min/1.73 m², and the final component was a need for continuous renal-replacement therapy. Our copy does not specify the stated UACR threshold. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [111] Zinman, 2015, Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes, N Engl J Med source

      The Abstract (p. 2) identifies the trial drug as empagliflozin, and the Results (p. 1) report cardiovascular outcomes for empagliflozin versus placebo. A search for semaglutide and the specified 36% nephropathy reduction found no passage addressing that claim in our copy; the paper does not establish or contradict a result for semaglutide. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
  • Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Canagliflozin reduced the risk of reduction in eGFR, ESKD, or death from ESKD by 40%.

    “and the risk of reduction in eGFR, ESKD, or death from ESKD by 40%”
    Quote in the paperSubstantial claim4 of 4 sources checked
    • cites [91] Neal, 2017, Canagliflozin and cardiovascular and renal events in type 2 diabetes, N Engl J Med source

      The Renal Outcomes section reports a hazard ratio of 0.60, consistent with a 40% lower observed risk for the composite outcome. But the measured outcome was a sustained 40% reduction in eGFR, need for renal-replacement therapy, or death from renal causes—not any reduction in eGFR, ESKD, or death from ESKD. The Results section also cautions that the renal findings were not considered statistically significant under the prespecified testing sequence. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [95] Marso, 2016, Liraglutide and cardiovascular outcomes in type 2 diabetes, N Engl J Med source

      The Results (Microvascular Outcomes; page not provided) report fewer nephropathy events with liraglutide than with placebo, with a hazard ratio of 0.78. A search for canagliflozin and the claimed 40% reduction found no passage in our copy addressing that drug or that result; the liraglutide finding does not establish or contradict the claim about canagliflozin. (LLM, conf=0.78)

      Experimental — accuracy not yet measured
    • cites [98] Marso, 2016, Semaglutide and cardiovascular outcomes in patients with type 2 diabetes, N Engl J Med source

      The Results (section “A Primary Outcome”; page unavailable) report a lower risk of new or worsening nephropathy with semaglutide, not a 40% reduction in the stated kidney-disease composite with canagliflozin. The paper reports a hazard ratio of 0.64 for its different nephropathy outcome. (LLM, conf=0.85)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [111] Zinman, 2015, Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes, N Engl J Med source

      The Results (p. 1) identify empagliflozin, not canagliflozin, as the treatment studied and report reductions in cardiovascular death, heart-failure hospitalization, and all-cause death—not a 40% reduction in the claimed kidney composite. The discussion (p. 11) says renal function was maintained with empagliflozin, but does not report the claimed outcome or percentage. (LLM, conf=0.88)

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  • May combine two claims. 37
  • Classified as probably not a substantial claim. 8
  • The quote only partly states this claim. 1

  • May combine two claims.

    Premisecitation
    § Glycemic Goals

    Intensive lowering of blood glucose with the goal of achieving near-normoglycemia has been shown in large randomized studies to delay the onset and progression of albuminuria and reduce eGFR in people with type 1 diabetes and type 2 diabetes.

    “Intensive lowering of blood glucose with the goal of achieving near-normoglycemia has been shown in large, randomized studies to delay the onset and progression of albuminuria and reduce eGFR in people with type 1 diabetes (52,53) and type 2 diabetes (1,(54)(55)(56)(57)(58)(59).”
    Quote in the paperSubstantial claim8 of 9 sources checked
    • cites [52] 2014, DCCT/EDIC Research Group. Effect of intensive diabetes treatment on albuminuria in type 1 diabetes: long-term follow-up of the Diabetes Control and Complications Trial and Epidemiology of Diabetes Interventions and Complications study, Lancet Diabetes Endocrinol source

      Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured
    • cites [53] de Boer, 2011, Intensive diabetes therapy and glomerular filtration rate in type 1 diabetes, N Engl J Med source
    • cites [1] de Boer, 2022, Diabetes management in chronic kidney disease: a consensus report by the American Diabetes Association (ADA) and Kidney Disease: Improving Global Outcomes (KDIGO), Diabetes Care source

      Split into 2 atoms — 0 confirmed, 1 partially supported, 1 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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    • cites [54] 1998, UK Prospective Diabetes Study (UKPDS) Group, Lancet

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [55] Patel, 2008, Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes, N Engl J Med source

      In the Results (p. 9), intensive glucose control in patients with type 2 diabetes reduced new-onset microalbuminuria and development of macroalbuminuria, supporting the albuminuria portion of the claim. The paper does not report a reduction in eGFR; the same passage reports no effect on doubling of serum creatinine. This trial studied type 2 diabetes, while the sentence cites other studies for type 1 diabetes. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [56] Ismail-Beigi, 2010, Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the ACCORD randomised trial, Lancet source

      For the type 2 diabetes portion attributed to this source, the Results report less new macroalbuminuria with intensive treatment and a short-term decline in eGFR; the microalbuminuria difference was no longer significant at study end. The paper does not establish delayed progression of existing albuminuria, and the eGFR difference was not significant at study end. The type 1 diabetes portion has separate citations and is not assessed here. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [57] Zoungas, 2014, Follow-up of blood-pressure lowering and glucose control in type 2 diabetes, N Engl J Med source

      Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured
    • cites [58] Zoungas, 2017, Effects of intensive glucose control on microvascular outcomes in patients with type 2 diabetes: a meta-analysis of individual participant data from randomised controlled trials, Lancet Diabetes Endocrinol source

      The Results section reports that intensive glucose control reduced the development of microalbuminuria and macroalbuminuria and increased albuminuria regression in people with type 2 diabetes. It does not support the eGFR part: the same section says intensive control did not significantly reduce the risk of eGFR falling below 30 or declining by 40%. This source studies type 2 diabetes; the citing sentence assigns its type 1 diabetes claim to other citations. (LLM, conf=0.90)

      Experimental — accuracy not yet measured
    • cites [59] Agrawal, 2018, Long-term follow-up of intensive glycaemic control on renal outcomes in the Veterans Affairs Diabetes Trial (VADT), Diabetologia source

      Split into 2 atoms — 0 confirmed, 1 partially supported, 1 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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  • Classified as probably not a substantial claim.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Metformin should not be initiated for individuals with an eGFR <45 mL/min/1.73m2.

    “4) metformin should not be initiated for individuals with an eGFR <45 mL/min/1.73m 2”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [104] Lalau, 2018, Metformin treatment in patients with type 2 diabetes and chronic kidney disease stages 3A, 3B, or 4, Diabetes Care source

      The Conclusions (page not available in our copy) say the results “open the way for the initiation of metformin treatment in severe CKD,” provided the dose is adjusted to eGFR. The paper identifies CKD stages 3B and 4 as below 45 mL/min/1.73 m², so its conclusion runs counter to a blanket recommendation not to initiate treatment below that threshold. (LLM, conf=0.86)

      Checked by a reasoning model — may be wrong.

