Type 2-diabetesPhase 3NCT01835678
Effects of Linagliptin on Renal Endothelium Function in Patients With Type 2 Diabetes.
A Phase 3 study testing Linagliptin in people with Type 2-diabetes, run by University of Erlangen-Nürnberg Medical School at 2 sites in Germany.
Trial summary
Diabetes mellitus is a metabolic disease with a growing prevalence worldwide, affecting 171 million people in 2000 and an expected 366 million people in 2030 (1) and therefore diabetic nephropathy is rapidly increasing in the Western hemisphere and represents in up to 50 % the cause of end stage renal disease. Read more about this study
- Who is it for?
- Ages 18 to 70 years
- Conditions the study is for
- Type 2-diabetes
- What is being tested?
- Linagliptin
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 65 participants
- Where
- 2 sitesGermany
- Study dates
- Oct 2012to Apr 2014
- Phase
- Phase 3
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 70 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Female and male patients aged between 18 and 70 years
- Type 2 diabetes without diabetic nephropathy (definition see exclusion criteria)
Who cannot join
- Any other form of diabetes mellitus than type 2 diabetes mellitus
- Use of insulin, glitazone or gliptins within the past 3 months
- Any other oral antidiabetic drug that can not be discontinued for the study period.
- Any history of stroke, transient ischemic attack, instable angina pectoris, or myocardial infarction within the last 6 months prior to study inclusion
- Urinary albumin excretion (UACR) > 100 mg/g (early morning spot urine)
- eGFR <45 ml/min/1.73m² (MDRD Formula)
Show all 22Show fewer
- Uncontrolled arterial hypertension (RR ≥180/ ≥110mmHg)
- HbA1c ≥ 10%
- Fasting plasma glucose ≥ 240 mg/dl
- Body mass index ≥ 40 kg/m²
- Triglyceride levels ≥ 1000 mg/dl
- HDL-cholesterol levels <25 mg/dl
- Overt congestive heart failure (CHF) or history of CHF
- Severe disorders of the gastrointestinal tract or other diseases which interfere the pharmacodynamics and pharmacokinetics of study drugs
- Significant laboratory abnormalities such as SGOT or SGPT levels more than 3 x above the upper limit of normal range, serum creatinine > 2mg/dl
- Drug or alcohol abuses
- Pregnant or breast-feeding patients
- Any patient currently receiving chronic (>30 consecutive days) treatment with an oral corticosteroid
- Patients being treated for severe auto immune disease e.g. lupus
- Participation in another clinical study within 30 days prior to visit 1
- Individuals at risk for poor protocol or medication compliance
- Subject who do not give written consent, that pseudonymous data will be transferred in line with the duty of documentation and the duty of notification according to § 12 and § 13 GCP-V
Trial locations and contacts
2 sites in 1 country.
Germany2 sites
Clinical Research Unit, Department of Nephrology and Hypertension, University of Erlangen-Nürnberg
Erlangen, 91054
Clinical Research Unit, Department of Nephrology and Hypertension, University of Erlangen-Nürnberg
Nuremberg, 90471
About this study
Official title: Effects of Linagliptin on Renal Endothelium Function in Patients With Type 2 Diabetes
Diabetes mellitus is a metabolic disease with a growing prevalence worldwide, affecting 171 million people in 2000 and an expected 366 million people in 2030 (1) and therefore diabetic nephropathy is rapidly increasing in the Western hemisphere and represents in up to 50 % the cause of end stage renal disease. Hence, early intervention is desirable to prevent any damage to the kidneys. In the early stage of diabetic nephropathy, endothelium dysfunction is a key pathogenetic process as indicated by increased leakage of albumin through the glomerular barrier (2).
Hence, improvement of endothelium function is an attractive therapeutic goal of antidiabetic medication. Endothelial dysfunction, in particular basal nitric oxide activity, has been also identified as pivotal determinant of glomerular filtration rate (3).
Read more
A new and promising class of antidiabetic drugs are the gliptins. Gliptins act by inhibiting the enzyme dipeptidyl peptidase-4 (DPP-4), which is responsible for the rapid inactivation of glucagon-like peptide-1 (GLP-1) - an incretin hormone of the gut (6 - 8), thereby enhancing and prolonging the effects of GLP-1. GLP-1 - member of the incretin hormones - is released into the blood after meal ingestion and stimulates the insulin secretion in a glucose dependent manner. This accounts for the marked prandial insulin response, which prevents prandial hyperglycemia.
