The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index; 1 of the 20 sources its claims cite were checked for support.
Effects of Losartan on Renal and Cardiovascular Outcomes in Patients with Type 2 Diabetes and Nephropathy
Open accessAbstract
BACKGROUND: Diabetic nephropathy is the leading cause of end-stage renal disease. Interruption of the renin-angiotensin system slows the progression of renal disease in patients with type 1 diabetes, but similar data are not available for patients with type 2, the most common form of diabetes. We assessed the role of the angiotensin-II-receptor antagonist losartan in patients with type 2 diabetes and nephropathy. METHODS: A total of 1513 patients were enrolled in this randomized, double-blind study comparing losartan (50 to 100 mg once daily) with placebo, both taken in addition to conventional antihypertensive treatment (calcium-channel antagonists, diuretics, alpha-blockers, beta-blockers, and centrally acting agents), for a mean of 3.4 years. The primary outcome was the composite of a doubling of the base-line serum creatinine concentration, end-stage renal disease, or death. Secondary end points included a composite of morbidity and mortality from cardiovascular causes, proteinuria, and the rate of progression of renal disease. RESULTS: A total of 327 patients in the losartan group reached the primary end point, as compared with 359 in the placebo group (risk reduction, 16 percent; P=0.02). Losartan reduced the incidence of a doubling of the serum creatinine concentration (risk reduction, 25 percent; P=0.006) and end-stage renal disease (risk reduction, 28 percent; P=0.002) but had no effect on the rate of death. The benefit exceeded that attributable to changes in blood pressure. The composite of morbidity and mortality from cardiovascular causes was similar in the two groups, although the rate of first hospitalization for heart failure was significantly lower with losartan (risk reduction, 32 percent; P=0.005). The level of proteinuria declined by 35 percent with losartan (P<0.001 for the comparison with placebo). CONCLUSIONS: Losartan conferred significant renal benefits in patients with type 2 diabetes and nephropathy, and it was generally well tolerated.
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In the paper
“In this regard, it should be noted that in related studies in patients with type 1 and type 2 diabetes, 1,28,29 the benefits of captopril or irbesartan were not tested in the presence of concurrent calcium-channel-antagonist therapy.”
What the sources say
- Not checked — no full text of the sourcecites [1] source
- Supportedcites [28] source
The Randomization and Treatment Plan states that calcium-channel blockers were discontinued before screening and excluded as additional antihypertensive treatment. Irbesartan and the calcium-channel blocker amlodipine were assigned as separate regimens, so this type 2 diabetes study did not test irbesartan's benefit with concurrent calcium-channel-blocker therapy. The captopril study in type 1 diabetes is covered by the sentence's other citations, not this source. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [29] source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The level of proteinuria declined by 35 percent with losartan (P<0.001 for the comparison with placebo).”
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Losartan also reduced the risk of end-stage renal disease by 28 percent (P=0.002)”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“according to the per-protocol analysis, among the patients who continued to receive their assigned study treatment, losartan conferred a 22 percent reduction in the risk of the primary composite end point (P=0.008).”
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We did find a significant difference in favor of losartan with regard to the rate of a first hospitalization for heart failure, a component of this secondary composite end point.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The risk of the combined end point of end-stage renal disease or death was 20 percent lower in the losartan group than in the placebo group (P=0.01)”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In this population, losartan (plus conventional antihypertensive therapy) demonstrated excellent tolerability, similar to that of placebo (plus conventional antihypertensive therapy), as evidenced by the similar numbers of patients in the two groups in whom the study treatment was discontinued because of adverse events.”
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Treatment with losartan resulted in a 16 percent reduction in the risk of the primary composite end point (P= 0.02)”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Similarly, simultaneous therapy with calcium-channel antagonists did not detract from the beneficial effects of losartan, despite the recent controversy regarding the role of calcium-channel antagonists in the protection of the kidneys and the heart. 25-27”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Approximately one third of the patients had a fatal or nonfatal cardiovascular event (247 in the losartan group [32.9 percent] and 268 in the placebo group [35.2 percent]; risk reduction, 10 percent; P=0.26).”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 14
- Probably not a substantial claim. 16
- The quote only partly states this claim. 1
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was a difference between the number of myocardial infarctions in the losartan group (50 patients [6.7 percent]) and the number in the placebo group (68 patients [8.9 percent]; risk reduction, 28 percent), but this difference was not statistically significant (P=0.08).”
Strength:plain· not yet calibratedn = 50Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“There was a small, time-averaged difference in the trough blood pressure between the losartan group”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Approximately 20 percent of the patients died, but there was no significant difference in mortality between the two groups (P=0.88).”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Losartan also led to an average reduction in the level of proteinuria (the urinary albumin-to-creatinine ratio) of 35 percent, whereas in the patients in the placebo group, the urinary albumin-to-creatinine ratio tended to increase (P<0.001 for the overall treatment effect) (Fig. 3).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“mean arterial pressure, 95.9 mm Hg and 96.8 mm Hg, respectively [P=0.59]; pulse pressure, 66.7 mm Hg and 67 .4 mm Hg, respectively [P= 0.77]”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“mean arterial pressure, 99.1 mm Hg and 99.7 mm Hg, respectively [P= 0.38]; pulse pressure, 66.2 mm Hg and 67 .1 mm Hg, respectively [P=0.37]”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“mean arterial pressure, 100.9 mm Hg and 103.1 mm Hg, respectively [P<0.001]; pulse pressure, 67 .8 mm Hg and 69.8 mm Hg, respectively [P=0.05]”
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There were no significant differences in the rates of most of the cardiovascular end points; the exception was the first hospitalization with heart failure (89 patients in the losartan group [11.9 percent], as compared with 127 in the placebo group [16.7 percent]), for which the risk was reduced by 32 percent (P=0.005)”
- Also stated in: § A BSTRACT · p. 1 · plain
“although the rate of first hospitalization for heart failure was significantly lower with losartan (risk reduction, 32 percent; P=0.005)”
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Also stated in: § A BSTRACT · p. 1 · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At base line, 93.5 percent of the patients (92.3 percent in the losartan group and 94.6 percent in the placebo group) were receiving antihypertensive therapy.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The benefits of losartan were observed among our patients, many of whom were already receiving other therapies, such as aspirin, beta-blockers, and lipidlowering agents, as part of sound medical practice.”