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    • cites [105] Chu, 2020, Hospitalization for lactic acidosis among patients with reduced kidney function treated with metformin or sulfonylureas, Diabetes Care source

      The Introduction describes an FDA contraindication at eGFR <30 mL/min/1.73 m², while the study examines continued metformin use rather than starting treatment. The Conclusions discuss guidance on continuation at reduced eGFR. Neither passage states whether metformin should be initiated below 45 mL/min/1.73 m²; searches for initiation and that threshold found no such recommendation. (LLM, conf=0.75)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § EPIDEMIOLOGY OF DIABETES AND CHRONIC KIDNEY DISEASE

    CKD is the leading cause of end-stage kidney disease in the U.S.

    “CKD can progress to kidney failure requiring dialysis or kidney transplantation and is the leading cause of end-stage kidney disease (ESKD) in the U.S. (5).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [5] Johansen, 2021, US Renal Data System 2020 annual data report: epidemiology of kidney disease in the United States, Am J Kidney Dis source

      The report’s opening section identifies CKD and end-stage renal disease (ESRD) as populations covered by its U.S. surveillance data, and the ESRD discussion reports dialysis and transplant counts. Neither passage says CKD is the leading cause of ESRD or ranks its causes; searches for that claim and for CKD progression to kidney failure found no supporting passage in our copy. (LLM, conf=0.74)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § ASSESSMENT OF ALBUMINURIA AND ESTIMATED GLOMERULAR FILTRATION RATE

    Measurement of a spot urine sample for albumin alone without simultaneously measuring urine creatinine is less expensive but susceptible to false-negative and false-positive determinations due to variation in urine concentration from hydration.

    “Measurement of a spot urine sample for albumin alone (whether by immunoassay or by using a sensitive dipstick test specific for albuminuria) without simultaneously measuring urine creatinine is less expensive but susceptible to false-negative and falsepositive determinations as a result of variation in urine concentration due to hydration (7).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [7] Yarnoff, 2017, The cost-effectiveness of using chronic kidney disease risk scores to screen for early-stage chronic kidney disease, BMC Nephrol source

      Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.

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  • May combine two claims.

    Premisecitation
    § ASSESSMENT OF ALBUMINURIA AND ESTIMATED GLOMERULAR FILTRATION RATE

    UACR is a continuous measurement, and differences within the normal and abnormal ranges are associated with kidney and cardiovascular outcomes.

    “However, UACR is a continuous measurement, and differences within the normal and abnormal ranges are associated with kidney and cardiovascular outcomes (6,10,11).”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [6] Fox, 2012, Associations of kidney disease measures with mortality and end-stage renal disease in individuals with and without diabetes: a meta-analysis, Lancet source
    • cites [10] Afkarian, 2013, Kidney disease and increased mortality risk in type 2 diabetes, J Am Soc Nephrol source
    • cites [11] Groop, 2009, The presence and severity of chronic kidney disease predicts all-cause mortality in type 1 diabetes, Diabetes source

      The Methods (Statistical analysis; page unavailable) say urinary albumin excretion (UAE) was entered as a categorical variable, and the Results report higher all-cause mortality across albuminuria categories. The paper does not establish that differences *within* the normal or abnormal ranges of UACR are associated with kidney and cardiovascular outcomes; it measured UAE rather than UACR and primarily analyzed mortality. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § EPIDEMIOLOGY OF DIABETES AND CHRONIC KIDNEY DISEASE

    Among people with type 1 or type 2 diabetes, the presence of CKD markedly increases cardiovascular risk and health care costs.

    “In addition, among people with type 1 or type 2 diabetes, the presence of CKD markedly increases cardiovascular risk and health care costs (6).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [6] Fox, 2012, Associations of kidney disease measures with mortality and end-stage renal disease in individuals with and without diabetes: a meta-analysis, Lancet source

      The Results report that cardiovascular mortality generally increased with lower eGFR and higher albuminuria in participants with diabetes. The paper does not report health care costs or distinguish findings for type 1 versus type 2 diabetes, so those parts of the claim are unsupported. (LLM, conf=0.90)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § EPIDEMIOLOGY OF DIABETES AND CHRONIC KIDNEY DISEASE

    CKD attributed to diabetes in adults occurs in 20-40% of people with diabetes.

    “In this section, the focus is on CKD attributed to diabetes in adults, which occurs in 20-40% of people with diabetes (1-4).”
    Quote in the paperNot a substantial claim4 of 4 sources checked
    • cites [1] de Boer, 2022, Diabetes management in chronic kidney disease: a consensus report by the American Diabetes Association (ADA) and Kidney Disease: Improving Global Outcomes (KDIGO), Diabetes Care source

      The Background reports that CKD prevalence among people with diabetes is greater than 25%, and estimates that 40% develop CKD during their lifetime. It does not give a 20–40% prevalence range specifically for CKD attributed to diabetes in adults; the 40% figure is a lifetime estimate, not a prevalence estimate. Screening and Diagnosis says CKD is usually attributed to diabetes when other causes are not indicated. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [2] Afkarian, 2016, Clinical manifestations of kidney disease among US adults with diabetes, 1988-2014, JAMA source

      The Clinical Manifestations of DKD section reports DKD in 26.2%–28.4% of US adults with diabetes across survey periods, within the claimed 20%–40% range. The claim is broader than this US study, and the limitations section says the underlying causes of kidney disease could not be determined; some cases were likely due to causes other than diabetes. (LLM, conf=0.82)

      Experimental — accuracy not yet measured
    • cites [3] de Boer, 2011, Temporal trends in the prevalence of diabetic kidney disease in the United States, JAMA source
    • cites [4] DCCT/EDIC Research Group, 2014, Kidney disease and related findings in the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study, Diabetes Care source

      The Introduction reports that up to 40% of patients with type 1 diabetes developed macroalbuminuria in early cohort studies. The Results (Clinical Course) report 30-year cumulative microalbuminuria incidences of 25% and 38% in two type 1 diabetes treatment groups. These findings concern specific kidney outcomes over time in type 1 diabetes; they do not establish that CKD occurs in 20–40% of all adults with diabetes. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • The quote only partly states this claim.

    Premisecitation
    § Prevention

    In the GRADE study, no differences between liraglutide, sitagliptin, glimeperide, and insulin glargine were observed for kidney and cardiovascular secondary outcomes.

    “No differences between the examined medications were observed, which suggests that there were no unique reno-protective effects among these medications for prevention.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [45] Wexler, 2023, Comparative effects of glucose-lowering medications on kidney outcomes in type 2 diabetes: the GRADE randomized clinical trial, JAMA Intern Med source

      The Results report no significant differences in kidney disease progression or secondary kidney outcomes across the four treatment groups. The Discussion, however, says GRADE found differential effects on total cardiovascular events, so the claim’s extension to cardiovascular outcomes is not supported. The Discussion also cautions that kidney benefits might emerge with longer follow-up. (LLM, conf=0.90)

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  • May combine two claims.

    Premisecitation
    § .2).

    Early changes in kidney function may be detected by increases in albuminuria before changes in eGFR, and this also significantly affects cardiovascular risk.