Apart from surrogate parameters like reduction of fasting and postprandial blood glucose levels or improvement of HbA1c, the effect of gliptins on micro- and macrovascular function and cardiovascular outcome has not been the primary focus of current studies. However, infusion of GLP-1, the incretin hormone affected by gliptins has been reported to ameliorate endothelial dysfunction in patients suffering from coronary artery disease (9) and it was recently shown that infusion of GLP-1 into healthy human subjects increases both normal and ACh-induced vasodilatation (10). In studies on rats with diabetes, GLP-1 infusion nearly re-established their normal vascular tone (11) and there are further data from experimental animals that indicate a beneficial effect of GLP-1 on endothelial function (12).
It is of major interest whether therapy with gliptins improves endothelial function of the micro- and macrovasculature. In face of the burden that diabetic nephropathy causes, the effect of linagliptin on the renal vasculature and endothelium integrity of the renal circulation (as measured by the availability of nitric oxide), is a key stone in order to claim that linagliptin is an effective antidiabetic agents. There is a need to demonstrate that linagliptin is effective beyond its blood glucose lowering actions and improves vascular endothelium function in the kidney.
Read the detailed description
Diabetes mellitus is a metabolic disease with a growing prevalence worldwide, affecting 171 million people in 2000 and an expected 366 million people in 2030 (1) and therefore diabetic nephropathy is rapidly increasing in the Western hemisphere and represents in up to 50 % the cause of end stage renal disease. Hence, early intervention is desirable to prevent any damage to the kidneys. In the early stage of diabetic nephropathy, endothelium dysfunction is a key pathogenetic process as indicated by increased leakage of albumin through the glomerular barrier (2).
Hence, improvement of endothelium function is an attractive therapeutic goal of antidiabetic medication. Endothelial dysfunction, in particular basal nitric oxide activity, has been also identified as pivotal determinant of glomerular filtration rate (3). Previously, blockade of the renin angiotensin system have been found to be effective in improving endothelium function (4). Furthermore, we observed that renal endothelium function is improved by cardiovascular risk factor control (e.g. blood pressure) and may be predictive for the development of diabetic nephropathy (5).
A new and promising class of antidiabetic drugs are the gliptins. Gliptins act by inhibiting the enzyme dipeptidyl peptidase-4 (DPP-4), which is responsible for the rapid inactivation of glucagon-like peptide-1 (GLP-1) - an incretin hormone of the gut (6 - 8), thereby enhancing and prolonging the effects of GLP-1. GLP-1 - member of the incretin hormones - is released into the blood after meal ingestion and stimulates the insulin secretion in a glucose dependent manner. This accounts for the marked prandial insulin response, which prevents prandial hyperglycemia. Several efficacy studies demonstrated a significant improvement of HbA1c with gliptins. In addition, gliptins improved fasting as well as prandial glucose levels and did not induce weight gain. Due to these positive metabolic effects in combination with a very small spectrum of side effects gliptins might very well be part of the standard therapy for type 2 diabetes in the future.
Apart from surrogate parameters like reduction of fasting and postprandial blood glucose levels or improvement of HbA1c, the effect of gliptins on micro- and macrovascular function and cardiovascular outcome has not been the primary focus of current studies. However, infusion of GLP-1, the incretin hormone affected by gliptins has been reported to ameliorate endothelial dysfunction in patients suffering from coronary artery disease (9) and it was recently shown that infusion of GLP-1 into healthy human subjects increases both normal and ACh-induced vasodilatation (10). In studies on rats with diabetes, GLP-1 infusion nearly re-established their normal vascular tone (11) and there are further data from experimental animals that indicate a beneficial effect of GLP-1 on endothelial function (12).
Diabetes mellitus is strongly associated with microangiopathy and macroangiopathy and is a strong independent risk factor for cardiovascular disease and cardiovascular mortality (13). Endothelial dysfunction which plays a crucial role in the atherosclerotic process is commonly observed in patients with diabetes mellitus and already prediabetes and has - amongst other factors - been linked to fasting and postprandial hyperglycemia. Gliptins reduce hyperglycemia and hyperglycemic peaks by preventing inactivation of GLP-1, which exerted beneficial effects on the endothelium in previous studies.