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Increased serum concentrations of creatinine or potassium led to the discontinuation of the study medication in 1.5 percent and 1.1 percent, respectively, of the patients in the losartan group, as compared with 1.2 percent and 0.5 percent of the patients in the placebo group.”
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Analyses of the primary and secondary end points were performed according to the intention-to-treat principle; we included data from all randomized patients (with the exception of three patients who were lost to follow-up), from the time of randomization through the date of study termination.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“An independent end-points committee whose members were unaware of the patients' treatment assignments reviewed the data to determine which patients had reached the end points.”
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“More patients discontinued the study treatment in the placebo group (53.5 percent) than in the losartan group (46.5 percent).”
Strength:plain· not yet calibratedn = 1,513Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan Study was an investigator-initiated, multinational, double-blind, randomized, placebo-controlled study designed to evaluate the renoprotective effects of losartan in 1513 patients with type 2 diabetes and nephropathy.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Because one interim analysis used a stopping boundary that was based on an alpha spending function of the O'Brien-Fleming type, 10 a critical P value of 0.048 was required for the primary hypothesis.”
What the sources say
- Not checked — no full text of the sourcecites [10] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In a second, per-protocol analysis, we excluded patients who violated the criteria for inclusion and exclusion and censored patients' data 14 days after they permanently discontinued the study medication.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The study protocol was approved by the institutional review board of each center, and all patients gave written informed consent.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“However, the study was discontinued early (February 10, 2001) by a unanimous vote of the steering committee, whose members were unaware of the treatment assignments.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We cannot exclude the possibility that this small difference had a beneficial effect on the renal outcomes.”
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The Heart Outcomes Prevention Evaluation (HOPE) Study 32 and its substudy of patients with diabetes, MICRO-HOPE, 20 showed benefits of angiotensin-I-converting enzyme inhibition in terms of the signs and symptoms of heart failure but failed to show significant differences in hospitalizations for heart failure.”
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Previous studies involving angiotensin-I-converting enzyme inhibitors have demonstrated beneficial effects on proteinuria but have not demonstrated the superiority of blockade of the renin-angiotensin system in slowing the progression to end-stage renal disease over nonblockade forms of therapy. 14-20”
What the sources say
- Not matchedcites [14] Walker WG, 1992, J Am Soc Nephrol
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites [15] source
- Not checked — no full text of the sourcecites [16] source
- Not checked — no full text of the sourcecites [17] source
- Not checked — no full text of the sourcecites [18] source
- Not checked — no full text of the sourcecites [19] Estacio RO, 2000, Diabetes Care
- Not checked — no full text of the sourcecites [20] source
Load-bearingStrength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, in the absence of a direct comparison between angiotensin-I-converting enzyme inhibitors and angiotensin II antagonists, any extrapolation from the results obtained with different classes of drugs is speculative at best.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We were able to determine the status of all patients (except for three patients in the losartan group who could not be contacted) with respect to dialysis, transplantation, and death.”
Strength:plain· not yet calibratedn = 3Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Subsequent hospitalizations for heart failure were not assessed.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, the Cox model accounts for the base-line level of proteinuria (which was a stratification factor) and the geographic region, as prespecified in the data analysis plan.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The difference results in part from the fact that the Cox regression model accounts for the time at risk - i.e., the longer average follow-up in the losartan group than in the placebo group.”
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
The paper relies on this without support.
Diabetic nephropathy is the leading cause of end-stage renal disease.
“Diabetic nephropathy is the leading cause of end-stage renal disease.”
The paper relies on this without support.
Type 2 diabetes is the most common form of diabetes.
“type 2, the most common form of diabetes”
The paper relies on this without support.
Similar data on interruption of the renin-angiotensin system are not available for patients with type 2 diabetes.
“similar data are not available for patients with type 2, the most common form of diabetes”
The paper relies on this without support.
Postponing end-stage renal disease in patients with type 2 diabetes remains an elusive goal.
“postponing end-stage renal disease in patients with type 2 diabetes, the leading cause of chronic renal failure in many countries, remains an elusive goal”
The paper relies on this without support.
Type 2 diabetes is the leading cause of chronic renal failure in many countries.
“type 2 diabetes, the leading cause of chronic renal failure in many countries”
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 cited source doesn’t support the claim as written.
In the citing paper
“In the IDNT trial, treatment with irbesartan compared with placebo resulted in a 33% decrease in the risk of doubling of serum creatinine concentration and was associated with a nonsigni fi cant reduction in the incidence of kidney failure, which was independent of blood pressure.”
From KDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease (2022) · cites this paper as [13]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Antihypertensive therapy reduces the risk of albuminuria (67)(68)(69)(70), and among people with type 1 or 2 diabetes with established CKD (eGFR <60 mL/min/1.73m 2 and UACR $300 mg/g creatinine), ACE inhibitor or ARB therapy reduces the risk of progression to ESKD (71)(72)(73)(74)(75)(76)(77)(78)(79)(80).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2025 (2025) · cites this paper as [71]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) has been shown to prevent major adverse kidney outcomes in people with diabetes, and these drugs are recommended by clinical practice guidelines for the treatment of people with type 2 diabetes who have, or are at high risk of, kidney disease.[4][5][6][7][8]”
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 [6]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The only currently approved treatment for renoprotection in patients with type 2 diabetes is reninangiotensin system blockade, which was first shown to be effective 18 years ago.3,4”
From Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy (2019) · cites this paper as [3]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, a sustained ≥57% decrease in eGFR (equivalent to doubling of serum creatinine) was selected in FIDELITY because it is a classic outcome in diabetic nephropathy studies2 , 12–14 and is a more robust kidney failure surrogate outcome than a ≥40% decrease in eGFR, particularly when initial changes in eGFR occur.14 , 15”
From Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis (2022) · cites this paper as [13]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Antihypertensive therapy reduces the risk of albuminuria (68-71), and among people with type 1 or 2 diabetes with established CKD (eGFR <60 mL/min/1.73m 2 and UACR ≥300 mg/g creatinine), ACE inhibitor or ARB therapy reduces the risk of progression to kidney failure (72)(73)(74)(75)(76)(77)(78)(79)(80)(81).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [72]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“ACE inhibitors or ARBs are the preferred first-line agents for blood pressure treatment among people with diabetes, hypertension, eGFR <60 mL/min/1.73m 2 , and UACR ≥300 mg/g creatinine because of their proven benefits for prevention of CKD progression (72,73,75).”
From 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [72]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This recommendation is based on RCTs where findings demonstrated decreased risk of CKD progression, for which patients with albuminuria are at elevated risk, with a maximally dosed RAS inhibitor compared with placebo or an active antihypertensive drug comparator (42–44).”
From Diabetes management in chronic kidney disease: a consensus report by the American Diabetes Association (ADA) and Kidney Disease: Improving Global Outcomes (KDIGO) (2022) · cites this paper as [42]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In patients with diabetic kidney disease with increased levels of albuminuria, large placebo-controlled trials have shown that renin-angiotensin system (RAS) inhibitors,3–5 sodium-glucose cotransporter 2 (SGLT2) inhibitors,6,7 and the non-steroidal mineralocorticoid receptor antagonist finerenone8,9 all reduced the risk of progression to kidney failure.”
From Empagliflozin in Patients with Chronic Kidney Disease (2023) · cites this paper as [3]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“In the IDNT trial, treatment with irbesartan compared with placebo resulted in a 33% decrease in the risk of doubling of serum creatinine concentration and was associated with a nonsigni fi cant reduction in the incidence of kidney failure, which was independent of blood pressure.”
From KDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease (2022) · cites this paper as [13]
Experimental — accuracy not yet measuredIn the citing paper
“For many years, the only agents that had demonstrated benefit in slowing kidney disease progression were the renin angiotensin aldosterone system blockers of angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) [11], [12], [13].”
From Glucagon-like peptide-1 receptor agonists in diabetic kidney disease: a review of their kidney and heart protection (2023) · cites this paper as [11]
In the citing paper
“ARBs (irbesartan/telmisartan) also slowed progression from microalbuminuria (albuminuria stage A2) to overt nephropathy.708,709”
From 2023 ESC guidelines for the management of cardiovascular disease in patients with diabetes. (2023) · cites this paper as [708]
In the citing paper
“Antagonism of the RAAS with ACE inhibitors or AngII receptor blockers also attenuates, but may not completely halt, the progression of kidney injury in patients with obesity, hypertension and T2DM67,68.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [67]
In the citing paper
“Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB)s improve endothelium-dependent vasodilation and reduce morbidity and mortality in heart failure and nephropathy, including diabetic nephropathy.218-221”
From The Vasculature in Prediabetes (2018) · cites this paper as [219]
In the citing paper
“Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB)s improve endothelium-dependent vasodilation and reduce morbidity and mortality in heart failure and nephropathy, including diabetic nephropathy.218-221”
From The Vasculature in Prediabetes (2018) · cites this paper as [219]
In the citing paper
“ARBs have also been shown to reduce the rate of progression from micro- to macroalbuminuria as well as ESRD in patients with type 2 diabetes (234–236).”
From Standards of Medical Care in Diabetes—2009 (2009) · cites this paper as [235]
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.
Mean follow-up of 3.4 years is not 42 months
MinorAt 12 months per year, 3.4 years is 40.8 months, not 42 months. Forty-two months is 3.5 years.
Reported 42 · recomputed 40.8
“The mean follow-up time was 3.4 years (42 months).”
Patients with prior heart failure were both excluded and included
MinorThe eligibility criteria excluded anyone with a history of heart failure before enrollment, but the paper later says 88 patients had preexisting heart failure at randomization. This affects the description of the population used for the heart-failure analysis.
“who had any history of heart failure before enrollment.”
“There were 88 patients (44 in each group) who had preexisting heart failure at the time of randomization.”