    “Early changes in kidney function may be detected by increases in albuminuria before changes in eGFR (41), and this also significantly affects cardiovascular risk.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [41] Zelniker, 2021, Effect of dapagliflozin on cardiovascular outcomes according to baseline kidney function and albuminuria status in patients with type 2 diabetes: a prespecified secondary analysis of a randomized clinical trial, JAMA Cardiol source

      The Study Population section (page not provided) identifies 4,650 patients with albuminuria as their only CKD marker, supporting that albuminuria can identify kidney dysfunction without reduced eGFR. But these are baseline measurements; the paper does not establish that albuminuria increases before an individual's eGFR changes. The CV Outcomes by Markers of CKD section (page not provided) also reports higher cardiovascular event rates among patients with albuminuria alone. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § DIAGNOSIS OF CHRONIC KIDNEY DISEASE IN PEOPLE WITH DIABETES

    Reduced eGFR without albuminuria has been frequently reported in type 1 and type 2 diabetes and is becoming more common over time as the prevalence of diabetes increases in the U.S.

    “Reduced eGFR without albuminuria has been frequently reported in type 1 and type 2 diabetes and is becoming more common over time as the prevalence of diabetes increases in the U.S. (2,3,16,(19)(20)(21).”
    Quote in the paperNot a substantial claim5 of 6 sources checked
    • cites [2] Afkarian, 2016, Clinical manifestations of kidney disease among US adults with diabetes, 1988-2014, JAMA source

      The Introduction (page not provided) says reduced GFR without albuminuria has been frequently described, and Clinical Manifestations of DKD (page not provided) reports that reduced eGFR became more prevalent among US adults with diabetes. The reported trend is for reduced eGFR overall, not specifically reduced eGFR without albuminuria. The paper does not establish that this pattern increased in both type 1 and type 2 diabetes or that rising diabetes prevalence caused it. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [3] de Boer, 2011, Temporal trends in the prevalence of diabetic kidney disease in the United States, JAMA source

      The Comment section reports that impaired GFR can occur without substantial albuminuria and describes it as increasingly frequent relative to albuminuria. The Results show an increase in impaired GFR with or without albuminuria, while the Comment says overall diabetic kidney disease prevalence rose in proportion to diabetes prevalence. The paper does not establish a separate temporal trend for reduced eGFR specifically without albuminuria, or that such a trend occurred in both type 1 and type 2 diabetes. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [16] Kramer, 2003, Renal insufficiency in the absence of albuminuria and retinopathy among adults with type 2 diabetes mellitus, JAMA source
    • cites [19] Molitch, 2010, Development and progression of renal insufficiency with and without albuminuria in adults with type 1 diabetes in the Diabetes Control and Complications Trial and the Epidemiology of Diabetes Interventions and Complications study, Diabetes Care source

      The introductory passage and Conclusions (pages not provided) report reduced GFR without increased albumin excretion in people with type 1 and type 2 diabetes. The paper does not establish that this condition is becoming more common in the U.S. because diabetes prevalence is increasing; its reported increase over time concerns cumulative incidence of reduced eGFR within the type 1 diabetes cohort. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [20] He, 2013, Diabetic retinopathy in predicting diabetic nephropathy in patients with type 2 diabetes and renal disease: a meta-analysis, Diabetologia source

      The Introduction (p. 1) says diabetes incidence and prevalence are increasing and reports a rising U.S. rate of ESRD due to diabetes. It does not establish that reduced eGFR without albuminuria is frequently reported in type 1 and type 2 diabetes, or that this specific condition is becoming more common in the U.S. (LLM, conf=0.78)

      Experimental — accuracy not yet measured
    • cites [21] Vistisen, 2019, Progressive decline in estimated glomerular filtration rate in patients with diabetes after moderate loss in kidney function-even without albuminuria, Diabetes Care source

      The Results report normoalbuminuria in participants with both type 1 and type 2 diabetes, and the Conclusions say that a substantial number enter CKD stage 3 without albuminuria and that this presentation is increasing, especially in type 2 diabetes. The paper does not establish that it is becoming more common in the U.S. or that rising U.S. diabetes prevalence is the reason. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation
    § STAGING OF CHRONIC KIDNEY DISEASE

    KDIGO recommends a more comprehensive CKD staging that incorporates albuminuria at all stages of eGFR; this system is more closely associated with risk but is also more complex.

    “Furthermore, Kidney Disease: Improving Global Outcomes (KDIGO) recommends a more comprehensive CKD staging that incorporates albuminuria at all stages of eGFR; this system is more closely associated with risk but is also more complex (1).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [1] de Boer, 2022, Diabetes management in chronic kidney disease: a consensus report by the American Diabetes Association (ADA) and Kidney Disease: Improving Global Outcomes (KDIGO), Diabetes Care source

      The Screening and Diagnosis section says KDIGO’s CKD classification uses both eGFR and albuminuria, and that risk rises with increasing albuminuria or decreasing eGFR. It does not say this system is more closely associated with risk than another staging system or that it is more complex. The copy provides no page number for this passage. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § STAGING OF CHRONIC KIDNEY DISEASE

    At any eGFR, the degree of albuminuria is associated with risk of cardiovascular disease, CKD progression, and mortality.

    “At any eGFR, the degree of albuminuria is associated with risk of cardiovascular disease (CVD), CKD progression, and mortality (6).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [6] Fox, 2012, Associations of kidney disease measures with mortality and end-stage renal disease in individuals with and without diabetes: a meta-analysis, Lancet source

      The Results report that all-cause and cardiovascular mortality generally increased with higher albuminuria categories across eGFR categories. The Discussion also identifies albuminuria as a predictor of end-stage renal disease. The study measured cardiovascular mortality and end-stage renal disease, not cardiovascular disease generally or all forms of CKD progression. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § SURVEILLANCE

    Diuretics can cause hypokalemia, which is associated with cardiovascular risk and mortality.

    “Serum potassium should also be monitored in individuals treated with diuretics because these medications can cause hypokalemia, which is associated with cardiovascular risk and mortality (38)(39)(40).”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [38] Hughes-Austin, 2017, The relation of serum potassium concentration with cardiovascular events and mortality in community-living individuals, Clin J Am Soc Nephrol source
    • cites [39] Bandak, 2017, Hyperkalemia after initiating renin-angiotensin system blockade: the Stockholm Creatinine Measurements (SCREAM) project, J Am Heart Assoc source

      The Results section discusses potassium-sparing diuretics as a risk factor for hyperkalemia after ACE-I or ARB initiation. The Discussion links hyperkalemia—not hypokalemia—to mortality. Searches for hypokalemia and diuretic-related low potassium found no passage addressing the attributed claim. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [40] Nilsson, 2017, Incidence and determinants of hyperkalemia and hypokalemia in a large healthcare system, Int J Cardiol source

      The Results (p. 5) associate loop/thiazide diuretic use with higher hypokalemia risk, and the Discussion (p. 6) calls diuretics its strongest baseline risk factor. The paper does not establish that hypokalemia is associated with cardiovascular outcomes or mortality; its Discussion (p. 6) links increased mortality risk to hyperkalemia events instead. (LLM, conf=0.89)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § INTERVENTIONS Nutrition

    Compared with higher levels of dietary protein intake, a dietary protein intake of 0.8 g/kg/day slowed GFR decline with evidence of a greater effect over time.