It is of major interest whether therapy with gliptins improves endothelial function of the micro- and macrovasculature. In face of the burden that diabetic nephropathy causes, the effect of linagliptin on the renal vasculature and endothelium integrity of the renal circulation (as measured by the availability of nitric oxide), is a key stone in order to claim that linagliptin is an effective antidiabetic agents. There is a need to demonstrate that linagliptin is effective beyond its blood glucose lowering actions and improves vascular endothelium function in the kidney.
- Conditions
- Type 2-diabetes
- Being tested
- Linagliptin, Placebo
- Medical subject headings
- Diabetes Mellitus, Type 2
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
LinagliptinDrug
orally 5 mg/d for 4 weeks
PlaceboDrug
orally once a day for 4 weeks
| Study group | Role | What they receive |
|---|---|---|
| Linagliptin | Active comparator | Linagliptin Receives: Drug: Linagliptin |
| Placebo | Placebo comparator | Placebo Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
effect of linagliptin compared to placebo on basal production and release of nitric oxide (NO) from renal vasculature
The primary objective of the study is the change of renal plasma flow to LNMMA infusion from baseline (given in ml/min) to determine the effect of linagliptin compared to placebo on basal production and release of nitric oxide (NO) from renal vasculature.
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
Secondary outcomes (10)
effects of linagliptin compared to placebo on other renal hemodynamic parameters
Renal plasma flow, glomerular filtration rate and filtration fraction, renal vascular resistance, calculated intraglomerular pressure.
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to placebo on urinary albumin creatinine ratio and tubular markers (e.g. NGAL).
effect of linagliptin compared to placebo on urinary albumin creatinine ratio and tubular markers (e.g. NGAL).
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to placebo on markers of oxidative stress (e.g. isoprostanes) and inflammation (e.g. hsCRP).
effect of linagliptin compared to placebo on markers of oxidative stress (e.g. isoprostanes) and inflammation (e.g. hsCRP).
Measured: Changes from baseline after 4 weeks with linagliptin versus placebo
effect of linagliptin compared to placebo on metabolic parameters (fasting glucose, fasting insulin, triglycerides, total-, LDL- and HDL-cholesterol)
effect of linagliptin compared to placebo on metabolic parameters (fasting glucose, fasting insulin, triglycerides, total-, LDL- and HDL-cholesterol)
Measured: Changes from baseline after 4 weeks of treatment with linaplitpin and placebo
effect of linagliptin compared to baseline on the change of renal plasma flow due to L-NMMA-infusion
effect of linagliptin compared to baseline on the change of renal plasma flow due to L-NMMA-infusion
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effects of linagliptin compared to baseline on other renal hemodynamic parameters
effects of linagliptin compared to baseline on other renal hemodynamic parameters: Renal plasma flow, glomerular filtration rate and filtration fraction, renal vascular resistance, calculated intraglomerular pressure
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
of linagliptin compared to baseline on urinary albumin creatinine ratio and tubular markers (e.g. NGAL)
of linagliptin compared to baseline on urinary albumin creatinine ratio and tubular markers (e.g. NGAL)
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to baseline on markers of oxidative stress (e.g. isoprostanes) and inflammation (e.g. hsCRP).
effect of linagliptin compared to baseline on markers of oxidative stress (e.g. isoprostanes) and inflammation (e.g. hsCRP)
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to baseline on metabolic parameters (fasting glucose, fasting insulin, triglycerides, total-, LDL- and HDL-cholesterol)
effect of linagliptin compared to baseline on metabolic parameters (fasting glucose, fasting insulin, triglycerides, total-, LDL- and HDL-cholesterol)
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
determine the relationship between changes of renal endothelial function with metabolic changes and changes of isoprostanes
determine the relationship between changes of renal endothelial function with metabolic changes and changes of isoprostanes
Measured: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 Apr 2013 (estimated)
- Study startOct 2012
- Primary completionMar 2014
- Study completionApr 2014
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (4)Papers the sponsor has linked to this study.
- Other trials for Type 2-diabetesStudies of the same condition, open and under way.
- More trials run by University of Erlangen-Nürnberg Medical SchoolThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 3
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 65 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Erlangen-Nürnberg Medical School
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Roland E Schmieder, MD, Principal investigator, University of Erlangen-Nürnberg
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01835678
- Sponsor's protocol ID
- CRC2012LINA
- Other IDs
- 2012-002278-30
- Status last verified
- Jan 2018
- First submitted
- 18 Mar 2013
- Last updated
- 12 Jan 2018
- Results posted
- No
- Data monitoring committee
- No
Publications
Ott C, Schneider MP, Delles C, Schlaich MP, Schmieder RE. Reduction in basal nitric oxide activity causes albuminuria. Diabetes. 2011 Feb;60(2):572-6. doi: 10.2337/db09-1630.