Citations
Cites
Nonparametric Estimation from Incomplete Observations
Kaplan, E. L., & Meier, P. (1992) · Springer series in statistics · doi:10.1007/978-1-4612-4380-9_25 · Cited by 45,239
Regression Models and Life-Tables
Cox, D. R. (1972) · Journal of the Royal Statistical Society Series B: Statistical Methodology · doi:10.1111/j.2517-6161.1972.tb00899.x · Cited by 39,793
Nonparametric Estimation from Incomplete Observations
Kaplan, E. L., & Meier, P. (1958) · Journal of the American Statistical Association · doi:10.1080/01621459.1958.10501452 · Cited by 39,158
Regression Models and Life-Tables
Cox, D. R. (1992) · Springer Series in Statistics · doi:10.1007/978-1-4612-4380-9_37 · Cited by 26,297
Levey, A. S., Bosch, J. P., Lewis, J. B., Greene, T., Rogers, N., Roth, D., & for the Modification of Diet in Renal Disease Study Group* (1999) · Annals of Internal Medicine · doi:10.7326/0003-4819-130-6-199903160-00002 · Cited by 15,079
(2000) · New England Journal of Medicine · doi:10.1056/nejm200001203420301 · Cited by 8,663
The SOLVD Investigators* (1991) · New England Journal of Medicine · doi:10.1056/nejm199108013250501 · Cited by 8,029
Lewis, E. J., Hunsicker, L. G., Clarke, W. R., Berl, T., Pohl, M. A., Lewis, J. B., Ritz, E., Atkins, R. C., Rohde, R., & Raz, I. (2001) · New England Journal of Medicine · doi:10.1056/nejmoa011303 · Cited by 5,987
The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy
Lewis, E. J., Hunsicker, L. G., Bain, R. P., & Rohde, R. D. (1993) · New England Journal of Medicine · doi:10.1056/nejm199311113292004 · Cited by 5,394
(1992) · New England Journal of Medicine · doi:10.1056/nejm199209033271003 · Cited by 3,725
Flagged first, then by citations
Research works printed but not linked: 5
- Black HR, 1999, J Hypertens, 17, S3
- Levey AS, 2000, J Am Soc Nephrol, 11, 155A
- Walker WG, 1992, J Am Soc Nephrol, 3, 339
- Estacio RO, 2000, Diabetes Care, 23, B54
- Bauer JH, Reams GP. Antihypertensive drugs. In: Brenner BM, ed. The kidney. 6th ed. Philadelphia: W.B. Saunders, 2000:2253-97.
Cited by
Sorted by citations
Items 1,801–1,900 of 7,495
The Selective A3AR Antagonist LJ-1888 Ameliorates UUO-Induced Tubulointerstitial Fibrosis
Lee, J., Hwang, I., Lee, H., Lee, H. W., Jeong, L. S., & Ha, H. (2013) · American Journal Of Pathology · doi:10.1016/j.ajpath.2013.07.010 · Cited by 50
Sawaguchi, M., Araki, S., Kobori, H., et al. (2011) · Journal of Diabetes Investigation · doi:10.1111/j.2040-1124.2011.00172.x · Cited by 48
Ji, Z., & Xu, Y. (2016) · Molecular Medicine Reports · doi:10.3892/mmr.2016.5313 · Cited by 49
Management of autosomal-dominant polycystic kidney disease—state-of-the-art
Müller, R., & Benzing, T. R. (2018) · Clinical Kidney Journal · doi:10.1093/ckj/sfy103 · Cited by 50
Urinary Renin in Patients and Mice With Diabetic Kidney Disease
Tang, J., Wysocki, J. A., Ye, M., Vallés, P. G., Rein, J., Shirazi, M., Bäder, M., Gómez, R. A., Sequeira-Lόpez, M. L. S., Afkarian, M., et al. (2019) · Hypertension · doi:10.1161/hypertensionaha.119.12873 · Cited by 48
Barriers to initiating SGLT2 inhibitors in diabetic kidney disease: a real-world study
Jeong, S. J., Lee, S. E., Shin, D. H., Park, I. B., Lee, H. S., & Kim, K. (2021) · BMC Nephrology · doi:10.1186/s12882-021-02381-3 · Cited by 49
Suzaki, Y., Ozawa, Y., & Kobori, H. (2007) · International Journal of Biological Sciences · doi:10.7150/ijbs.3.40 · Cited by 48
Ohishi, M., TAKAGI, T., Ito, N., et al. (2007) · Hypertension Research · doi:10.1291/hypres.30.797 · Cited by 48
Heart and Kidney: Fatal Twins?