    “Compared with higher levels of dietary protein intake, this level slowed GFR decline with evidence of a greater effect over time.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [1] de Boer, 2022, Diabetes management in chronic kidney disease: a consensus report by the American Diabetes Association (ADA) and Kidney Disease: Improving Global Outcomes (KDIGO), Diabetes Care source

      The Lifestyle section recommends 0.8 g/kg/day and describes a theoretical risk that higher protein intake could accelerate kidney-function decline. It does not report that 0.8 g/kg/day slowed GFR decline compared with higher intake, or that the effect grew over time. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § INTERVENTIONS Nutrition

    Reducing dietary protein below the recommended daily allowance of 0.8 g/kg/day does not alter blood glucose levels, cardiovascular risk measures, or the course of GFR decline.

    “Reducing the amount of dietary protein below the recommended daily allowance of 0.8 g/kg/day is not recommended because it does not alter blood glucose levels, cardiovascular risk measures, or the course of GFR decline (46).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [46] Klahr, 1994, The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease, N Engl J Med source

      Study 2 (p. 5) found no statistically significant difference in GFR decline between the low- and very-low-protein groups, but the Discussion (p. 7) notes a nonsignificant trend toward slower decline with very low protein intake. The paper does not report that protein restriction leaves blood glucose unchanged; Adverse Events (p. 5) instead reports significant differences in serum cholesterol changes between diet groups. It does not establish the broad recommendation against intake below 0.8 g/kg/day. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Blood Pressure and Use of ACE Inhibitors and Angiotensin Receptor Blockers

    Two clinical trials studied the combinations of ACE inhibitors and ARBs and found no benefits on CVD or CKD, and the medication combination had higher adverse event rates (hyperkalemia and/or AKI).

    “Two clinical trials studied the combinations of ACE inhibitors and ARBs and found no benefits on CVD or CKD, and the medication combination had higher adverse event rates (hyperkalemia and/or AKI) (87,88).”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [87] Yusuf, 2008, Telmisartan, ramipril, or both in patients at high risk for vascular events, N Engl J Med source

      The Discussion reports that telmisartan plus ramipril provided no significant benefit on the cardiovascular primary outcome and increased hyperkalemia and renal dysfunction. The paper reports renal harm, but does not establish the claim that the combination provided no benefit on CKD outcomes; its stated prevention outcome was vascular events. This citation supports the ONTARGET trial's findings, not the findings of both trials cited in the sentence. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [88] Fried, 2013, Combined angiotensin inhibition for the treatment of diabetic nephropathy, N Engl J Med source

  • May combine two claims.

    Premisecitation
    § Blood Pressure and Use of ACE Inhibitors and Angiotensin Receptor Blockers

    In people with CKD (eGFR 10-60) who had ACE inhibitors or ARBs stopped, restarting the ACE inhibitor or ARB was associated with better long-term kidney outcomes and lower mortality.

    “Hattori et al. (83) evaluated 6,065 participants between 2005 and 2021 (approximately 40% had diabetes) with eGFR ranging from 10 to 60 mL/min/1.73m 2 who had ACE inhibitors or ARBs stopped (usually due to hyperkalemia or AKI) and found that those who restarted the ACE inhibitor or ARB had better long-term kidney outcomes and lower mortality”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [83] Hattori, 2024, Estimated effect of restarting renin-angiotensin system inhibitors after discontinuation on kidney outcomes and mortality, J Am Soc Nephrol source

      The eligibility criteria specify eGFR of 10–60 mL/min/1.73 m² after RAS inhibitor discontinuation, and the Discussion reports lower hazards of kidney outcomes and mortality with restarting. However, the Discussion says the precise reasons for discontinuation were unknown, so the citing sentence’s assertion that treatment was usually stopped because of hyperkalemia or AKI is not supported. (LLM, conf=0.89)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Direct Kidney Effects of Glucose-Lowering Medications

    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.

    “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).”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [31] Wanner, 2016, Empagliflozin and progression of kidney disease in type 2 diabetes, N Engl J Med source

      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 measured
    • cites (89)(90)(91)(92)

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    eGFR should be monitored while taking metformin.

    “2) eGFR should be monitored while taking metformin”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [104] Lalau, 2018, Metformin treatment in patients with type 2 diabetes and chronic kidney disease stages 3A, 3B, or 4, Diabetes Care source

      The ‘Concerning the metformin dose’ section recommends assessing eGFR every six months in patients with CKD stage 3 taking metformin. The citing sentence omits that population limit and presents monitoring as a recommendation for everyone taking metformin. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [105] Chu, 2020, Hospitalization for lactic acidosis among patients with reduced kidney function treated with metformin or sulfonylureas, Diabetes Care source

  • Classified as probably not a substantial claim.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Metformin should be temporarily discontinued at the time of or before iodinated contrast imaging procedures in individuals with eGFR 30-60 mL/min/1.73m2.

    “5) metformin should be temporarily discontinued at the time of or before iodinated contrast imaging procedures in individuals with eGFR 30-60 mL/min/1.73m 2 .”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [104] Lalau, 2018, Metformin treatment in patients with type 2 diabetes and chronic kidney disease stages 3A, 3B, or 4, Diabetes Care source

      The Conclusions discuss continuing metformin at eGFR-adjusted doses, and the dosing recommendations advise withdrawal when acute kidney injury is likely. Searches for iodinated contrast, imaging procedures, and withdrawal before imaging found no passage addressing the claimed temporary discontinuation rule for eGFR 30–60 mL/min/1.73 m². (LLM, conf=0.74)

      Experimental — accuracy not yet measured
    • cites [105] Chu, 2020, Hospitalization for lactic acidosis among patients with reduced kidney function treated with metformin or sulfonylureas, Diabetes Care source

      The Introduction and Conclusions discuss metformin use at reduced eGFR, but neither addresses iodinated contrast imaging or temporary discontinuation around a procedure. Searches for iodinated contrast and for holding metformin before imaging found no passage supporting that specific recommendation; page numbers were not available in our copy. (LLM, conf=0.72)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Blood Pressure and Use of ACE Inhibitors and Angiotensin Receptor Blockers

    In the absence of kidney disease, ACE inhibitors or ARBs are useful to manage blood pressure but have not proven superior to alternative classes of antihypertensive therapy, including thiazide-like diuretics and dihydropyridine calcium channel blockers.

    “In the absence of kidney disease, ACE inhibitors or ARBs are useful to manage blood pressure but have not proven superior to alternative classes of antihypertensive therapy, including thiazide-like diuretics and dihydropyridine calcium channel blockers (85).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [85] Bangalore, 2016, Diabetes mellitus as a compelling indication for use of renin angiotensin system blockers: systematic review and meta-analysis of randomized trials, BMJ source

      Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    The benefits and risks of continuing metformin treatment should be reassessed when eGFR falls to <45 mL/min/1.73m2.