PubMed 21270268Schlaich MP, Schmitt D, Ott C, Schmidt BM, Schmieder RE. Basal nitric oxide synthase activity is a major determinant of glomerular haemodynamics in humans. J Hypertens. 2008 Jan;26(1):110-6. doi: 10.1097/HJH.0b013e3282f1a93e.
PubMed 18090547Ritt M, Ott C, Raff U, Schneider MP, Schuster I, Hilgers KF, Schlaich MP, Schmieder RE. Renal vascular endothelial function in hypertensive patients with type 2 diabetes mellitus. Am J Kidney Dis. 2009 Feb;53(2):281-9. doi: 10.1053/j.ajkd.2008.10.041. Epub 2008 Dec 19.
PubMed 19100670Ott C, Kistner I, Keller M, Friedrich S, Willam C, Bramlage P, Schmieder RE. Effects of linagliptin on renal endothelial function in patients with type 2 diabetes: a randomised clinical trial. Diabetologia. 2016 Dec;59(12):2579-2587. doi: 10.1007/s00125-016-4083-4. Epub 2016 Sep 1.
PubMed 27586249
Study at a glance
From the registry record, last updated by the sponsor on 12 Jan 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effects of Linagliptin on Renal Endothelium Function in Patients With Type 2 Diabetes
- ClinicalTrials.gov ID
- NCT01835678
- Acronym / sponsor ID
- CRC2012LINA
- Conditions
- Type 2-diabetes
- Phase
- Phase 3
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 65 participants (actual)
- Lead sponsor
- University of Erlangen-Nürnberg Medical SchoolUniversity, hospital or other
- Study start
- Oct 2012
- Primary completion
- Mar 2014 (actual)
- Study completion
- Apr 2014 (actual)
- First posted
- 19 Apr 2013 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Diabetes mellitus is a metabolic disease with a growing prevalence worldwide, affecting 171 million people in 2000 and an expected 366 million people in 2030 (1) and therefore diabetic nephropathy is rapidly increasing in the Western hemisphere and represents in up to 50 % the cause of end stage renal disease. Hence, early intervention is desirable to prevent any damage to the kidneys. In the early stage of diabetic nephropathy, endothelium dysfunction is a key pathogenetic process as indicated by increased leakage of albumin through the glomerular barrier (2).
Hence, improvement of endothelium function is an attractive therapeutic goal of antidiabetic medication. Endothelial dysfunction, in particular basal nitric oxide activity, has been also identified as pivotal determinant of glomerular filtration rate (3).
A new and promising class of antidiabetic drugs are the gliptins. Gliptins act by inhibiting the enzyme dipeptidyl peptidase-4 (DPP-4), which is responsible for the rapid inactivation of glucagon-like peptide-1 (GLP-1) - an incretin hormone of the gut (6 - 8), thereby enhancing and prolonging the effects of GLP-1. GLP-1 - member of the incretin hormones - is released into the blood after meal ingestion and stimulates the insulin secretion in a glucose dependent manner. This accounts for the marked prandial insulin response, which prevents prandial hyperglycemia.
Apart from surrogate parameters like reduction of fasting and postprandial blood glucose levels or improvement of HbA1c, the effect of gliptins on micro- and macrovascular function and cardiovascular outcome has not been the primary focus of current studies. However, infusion of GLP-1, the incretin hormone affected by gliptins has been reported to ameliorate endothelial dysfunction in patients suffering from coronary artery disease (9) and it was recently shown that infusion of GLP-1 into healthy human subjects increases both normal and ACh-induced vasodilatation (10). In studies on rats with diabetes, GLP-1 infusion nearly re-established their normal vascular tone (11) and there are further data from experimental animals that indicate a beneficial effect of GLP-1 on endothelial function (12).
It is of major interest whether therapy with gliptins improves endothelial function of the micro- and macrovasculature. In face of the burden that diabetic nephropathy causes, the effect of linagliptin on the renal vasculature and endothelium integrity of the renal circulation (as measured by the availability of nitric oxide), is a key stone in order to claim that linagliptin is an effective antidiabetic agents. There is a need to demonstrate that linagliptin is effective beyond its blood glucose lowering actions and improves vascular endothelium function in the kidney.