Ritz, E. (2006) · The American Journal of Medicine · doi:10.1016/j.amjmed.2006.01.012 · Cited by 48
Resistant Hypertension: Prevalence and Evolving Concepts
Epstein, M. (2007) · Journal of Clinical Hypertension · doi:10.1111/j.1524-6175.2007.06171.x · Cited by 49
Compliance and persistence with newer antihypertensive agents
Gerth, W. C. (2002) · Current Hypertension Reports · doi:10.1007/s11906-002-0021-6 · Cited by 48
Benigni, A., Gagliardini, E., & Remuzzi, G. (2004) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2003.11.005 · Cited by 48
Self-citationFéliers, D., Duraisamy, S., Barnes, J. L., et al. (2004) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00271.2004 · Cited by 48
Izuhara, Y., Nangaku, M., Takizawa, S., et al. (2007) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfm601 · Cited by 48
Interaction Between Renal Function and Microalbuminuria for Cardiovascular Risk in Hypertension
Färbom, P., Wahlstrand, B., Almgren, P., Skrtic, S., Lanke, J., Weiss, L. G., Kjeldsen, S. E., Hedner, T., & Melander, O. (2008) · Hypertension · doi:10.1161/hypertensionaha.107.109264 · Cited by 48
Age distribution and yearly changes in the incidence of ESRD in Japan
Yamagata, K., Takahashi, H., Suzuki, S., Mase, K., Hagiwara, M., Shimizu, Y., Hirayama, K., Kobayashi, M., Narita, M., & Kôyama, A. (2004) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2003.11.005 · Cited by 48
Beddhu, S., Logar, C. M., & Herzog, C. A. (2003) · The American Journal of the Medical Sciences · doi:10.1097/00000441-200304000-00008 · Cited by 48
Antagonistes des r??cepteurs de l???angiotensine II
Corvol, P. L., & Plouin, P. (2002) · Drugs · doi:10.2165/00003495-200262991-00006 · Cited by 48
Diabetic renal disease: from recent studies to improved clinical practice
Mogensen, C. E., & Cooper, M. E. (2004) · Diabetic Medicine · doi:10.1111/j.1464-5491.2004.01121.x · Cited by 48
Self-citationBlood Pressure and Cardiovascular Disease
Furberg, C. D., Psaty, B. M., & Soliman, E. Z. (2009) · Wiley eBooks · doi:10.1002/9781444309768.ch13 · Cited by 48
Therapeutic Targeting of Fibrotic Epithelial-Mesenchymal Transition–An Outstanding Challenge
Fintha, A., Gasparics, Á., Rosivall, L., & Sebe, A. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.00388 · Cited by 47
Fernández‐Fernández, B., Fernández-Prado, R., Górriz, J. L., Martínez‐Castelao, A., Navarro‐González, J. F., Porrini, E., Soler, M. J., & Ortíz, A. (2019) · Clinical Kidney Journal · doi:10.1093/ckj/sfz070 · Cited by 48
Malek, V., Suryavanshi, S. V., Sharma, N., Kulkarni, Y. A., Mulay, S. R., & Gaikwad, A. B. (2020) · Reviews of physiology, biochemistry and pharmacology · doi:10.1007/112_2020_50 · Cited by 48
Losartan and enalapril are comparable in reducing proteinuria in children with Alport syndrome
Webb, N. J. A., Shahinfar, S., Wells, T. G., et al. (2012) · Pediatric Nephrology · doi:10.1007/s00467-012-2372-9 · Cited by 47
Self-citationAT1 Receptors and Control of Blood Pressure: The Kidney and More…
Crowley, S. D., Gurley, S. B., & Coffman, T. M. (2007) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2006.11.002 · Cited by 45
Ripley, E. B. D. (2010) · International Journal of Nephrology and Renovascular Disease · doi:10.2147/ijnrd.s7038 · Cited by 47
Reduction of proteinuria with angiotensin receptor blockers
Galle, J. C. (2008) · Nature Clinical Practice Cardiovascular Medicine · doi:10.1038/ncpcardio0806 · Cited by 47
The Genetics of Diabetic Nephropathy
Brennan, E. P., McEvoy, C. M., Sadlier, D. M., Godson, C., & Martin, F. (2013) · Genes · doi:10.3390/genes4040596 · Cited by 46
Effect of tranilast in early-stage diabetic nephropathy
Soma, J., Satô, K., Saito, H., et al. (2006) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfl325 · Cited by 47
The role of renin angiotensin system inhibition in kidney repair
van der Meer, I. M., Cravedi, P., & Remuzzi, G. (2010) · Fibrogenesis & Tissue Repair · doi:10.1186/1755-1536-3-7 · Cited by 47
Self-citationOnuigbo, M. A. C. (2010) · Renal Failure · doi:10.3109/0886022x.2010.502608 · Cited by 48
Elliott, W. J. (2009) · Yearbook of Cardiology · doi:10.1016/s0145-4145(08)79418-8 · Cited by 47
Velde‐Keyzer, C. A. T., van Breda, G. F., Vervloet, M. G., de Jong, M. A., Laverman, G. D., Hemmelder, M. H., Janssen, W. M. T., Heerspink, H. J. L., Kwakernaak, A. J., Bakker, S. J. L., et al. (2016) · Journal of the American Society of Nephrology · doi:10.1681/asn.2016040407 · Cited by 48
Albuminuria and Cerebral Small Vessel Disease: A Systematic Review and Meta‐Analysis
Georgakis, M. K., Chatzopoulou, D., Tsivgoulis, G. K., & Petridou, E. T. (2018) · Journal of the American Geriatrics Society · doi:10.1111/jgs.15240 · Cited by 50
MicroRNA as novel biomarkers and therapeutic targets in diabetic kidney disease: An update
Cao, Q., Chen, X., Huang, C., & Pollock, C. A. (2019) · FASEB BioAdvances · doi:10.1096/fba.2018-00064 · Cited by 48
New Therapies for the Treatment of Renal Fibrosis
Liu, F., & Zhuang, S. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-8871-2_31 · Cited by 48
Fu, E. L., Clase, C. M., Evans, M., Lindholm, B., Rotmans, J. I., Dekker, F. W., van Diepen, M., & Carrero, J. J. (2020) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2020.10.006 · Cited by 48
Nichols, G. A., Déruaz‐Luyet, A., Brodovicz, K. G., Kimes, T. M., Rosales, A. G., & Hauske, S. J. (2020) · BMC Nephrology · doi:10.1186/s12882-020-01792-y · Cited by 48