    “3) the benefits and risks of continuing treatment should be reassessed when eGFR falls to <45 mL/min/1.73m 2 (104,105)”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [104] Lalau, 2018, Metformin treatment in patients with type 2 diabetes and chronic kidney disease stages 3A, 3B, or 4, Diabetes Care source

      The Conclusions define CKD stage 3B as eGFR 44–30 mL/min/1.73 m² and recommend a lower metformin dose than for stage 3A. The paper thus supports reviewing treatment when eGFR falls below 45, but it does not specifically say to reassess the benefits and risks of continuing it. (LLM, conf=0.83)

      Experimental — accuracy not yet measured
    • cites [105] Chu, 2020, Hospitalization for lactic acidosis among patients with reduced kidney function treated with metformin or sulfonylureas, Diabetes Care source

      The Conclusions discuss guidance to continue metformin at reduced eGFR, and the Results (Sensitivity and Subgroup Analysis; page unavailable) examine patients with eGFR <45 mL/min/1.73 m². The paper does not say that the benefits and risks of continuing treatment should be reassessed at that threshold. (LLM, conf=0.76)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    GLP-1 RAs reduce risks of CVD events and hypoglycemia and slow progression of CKD.

    “GLP-1 RAs are suggested for cardiovascular risk reduction if such risk is a predominant problem, as they reduce risks of CVD events and hypoglycemia and slow progression of CKD (100,107-110).”
    Quote in the paperSubstantial claim1 of 5 sources checked
    • cites [100] Perkovic, 2024, Effects of semaglutide on chronic kidney disease in patients with type 2 diabetes, N Engl J Med source
    • cites [107] Zelniker, 2019, Comparison of the effects of glucagon-like peptide receptor agonists and sodium-glucose cotransporter 2 inhibitors for prevention of major adverse cardiovascular and renal outcomes in type 2 diabetes mellitus, Circulation source
    • cites [108] Mann, 2020, Effects of once-weekly subcutaneous semaglutide on kidney function and safety in patients with type 2 diabetes: a post-hoc analysis of the SUSTAIN 1-7 randomised controlled trials, Lancet Diabetes Endocrinol source
    • cites [109] Mann, 2021, Incretin-based drugs and the kidney in type 2 diabetes: choosing between DPP-4 inhibitors and GLP-1 receptor agonists, Kidney Int source
    • cites [110] Bakris, 2019, Major advancements in slowing diabetic kidney disease progression: focus on SGLT2 inhibitors, Am J Kidney Dis source

      In the main text (page unavailable), Bakris reports that GLP-1 receptor agonist trials reduced cardiovascular event rates and albuminuria, and describes kidney-progression benefits as promising. The paper does not report reduced hypoglycemia risk or establish that GLP-1 receptor agonists slow CKD progression; it attributes the observed slowing of kidney disease progression to SGLT2 inhibitor trials. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    SGLT2 inhibitors slow CKD progression and reduce heart failure risk independent of glucose management in people with type 2 diabetes and eGFR ≥20 mL/min/1.73m2.

    “SGLT2 inhibitors are recommended for people with eGFR $20 mL/min/1.73m 2 and type 2 diabetes, as they slow CKD progression and reduce heart failure risk independent of glucose management (106).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [106] McGuire, 2021, Association of SGLT2 inhibitors with cardiovascular and kidney outcomes in patients with type 2 diabetes: a meta-analysis, JAMA Cardiol source

      The Results report reduced kidney-disease progression, and the Discussion reports reduced heart-failure hospitalization and recommendations independent of glucose control. But the Discussion specifies recommendations for eGFR ≥30 mL/min/1.73 m², not ≥20; the cited paper does not support the lower threshold. Page numbers are unavailable in our copy. (LLM, conf=0.90)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Blood Pressure and Use of ACE Inhibitors and Angiotensin Receptor Blockers

    ACE inhibitors and ARBs are considered to have similar benefits and risks.

    “ACE inhibitors and ARBs are considered to have similar benefits (75,76) and risks.”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [75] Barnett, 2004, Angiotensin-receptor blockade versus converting-enzyme inhibition in type 2 diabetes and nephropathy, N Engl J Med source
    • cites [76] Wu, 2017, Comparative effectiveness of angiotensin-converting enzyme inhibitors versus angiotensin II receptor blockers for major renal outcomes in patients with diabetes: a 15-year cohort study, PLoS One source

  • May combine two claims.

    Premisecitation
    § Blood Pressure and Use of ACE Inhibitors and Angiotensin Receptor Blockers

    In a trial of people with type 2 diabetes and normal urinary albumin excretion, an ARB reduced or suppressed the development of albuminuria but increased the rate of cardiovascular events.

    “In a trial of people with type 2 diabetes and normal urinary albumin excretion, an ARB reduced or suppressed the development of albuminuria but increased the rate of cardiovascular events (86).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [86] Haller, 2011, Olmesartan for the delay or prevention of microalbuminuria in type 2 diabetes, N Engl J Med source

      The Background describes a trial in people with type 2 diabetes and normoalbuminuria, and the Discussion reports that ARB therapy delayed the onset of microalbuminuria by 23%. The Cardiovascular End Points section reports more cardiovascular deaths with olmesartan (15 vs. 3), but the overall cardiovascular composite was similar between groups (4.3% vs. 4.2%). The claim therefore overstates the finding by saying cardiovascular events increased generally. (LLM, conf=0.90)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    In EMPA-KIDNEY, the empagliflozin-treated participants had lower risk of progression of kidney disease and lower risk of death from cardiovascular causes (HR 0.72 [95% CI 0.64-0.82]; P < 0.001).

    “The empagliflozintreated participants had lower risk of progression of kidney disease and lower risk of death from cardiovascular causes (HR 0.72 [95% CI 0.64-0.82];P < 0.001).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [115] Herrington, 2023, Empagliflozin in patients with chronic kidney disease, N Engl J Med source

      The Results section reports HR 0.72 (95% CI 0.64–0.82; P<0.001) for the composite outcome of kidney disease progression or cardiovascular death, not for each outcome separately. Kidney disease progression had HR 0.71, while cardiovascular death had HR 0.84 (95% CI 0.60–1.19), so the paper does not establish a statistically significant reduction in cardiovascular death on its own. (LLM, conf=0.90)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    Most participants with CKD in these trials also had diagnosed atherosclerotic cardiovascular disease (ASCVD) at baseline, although 28% of CANVAS participants with CKD did not have diagnosed ASCVD.

    “Most participants with CKD in these trials also had diagnosed atherosclerotic cardiovascular disease (ASCVD) at baseline, although 28% of CANVAS participants with CKD did not have diagnosed ASCVD (32).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [32] Neuen, 2018, Cardiovascular and renal outcomes with canagliflozin according to baseline kidney function, Circulation source

  • May combine two claims.

    Premisecitation
    § Renal and Cardiovascular Outcomes of Mineralocorticoid Receptor Antagonists in Chronic Kidney Disease

    There are two different classes of MRAs, steroidal and nonsteroidal, with one group not extrapolatable to the other.

    “There are two different classes of MRAs, steroidal and nonsteroidal, with one group not extrapolatable to the other (124).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [124] Agarwal, 2021, Steroidal and non-steroidal mineralocorticoid receptor antagonists in cardiorenal medicine, Eur Heart J source

      The Introduction and the finerenone comparison section (page numbers unavailable) distinguish steroidal from nonsteroidal MRAs and describe differences in their mechanisms and effects. Those passages support treating them as different classes, but do not establish the categorical claim that findings for one class cannot be extrapolated to the other. (LLM, conf=0.82)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    CREDENCE was stopped early due to positive efficacy and showed a 32% risk reduction for development of ESKD over control.