Pfeffer, M. A., & Frohlich, E. D. (2006) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00647.2006 · Cited by 47
Angiotensin II Upregulates RAGE Expression on Podocytes: Role of AT2 Receptors
Rüster, C., Bondeva, T., Franke, S., Tanaka, N., Yamamoto, H., & Wolf, G. (2009) · American Journal of Nephrology · doi:10.1159/000191467 · Cited by 47
The Role of Glycosaminoglycans and Sulodexide in the Treatment of Diabetic Nephropathy
Abaterusso, C., & Gambaro, G. (2006) · Treatments in Endocrinology · doi:10.2165/00024677-200605040-00002 · Cited by 49
The Kidney, Hypertension, and Remaining Challenges
Khosla, N., Kalaitzidis, R., & Bakris, G. L. (2009) · Medical Clinics of North America · doi:10.1016/j.mcna.2009.02.001 · Cited by 45
Rosen, A. B., Karter, A. J., Liu, J. Y., Selby, J. V., & Schneider, E. C. (2004) · Journal of General Internal Medicine · doi:10.1111/j.1525-1497.2004.30264.x · Cited by 47
Recent clinical trials with omapatrilat: New developments
Zanchi, A., Maillard, M. P., & Burnier, M. (2003) · Current Hypertension Reports · doi:10.1007/s11906-003-0045-6 · Cited by 47
Campbell, N. R. C., Khan, N. A., Hill, M. D., Tremblay, G., Lebel, M., Kaczorowski, J. A., McAlister, F. A., Lewanczuk, R. Z., & Tobe, S. W. (2009) · Canadian Journal of Cardiology · doi:10.1016/s0828-282x(09)70490-8 · Cited by 47
Evaluation of a technique of inducing hypertensive renal insufficiency in cats
Mathur, S., Brown, C. A., Dietrich, U. M., Munday, J. S., Newell, M. A., Sheldon, S. E., Cartier, L. M., & Brown, S. A. (2004) · American Journal of Veterinary Research · doi:10.2460/ajvr.2004.65.1006 · Cited by 47
Clinical studies of advanced glycation end product inhibitors and diabetic kidney disease
Williams, M. E. (2004) · Current Diabetes Reports · doi:10.1007/s11892-004-0054-0 · Cited by 47
Stehle, D., Xu, M., Schomber, T., Hahn, M. G., Schweda, F., Feil, S. C., Kraehling, J. R., Eitner, F., Patzak, A. R., Sandner, P., et al. (2021) · British Journal of Pharmacology · doi:10.1111/bph.15586 · Cited by 45
Heart Failure in Patients with Chronic Kidney Disease
Xanthopoulos, A. V., Papamichail, A., Briasoulis, Α., Loritis, K., Bourazana, A., Magouliotis, D. E., Sarafidis, P. A., Stefanidis, I., Skoularigis, J. S., & Triposkiadis, F. K. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12186105 · Cited by 56
Benigni, A., Zoja, C., Campana, M., et al. (2006) · Nephron Experimental Nephrology · doi:10.1159/000094967 · Cited by 46
Self-citationResveratrol attenuates angiotensin II-induced interleukin-6 expression and perivascular fibrosis
Inanaga, K., Ichiki, T., Matsuura, H., Miyazaki, R., Hashimoto, T., Takeda, K., & Sunagawa, K. (2009) · Hypertension Research · doi:10.1038/hr.2009.47 · Cited by 45
Is diabetic nephropathy reversible?
Fioretto, P., Barzon, I., & Mauer, M. S. (2014) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2014.01.017 · Cited by 46
Renin-angiotensin-aldosterone system-mediated redox effects in chronic kidney disease
Nistala, R., Wei, Y., Sowers, J. R., & Whaley‐Connell, A. T. (2009) · Translational research · doi:10.1016/j.trsl.2008.12.008 · Cited by 46
Achieving Blood Pressure Goals: Why Aren't We?
Cushman, W. C., & Basile, J. (2006) · Journal of Clinical Hypertension · doi:10.1111/j.1524-6175.2006.05789.x · Cited by 46
Nerpin, E., Ingelsson, E., Risérus, U., Sundström, J., Larsson, A. O., Jobs, E. N., Jobs, M., Hallan, S. I., Zethelius, B., Berglund, L., et al. (2011) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfq848 · Cited by 45
Mineralocorticoid receptor as a therapeutic target in chronic kidney disease and hypertension
Shibata, S., Ishizawa, K., & Uchida, S. (2016) · Hypertension Research · doi:10.1038/hr.2016.137 · Cited by 48
Loffler, K. A., Heeley, E., Freed, R., Anderson, C. S., Brockway, B., Corbett, A., Chang, C. L., Douglas, J. A., Ferrier, K., Graham, N., et al. (2017) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201703-0603oc · Cited by 46
Mineralocorticoid Antagonism and Diabetic Kidney Disease
Lytvyn, Y., Godoy, L. C., Scholtes, R. A., van Raalte, D. H., & Cherney, D. Z. I. (2019) · Current Diabetes Reports · doi:10.1007/s11892-019-1123-8 · Cited by 48
Martin, W. P., White, J. P., López-Hernández, F. J., Docherty, N. G., & le Roux, C. W. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00289 · Cited by 49
Morales, E., Cravedi, P., & Manrique, J. (2021) · Frontiers in Medicine · doi:10.3389/fmed.2021.653634 · Cited by 48
Sánchez, J. J. G., Thompson, J. C., Scott, D. A., Evans, R., Rao, N., Sörstadius, E., James, G., NOLAN, S. T., Wittbrodt, E. T., Sultan, A. A., et al. (2021) · Advances in Therapy · doi:10.1007/s12325-021-02006-z · Cited by 53
Yokozawa, T., Nakagawa, T., Oya, T., et al. (2005) · Journal of Pharmacy and Pharmacology · doi:10.1211/0022357056154 · Cited by 46
Evolving strategies for the use of combination therapy in hypertension
Gradman, A. H., & Acevedo, C. (2002) · Current Hypertension Reports · doi:10.1007/s11906-002-0062-x · Cited by 46
Progression and regression in renal vascular and glomerular fibrosis
Chatziantoniou, C., Boffa, J., Tharaux, P., Flamant, M., Ronco, P. M., & Dussaule, J. (2004) · International Journal of Experimental Pathology · doi:10.1111/j.0959-9673.2004.00376.x · Cited by 46
Trends in cardiovascular drug utilization and drug expenditures in Canada between 1996 and 2001.
Jackevicius, C. A., Tu, K., Filate, W. A., Brien, S., & Tu, J. V. (2003) · PubMed · Cited by 45
Nakao, N., Seno, H., Kasuga, H., et al. (2004) · American Journal of Nephrology · doi:10.1159/000081953 · Cited by 46
RetractedAgarwal, R., & Fouque, D. P. (2022) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfac331 · Cited by 47
Stringer, S. J., Sharma, P., Dutton, M., Jesky, M., Ng, K. P., Kaur, O., Chapple, I., Dietrich, T., Ferro, C. J., & Cockwell, P. (2013) · BMC Nephrology · doi:10.1186/1471-2369-14-95 · Cited by 47
Microalbuminuria breakthrough under chronic renin–angiotensin–aldosterone system suppression
Cerezo, C., Ruilope, L. M., Segura, J., García‐Donaire, J. A., de la Cruz, J. J., Banegas, J. R., Waeber, B., Rabelink, T. J., & Messerli, F. H. (2011) · Journal of Hypertension · doi:10.1097/hjh.0b013e32834d9e0f · Cited by 44
Whaley‐Connell, A. T. (2008) · Vascular Health and Risk Management · doi:10.2147/vhrm.s3121 · Cited by 46
Assessing the Validity of Surrogate Outcomes for ESRD
Jun, M., Turin, T. C., Woodward, M., Perkovic, V., Heerspink, H. J. L., Manns, B., Tonelli, M. A., & Hemmelgarn, B. R. (2015) · Journal of the American Society of Nephrology · doi:10.1681/asn.2014040396 · Cited by 44
Hypertension in diabetes: A call to action
Campbell, N. R. C., Leiter, L. A., Larochelle, P. M., Tobe, S. W., Chockalingam, A., Ward, R., Morris, D., & Tsuyuki, R. T. (2009) · Canadian Journal of Cardiology · doi:10.1016/s0828-282x(09)70493-3 · Cited by 46
ARB candesartan and CCB amlodipine in hypertensive patients: the CASE-J trial
Ogihara, T., Fujimoto, A., Nakao, K., & Saruta, T. (2008) · Expert Review of Cardiovascular Therapy · doi:10.1586/14779072.6.9.1195 · Cited by 46
Heerspink, H. J. L., Gao, P., de Zeeuw, D., Clase, C. M., Dagenais, G. R., Sleight, P., Lonn, E., Teo, K. K., Yusuf, S., & Mann, J. F. E. (2013) · European Journal of Preventive Cardiology · doi:10.1177/2047487313510678 · Cited by 48
Leporini, C., Pisano, A., Russo, E., D’Arrigo, G., Sarro, G. D., Coppolino, G., & Bolignano, D. (2016) · Pharmacological Research · doi:10.1016/j.phrs.2016.03.001 · Cited by 45
Ma, R., Chaudhari, S. K., & Li, W. (2016) · Antioxidants and Redox Signaling · doi:10.1089/ars.2016.6661 · Cited by 45
Unmet need in diabetic nephropathy: failed drugs or trials?
de Zeeuw, D., & Heerspink, H. J. L. (2016) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(16)30045-6 · Cited by 45
Mega clinical trials which have shaped the RAS intervention clinical practice
Düsing, R. (2016) · Therapeutic Advances in Cardiovascular Disease · doi:10.1177/1753944716644131 · Cited by 44
Yamanouchi, M., SKUPIEN, J. K., Niewczas, M. A., Smiles, A. M., Doria, A., Stanton, R. C., Gałecki, A. T., Duffin, K. L., Pullen, N., Breyer, M. D., et al. (2017) · Kidney International · doi:10.1016/j.kint.2017.02.010 · Cited by 45
Chou, Y., Huang, T., & Chu, T. (2017) · Journal of the Formosan Medical Association · doi:10.1016/j.jfma.2017.04.026 · Cited by 45
Early and late scanning electron microscopy findings in diabetic kidney disease
Conti, S., Perico, N., Novelli, R., Carrara, C., Benigni, A., & Remuzzi, G. (2018) · Scientific Reports · doi:10.1038/s41598-018-23244-2 · Cited by 45
Self-citationChen, P., Shi, X., Xu, X., Lin, Y., Shao, Z., Wu, R., & Huang, L. (2018) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2017.09.006 · Cited by 45
Impaired Glucose Metabolism in Patients with Heart Failure
Tenenbaum, A., & Fisman, E. Z. (2004) · American Journal of Cardiovascular Drugs · doi:10.2165/00129784-200404050-00001 · Cited by 46
Reversal of diabetic nephropathy: lessons from pancreas transplantation
Fioretto, P., & Mauer, M. S. (2012) · Journal of Nephrology · doi:10.5301/jn.5000061 · Cited by 45
Mechanisms of kidney fibrosis and the role of antifibrotic therapies
Deelman, L., & Sharma, K. (2008) · Current Opinion in Nephrology & Hypertension · doi:10.1097/mnh.0b013e32831c50a1 · Cited by 45
Tonolo, G., Velussi, M., Brocco, E., Abaterusso, C., Carraro, A., Morgia, G., Satta, A. E., Faedda, R., Abhyankar, A., Luthman, H., et al. (2006) · Kidney International · doi:10.1038/sj.ki.5001515 · Cited by 44
Hypertensive renal damage: Insights from animal models and clinical relevance
Griffin, K. A., & BIDANI, A. K. (2004) · Current Hypertension Reports · doi:10.1007/s11906-004-0091-8 · Cited by 45