    “It was stopped early due to positive efficacy and showed a 32% risk reduction for development of ESKD over control (29).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [29] Perkovic, 2019, Canagliflozin and renal outcomes in type 2 diabetes and nephropathy, N Engl J Med source

  • May combine two claims.

    Premiseown data
    § Renal and Cardiovascular Outcomes of Mineralocorticoid Receptor Antagonists in Chronic Kidney Disease

    In FIDELIO-DKD, the study was completed, and there were no deaths related to hyperkalemia.

    “However, the study was completed, and there were no deaths related to hyperkalemia.”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [33] Bakris, 2020, Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes, N Engl J Med source
    • cites [125] Filippatos, 2021, Finerenone and cardiovascular outcomes in patients with chronic kidney disease and type 2 diabetes, Circulation source

      The Results (Patients; page not provided) report outcomes through the end of FIDELIO-DKD, supporting that the study was completed. The Results (Safety Outcomes; page not provided) report hyperkalemia-related hospitalizations and treatment discontinuations, but do not state whether any deaths were related to hyperkalemia. That part of the claim is not supported by our copy. (LLM, conf=0.83)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Renal and Cardiovascular Outcomes of Mineralocorticoid Receptor Antagonists in Chronic Kidney Disease

    FIDELIO-DKD demonstrated a significant reduction in CKD progression and cardiovascular events in people with diabetes and advanced CKD.

    “Late in 2020, the results of the first of two trials, the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease (FIDELIO-DKD) trial, which examined the kidney effects of finerenone, demonstrated a significant reduction in CKD progression and cardiovascular events in people with diabetes and advanced CKD (33,125).”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [33] Bakris, 2020, Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes, N Engl J Med source
    • cites [125] Filippatos, 2021, Finerenone and cardiovascular outcomes in patients with chronic kidney disease and type 2 diabetes, Circulation source

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    In CREDENCE, there were clear benefits on cardiovascular outcomes demonstrating a 31% reduction in cardiovascular death or heart failure hospitalization and a 20% reduction in cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke.

    “Moreover, in this advanced CKD group, there were clear benefits on cardiovascular outcomes demonstrating a 31% reduction in cardiovascular death or heart failure hospitalization and a 20% reduction in cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke (29,110,113).”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites [29] Perkovic, 2019, Canagliflozin and renal outcomes in type 2 diabetes and nephropathy, N Engl J Med source
    • cites [110] Bakris, 2019, Major advancements in slowing diabetic kidney disease progression: focus on SGLT2 inhibitors, Am J Kidney Dis source

      The main text (page not provided) describes CREDENCE and says SGLT2 inhibitors reduce cardiovascular risk in people with type 2 diabetes. It does not report either the 31% reduction in cardiovascular death or heart-failure hospitalization or the 20% reduction in cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke. Its 31% figure instead refers to the proportion of CREDENCE participants with CKD stages 3b–4. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites [113] Mahaffey, 2019, Canagliflozin and cardiovascular and renal outcomes in type 2 diabetes mellitus and chronic kidney disease in primary and secondary cardiovascular prevention groups, Circulation source

      The Results section (Cardiovascular Outcomes by Primary and Secondary Prevention; page unavailable) reports that canagliflozin reduced the cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke composite, with consistent effects across prevention groups. The Results section (Numbers Needed to Treat; page unavailable) also reports benefit for cardiovascular death or heart-failure hospitalization. Our copy does not state the claimed 31% and 20% reductions, so it supports the direction and outcomes but not those precise magnitudes. (LLM, conf=0.82)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Interpretationcitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    SGLT2 inhibitors are safe and effective at eGFR levels of >20 mL/min/1.73m2.

    “Subgroup analyses from DAPA-CKD (117) and analyses from the EMPEROR heart failure trials suggest that SGLT2 inhibitors are safe and effective at eGFR levels of >20 mL/min/1.73m 2 .”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites [117] Chertow, 2021, Effects of dapagliflozin in stage 4 chronic kidney disease, J Am Soc Nephrol source

      The Abstract and Discussion report benefits of dapagliflozin in stage 4 CKD without increased adverse-event rates. But DAPA-CKD enrolled participants with baseline eGFR of at least 25 mL/min/1.73 m², so its subgroup analysis does not itself establish safety and effectiveness throughout the claimed range above 20; the Discussion attributes enrollment down to 20 to EMPEROR-Reduced. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites [118] Anker, 2021, Empagliflozin in heart failure with a preserved ejection fraction, N Engl J Med source

      The Primary Outcome and Safety sections report that empagliflozin improved heart-failure outcomes and give overall adverse-event results. The trial analyzed kidney-function subgroups at an eGFR cutoff of 60 mL/min/1.73 m², but our copy does not establish efficacy or safety specifically down to >20 mL/min/1.73 m². (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [119] Packer, 2020, Cardiovascular and renal outcomes with empagliflozin in heart failure, N Engl J Med source

      The Results and Discussion report cardiovascular and renal benefits with empagliflozin in patients with heart failure, and the Discussion says several safety concerns were not evident. Our copy does not establish that these findings hold specifically down to an eGFR just above 20 mL/min/1.73 m², or for SGLT2 inhibitors as a class; searches for that threshold and low-eGFR subgroup findings did not locate supporting passages. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Interpretationcitation
    § Renal and Cardiovascular Outcomes of Mineralocorticoid Receptor Antagonists in Chronic Kidney Disease

    The pooled FIDELITY trial analysis confirms and strengthens the positive cardiovascular and kidney outcomes with finerenone across the spectrum of CKD, irrespective of baseline ASCVD history (with the exclusion of those with heart failure with reduced ejection fraction).

    “The pooled FIDELITY trial analysis confirms and strengthens the positive cardiovascular and kidney outcomes with finerenone across the spectrum of CKD, irrespective of baseline ASCVD history (with the exclusion of those with heart failure with reduced ejection fraction).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [127] Agarwal, 2022, Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis, Eur Heart J source

      Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation
    § Renal and Cardiovascular Outcomes of Mineralocorticoid Receptor Antagonists in Chronic Kidney Disease

    In FIGARO-DKD, there was a higher incidence of hyperkalemia in the finerenone group, 10.8% vs. 5.3%, although only 1.2% of the 3,686 individuals on finerenone stopped the study due to hyperkalemia.

    “There was a higher incidence of hyperkalemia in the finerenone group, 10.8% vs. 5.3%, although only 1.2% of the 3,686 individuals on finerenone stopped the study due to hyperkalemia.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [126] Pitt, 2021, Cardiovascular events with finerenone in kidney disease and type 2 diabetes, N Engl J Med source

      The Safety Outcomes and Vital Signs section reports hyperkalemia in 10.8% of finerenone patients versus 5.3% of placebo patients, and permanent discontinuation of the trial regimen in 1.2% of finerenone patients. The Results section gives 3,686 patients in the finerenone analysis group. The paper says those patients stopped the regimen, not that they stopped participating in the study. (LLM, conf=0.87)

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim. May combine two claims.

    Interpretationreasoning
    § DIAGNOSIS OF CHRONIC KIDNEY DISEASE IN PEOPLE WITH DIABETES

    In most people with diabetes and CKD, there is no need for a kidney biopsy, as other possible diagnoses would not change treatment.

    “In most people, there is no need for a kidney biopsy, as the other possible diagnoses would not change treatment.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    The FDA revised its guidance for the use of metformin in CKD in 2016, recommending use of eGFR instead of serum creatinine to guide treatment and expanding the pool of people with kidney disease for whom metformin treatment should be considered.

    “The FDA revised its guidance for the use of metformin in CKD in 2016 (103), recommending use of eGFR instead of serum creatinine to guide treatment and expanding the pool of people with kidney disease for whom metformin treatment should be considered.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [103] U.S. Food and Drug Administration . FDA drug safety communication: FDA revises warnings regarding use of the diabetes medicine metformin in certain patients with reduced kidney function, 2017. Accessed 25 August 2024. Available from https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-fda-revises-warnings-regarding-use-diabetes-medicine-metformin-certain

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation
    § Blood Pressure and Use of ACE Inhibitors and Angiotensin Receptor Blockers

    In the setting of lower levels of albuminuria (30-299 mg/g creatinine), ACE inhibitor or ARB therapy at maximum tolerated doses in trials has reduced progression to more advanced albuminuria, slowed CKD progression, and reduced cardiovascular events but has not reduced progression to ESKD.

    “In the setting of lower levels of albuminuria (30-299 mg/g creatinine), ACE inhibitor or ARB therapy at maximum tolerated doses in trials has reduced progression to more advanced albuminuria ($300 mg/g creatinine), slowed CKD progression, and reduced cardiovascular events but has not reduced progression to ESKD (74,77).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [74] 2000, Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy, Lancet source
    • cites [77] Parving, 2001, The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes, N Engl J Med source

  • May combine two claims.

    Premisecitation
    § Direct Kidney Effects of Glucose-Lowering Medications

    Recent data support the notion that SGLT2 inhibitors reduce oxidative stress in the kidney by >50% and blunt increases in angiotensinogen as well as reduce NLRP3 inflammasome activity.

    “Moreover, recent data support the notion that SGLT2 inhibitors reduce oxidative stress in the kidney by >50% and blunt increases in angiotensinogen as well as reduce NLRP3 inflammasome activity (92)(93)(94).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites (92)(93)(94)

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    While the glucose-lowering effects of SGLT2 inhibitors are blunted with eGFR <45 mL/min/1.73m2, the renal and cardiovascular benefits were still seen at eGFR levels as low as 20 mL/min/1.73m2 even with no significant change in glucose.

    “Of note, while the glucose-lowering effects of SGLT2 inhibitors are blunted with eGFR <45 mL/min/1.73m 2 , the renal and cardiovascular benefits were still seen at eGFR levels as low as 20 mL/min/1.73m 2 even with no significant change in glucose (29,31,52,63,98,111,(114)(115)(116).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites 29,31,52,63,98,111,(114)(115)(116)

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Interpretationcitation
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    The FLOW study supports a beneficial effect of semaglutide in slowing decline in kidney function as well as being cardioprotective in people with CKD and type 2 diabetes.

    “Thus, the study supports a beneficial effect of semaglutide in slowing decline in kidney function as well as being cardioprotective in people with CKD and type 2 diabetes.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [100] Perkovic, 2024, Effects of semaglutide on chronic kidney disease in patients with type 2 diabetes, N Engl J Med source

  • May combine two claims.

    Study design and conductnone given
    § Selection of Glucose-Lowering Medications for People With Chronic Kidney Disease

    These analyses were limited by evaluation of study populations not selected primarily for CKD and examination of kidney effects as secondary outcomes.

    “These analyses were limited by evaluation of study populations not selected primarily for CKD and examination of kidney effects as secondary outcomes.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation
    § REFERRAL TO A NEPHROLOGIST

    Consultation with a nephrologist when stage 4 CKD develops (eGFR <30 mL/min/1.73m2) has been found to reduce cost, improve quality of care, and delay dialysis.

    “Consultation with a nephrologist when stage 4 CKD develops (eGFR <30 mL/min/1.73m 2 ) has been found to reduce cost, improve quality of care, and delay dialysis (128).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [128] Smart, 2014, Early referral to specialist nephrology services for preventing the progression to end-stage kidney disease, Cochrane Database Syst Rev source
44 of 44

  • The paper relies on this without support.

    Race is a social and not a biologic construct.

    “Historically, a correction factor for muscle mass was included in a modified equation for African American people; however, race is a social and not a biologic construct, making it problematic to apply race to clinical algorithms.”

  • The paper relies on this without support.

    Combining filtration markers (creatinine and cystatin C) is more accurate and would support better clinical decisions than either marker alone.

    “Additionally, increased use of cystatin C (another marker of eGFR) is suggested in combination with serum creatinine because combining filtration markers (creatinine and cystatin C) is more accurate and would support better clinical decisions than either marker alone.”

  • The paper relies on this without support.

    CKD in people with diabetes typically develops after a duration of 10 years in type 1 diabetes (most common presentation 5-15 years after diagnosis) but may be present at diagnosis of type 2 diabetes.

    “CKD in people with diabetes typically develops after a duration of 10 years in type 1 diabetes (the most common presentation is 5-15 years after the diagnosis of type 1 diabetes) but may be present at diagnosis of type 2 diabetes.”

  • The paper relies on this without support.

    Higher levels of dietary protein intake (>20% of daily calories from protein or >1.3 g/kg/day) are associated with increased albuminuria, more rapid kidney function loss, and CVD mortality.

    “Higher levels of dietary protein intake (>20% of daily calories from protein or >1.3 g/kg/day) have been associated with increased albuminuria, more rapid kidney function loss, and CVD mortality and therefore should be avoided.”

  • The paper relies on this without support.

    All trials that evaluated the benefits of SGLT2 inhibition or nonsteroidal MRA effects were done in individuals who were being treated with an ACE inhibitor or ARB, in some trials up to maximum tolerated doses.

    “Indeed, all the trials that evaluated the benefits of SGLT2 inhibition or nonsteroidal MRA effects were done in individuals who were being treated with an ACE inhibitor or ARB, in some trials up to maximum tolerated doses.”

  • The paper relies on this without support.

    People with CKD are at increased risk of CKD progression (particularly those with albuminuria) and CVD.

    “People with CKD are at increased risk of CKD progression (particularly those with albuminuria) and CVD; therefore, lower blood pressure goals may be suitable in some cases, especially in individuals with severely elevated albuminuria ($300 mg/g creatinine).”

  • The paper relies on this without support.

    The presence of CKD affects the risks and benefits of intensive lowering of blood glucose and a number of specific glucose-lowering medications.

    “The presence of CKD affects the risks and benefits of intensive lowering of blood glucose and a number of specific glucose-lowering medications.”

  • The paper relies on this without support.

    The effects of glucose-lowering therapies on CKD have helped define A1C goals.

    “The effects of glucose-lowering therapies on CKD have helped define A1C goals.”