Hypertension and antihypertensive treatment of diabetic nephropathy
Ritz, E., & Dikow, R. (2006) · Nature Reviews Nephrology · doi:10.1038/ncpneph0298 · Cited by 44
Seccia, T. M., Maniero, C., Belloni, A. S., Guidolin, D., Pothen, P., Pessina, A. C., & Rossi, G. P. (2008) · Journal of Hypertension · doi:10.1097/hjh.0b013e328309f00a · Cited by 45
Outcome research, nutrition, and reverse epidemiology in maintenance dialysis patients
Kalantar‐Zadeh, K., Fouque, D. P., & Kopple, J. D. (2004) · Journal of Renal Nutrition · doi:10.1053/j.jrn.2004.01.005 · Cited by 45
Desai, A. S., & Fang, J. C.-T. (2008) · Heart Failure Clinics · doi:10.1016/j.hfc.2007.11.001 · Cited by 45
RENAAL Investigators, Boner, G., Cooper, M. E., McCarroll, K., Brenner, B. M., de Zeeuw, D., Kowey, P. R., Shahinfar, S., Dickson, T. Z., Crow, R. S., et al. (2005) · Diabetologia · doi:10.1007/s00125-005-1893-1 · Cited by 44
Self-citationHotta, O. (2004) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2004.01.005 · Cited by 44
Lessons Learned from Recent Hypertension Trials about Kidney Disease
Khosla, N., & Bakris, G. L. (2005) · Clinical Journal of the American Society of Nephrology · doi:10.2215/cjn.00840805 · Cited by 45
Treatment of diabetic nephropathy with angiotensin II receptor antagonist
Lewis, E. J., & Lewis, J. B. (2003) · Clinical and Experimental Nephrology · doi:10.1007/s101570300000 · Cited by 45
The Renin-Angiotensin-Aldosterone System and Fibrinolysis in Progressive Renal Disease
Brown, N. J., Vaughan, D. E., & Fogo, A. B. (2002) · Seminars in Nephrology · doi:10.1053/snep.2002.34725 · Cited by 45
Blood Pressure Lowering for the Prevention and Treatment of Diabetic Kidney Disease
Thomas, M. C., & Atkins, R. C. (2006) · Drugs · doi:10.2165/00003495-200666170-00005 · Cited by 45
Prevention and Treatment of Diabetic Nephropathy
Tong, L., & Adler, S. G. (2010) · Elsevier eBooks · doi:10.1016/b978-0-323-05876-6.00030-7 · Cited by 46
Heerspink, H. J. L., Vart, P., Jongs, N., Neuen, B. L., Bakris, G. L., Claggett, B. L., Vaduganathan, M., McCausland, F. R., Docherty, K. F., Jhund, P. S., et al. (2023) · Diabetes Obesity and Metabolism · doi:10.1111/dom.15232 · Cited by 47
Novel drugs and intervention strategies for the treatment of chronic kidney disease
Heerspink, H. J. L., & de Zeeuw, D. (2013) · British Journal of Clinical Pharmacology · doi:10.1111/bcp.12195 · Cited by 46
Metadata
- Authors
- Brenner, B. M., Cooper, M. E., de Zeeuw, D., Keane, W. F., Mitch, W. E., Parving, H.-H., Remuzzi, G., Snapinn, S. M., Zhang, Z., & Shahinfar, S.
- Affiliations
- Brigham and Women's Hospital (US)
- The University of Melbourne (AU)
- Hennepin County Medical Center (US)
- Emory University (US)
- Mario Negri Institute for Pharmacological Research (IT)
- Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2001-09-20
- Volume
- 345
- Issue
- 12
- Pages
- 861-869
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2056976690
- Semantic Scholar
- 842bf4da2a50ee13464536c9dfa502f4eb80c5f1
- Cited by
- 7,493
- References
- 37
- Citations by year
- 2026: 180 · 2025: 233 · 2024: 211 · 2023: 248 · 2022: 235 · 2021: 240 · 2020: 263 · 2019: 204 · 2018: 212 · 2017: 233 · 2016: 243 · 2015: 249 · 2014: 289 · 2013: 288 · 2012: 341
- FWCI
- 280.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- RECERCAT (Consorci de Serveis Universitaris de Catalunya) (submittedVersion, public-domain)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
- Keywords
- losartan, type 2 diabetes, diabetic nephropathy, angiotensin receptor blockers, renin-angiotensin system blockade, end-stage renal disease, kidney disease progression, proteinuria, cardiovascular morbidity and mortality, heart failure hospitalization, serum creatinine doubling, antihypertensive therapy
- MeSH terms
- Adult, Aged, Antihypertensive Agents, Cardiovascular Diseases, Creatine, Creatinine, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Double-Blind Method, Female, Humans, Hypertension, Kidney Failure, Chronic, Male, Middle Aged, Proteinuria, Disease Progression, Losartan, Angiotensin Receptor Antagonists
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.
A language model drew the claims from the paper on 2026-10-16, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-16 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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