  • The paper relies on this without support.

    Many antihypertensive medications (e.g., diuretics, ACE inhibitors, and ARBs) can reduce intravascular volume, renal blood flow, and/or glomerular filtration.

    “In particular, many antihypertensive medications (e.g., diuretics, ACE inhibitors, and angiotensin receptor blockers [ARBs]) can reduce intravascular volume, renal blood flow, and/or glomerular filtration.”

  • The paper relies on this without support.

    It is rare for people with type 1 diabetes to develop kidney disease without retinopathy.

    “It is rare for people with type 1 diabetes to develop kidney disease without retinopathy.”

  • The paper relies on this without support.

    The typical presentation of CKD in people with diabetes includes long-standing duration of diabetes, retinopathy, albuminuria without gross hematuria, and gradually progressive loss of eGFR.

    “The typical presentation of CKD in people with diabetes is considered to include long-standing duration of diabetes, retinopathy, albuminuria without gross hematuria, and gradually progressive loss of eGFR.”

  • The paper relies on this without support.

    Signs of CKD may be present at diagnosis or without retinopathy in type 2 diabetes.

    “However, signs of CKD may be present at diagnosis or without retinopathy in type 2 diabetes.”

  • The paper relies on this without support.

    Active urinary sediment, rapidly increasing albuminuria or total proteinuria, presence of nephrotic syndrome, rapidly decreasing eGFR, or absence of retinopathy (in type 1 diabetes) suggests alternative or additional causes of kidney disease.

    “An active urinary sediment (containing red or white blood cells or cellular casts), rapidly increasing albuminuria or total proteinuria, the presence of nephrotic syndrome, rapidly decreasing eGFR, or the absence of retinopathy (in type 1 diabetes) suggests alternative or additional causes of kidney disease.”

  • The paper relies on this without support.

    Urinary excretion of sodium and potassium may be impaired in individuals with reduced eGFR.

    “These interventions may be most important for individuals with reduced eGFR, for whom urinary excretion of sodium and potassium may be impaired.”

  • The paper relies on this without support.

    Outcome trials have not been performed to determine whether ACE inhibitors or ARBs improve kidney outcomes in people with moderately increased albuminuria (30-299 mg/g creatinine) without hypertension.

    “While ACE inhibitors or ARBs are often prescribed for moderately increased albuminuria (30-299 mg/g creatinine) without hypertension, outcome trials have not been performed in this setting to determine whether they improve kidney outcomes.”

  • The paper relies on this without support.

    ACE inhibitors and ARBs are commonly not dosed at maximum tolerated doses because of concerns that serum creatinine will rise.

    “It should be noted that ACE inhibitors and ARBs are commonly not dosed at maximum tolerated doses because of concerns that serum creatinine will rise.”

  • The paper relies on this without support.

    In all clinical trials demonstrating efficacy of ACE inhibitors and ARBs in slowing kidney disease progression, the maximum tolerated doses were used—not very low doses that do not provide benefit.

    “Note that in all clinical trials demonstrating efficacy of ACE inhibitors and ARBs in slowing kidney disease progression, the maximum tolerated doses were usednot very low doses that do not provide benefit.”

  • The paper relies on this without support.

    There has not been a direct comparison of MRAs and SGLT2 inhibitors.

    “Of note, there has not been a direct comparison of MRAs and SGLT2 inhibitors.”

  • The paper relies on this without support.

    There have also been no studies directly comparing MRAs, SGLT2 inhibitors, and GLP-1 RAs.

    “There have also been no studies directly comparing MRAs, SGLT2 inhibitors, and GLP-1 RAs.”

  • The paper relies on this without support.

    All of these studies included participants taking either an ACE inhibitor or an ARB, often at maximally tolerated doses.

    “As noted, all of these studies included participants taking either an ACE inhibitor or an ARB, often at maximally tolerated doses.”

  • The paper relies on this without support.

    Complications of CKD generally become prevalent when eGFR falls below 60 mL/min/1.73m2 (stage G3 CKD or greater) and become more common and severe as CKD progresses.

    “Complications of chronic kidney disease (CKD) generally become prevalent when estimated glomerular filtration rate falls below 60 mL/min/1.73m 2 (stage G3 CKD or greater) and become more common and severe as CKD progresses.”

  • The paper relies on this without support.

    Finerenone is currently the only ns-MRA with proven clinical kidney and cardiovascular benefits.

    “†Finerenone is currently the only ns-MRA with proven clinical kidney and cardiovascular benefits.”

  • The paper relies on this without support.

    Data that do exist suggest sustained benefit on albuminuria reduction with MRAs.

    “However, data that do exist suggest sustained benefit on albuminuria reduction.”
23 of 23

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The ADA states that high-protein diets providing 20% of total calories, or more than 1.3 g/kg/day are not recommended for patients with chronic kidney disease due to increased risk of albuminuria, more rapid kidney function loss, and increased CVD mortality.

    “The ADA states that high-protein diets providing 20% of total calories, or more than 1.3 g/kg/day are not recommended for patients with chronic kidney disease due to increased risk of albuminuria, more rapid kidney function loss, and increased CVD mortality [149].”

    From Lifestyle Medicine for Obesity in the Era of Highly Effective Anti-Obesity Treatment (2025) · cites this paper as [149]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Albuminuria categories overlap at 300 mg/g

    Minor

    One definition places 300 mg/g in both the moderate and severe categories; elsewhere, the moderate category ends at 299 mg/g.

  • Monitoring guidance gives different maximum frequencies

    Minor

    The recommendation caps monitoring at four times per year, while the figure description calls for four or more times per year in the highest-risk category.

  • Glucose-control passage reverses the direction of the eGFR benefit

    Minor

    One passage says intensive glucose lowering reduces eGFR, whereas a later passage describes its eventual effect as improved eGFR outcomes.

3 of 3

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. 1998, UK Prospective Diabetes Study (UKPDS) Group, Lancet, 352, 837

Cited by

Sorted by citations

Related

Authors
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., Garg, R., Khunti, K., Lal, R., Lingvay, I., Matfin, G., Pandya, N., Pekas, E. J., Pilla, S. J., Polsky, S., Segal, A. R., Seley, J. J., Stanton, R. C., & Bannuru, R. R.
ORCID
Venue
Diabetes Care
Publisher
American Diabetes Association
Published
2024-12-09
Volume
48
Issue
Supplement_1
Pages
S239-S251
ISSN
  • 0149-5992 (ISSN-L)
  • 1935-5548
DOI
10.2337/dc25-s011
PMC
PMC11635029
OpenAlex
W4405187720
Cited by
262
References
131
Citations by year
2026: 121 · 2025: 113 · 2024: 18 · 2023: 11
FWCI
61.04
Type
journal article
Language
en
Open access
Licence
www.diabetesjournals.org/journals/pages/license (vor)
Locations
  • Diabetes Care (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (submittedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
Keywords
chronic kidney disease, diabetes mellitus, risk management, clinical guidelines, quality of care, diabetic nephropathy
MeSH terms
Diabetes Mellitus, Humans, Risk Management

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-11.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-11.

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Statistics and arithmetic are recomputed, not judged.

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