Detailed description
Diabetes mellitus is a metabolic disease with a growing prevalence worldwide, affecting 171 million people in 2000 and an expected 366 million people in 2030 (1) and therefore diabetic nephropathy is rapidly increasing in the Western hemisphere and represents in up to 50 % the cause of end stage renal disease. Hence, early intervention is desirable to prevent any damage to the kidneys. In the early stage of diabetic nephropathy, endothelium dysfunction is a key pathogenetic process as indicated by increased leakage of albumin through the glomerular barrier (2).
Hence, improvement of endothelium function is an attractive therapeutic goal of antidiabetic medication. Endothelial dysfunction, in particular basal nitric oxide activity, has been also identified as pivotal determinant of glomerular filtration rate (3). Previously, blockade of the renin angiotensin system have been found to be effective in improving endothelium function (4). Furthermore, we observed that renal endothelium function is improved by cardiovascular risk factor control (e.g. blood pressure) and may be predictive for the development of diabetic nephropathy (5).
A new and promising class of antidiabetic drugs are the gliptins. Gliptins act by inhibiting the enzyme dipeptidyl peptidase-4 (DPP-4), which is responsible for the rapid inactivation of glucagon-like peptide-1 (GLP-1) - an incretin hormone of the gut (6 - 8), thereby enhancing and prolonging the effects of GLP-1. GLP-1 - member of the incretin hormones - is released into the blood after meal ingestion and stimulates the insulin secretion in a glucose dependent manner. This accounts for the marked prandial insulin response, which prevents prandial hyperglycemia. Several efficacy studies demonstrated a significant improvement of HbA1c with gliptins. In addition, gliptins improved fasting as well as prandial glucose levels and did not induce weight gain. Due to these positive metabolic effects in combination with a very small spectrum of side effects gliptins might very well be part of the standard therapy for type 2 diabetes in the future.
Apart from surrogate parameters like reduction of fasting and postprandial blood glucose levels or improvement of HbA1c, the effect of gliptins on micro- and macrovascular function and cardiovascular outcome has not been the primary focus of current studies. However, infusion of GLP-1, the incretin hormone affected by gliptins has been reported to ameliorate endothelial dysfunction in patients suffering from coronary artery disease (9) and it was recently shown that infusion of GLP-1 into healthy human subjects increases both normal and ACh-induced vasodilatation (10). In studies on rats with diabetes, GLP-1 infusion nearly re-established their normal vascular tone (11) and there are further data from experimental animals that indicate a beneficial effect of GLP-1 on endothelial function (12).
Diabetes mellitus is strongly associated with microangiopathy and macroangiopathy and is a strong independent risk factor for cardiovascular disease and cardiovascular mortality (13). Endothelial dysfunction which plays a crucial role in the atherosclerotic process is commonly observed in patients with diabetes mellitus and already prediabetes and has - amongst other factors - been linked to fasting and postprandial hyperglycemia. Gliptins reduce hyperglycemia and hyperglycemic peaks by preventing inactivation of GLP-1, which exerted beneficial effects on the endothelium in previous studies.
It is of major interest whether therapy with gliptins improves endothelial function of the micro- and macrovasculature. In face of the burden that diabetic nephropathy causes, the effect of linagliptin on the renal vasculature and endothelium integrity of the renal circulation (as measured by the availability of nitric oxide), is a key stone in order to claim that linagliptin is an effective antidiabetic agents. There is a need to demonstrate that linagliptin is effective beyond its blood glucose lowering actions and improves vascular endothelium function in the kidney.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Linagliptin | Active comparator | Drug: LinagliptinLinagliptin |
| Placebo | Placebo comparator | Drug: PlaceboPlacebo |
Who may qualify
- Ages
- 18 to 70 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (2 listed)
- Female and male patients aged between 18 and 70 years
- Type 2 diabetes without diabetic nephropathy (definition see exclusion criteria)
Key exclusion criteria (22 listed)
- Any other form of diabetes mellitus than type 2 diabetes mellitus
- Use of insulin, glitazone or gliptins within the past 3 months
- Any other oral antidiabetic drug that can not be discontinued for the study period.
- Any history of stroke, transient ischemic attack, instable angina pectoris, or myocardial infarction within the last 6 months prior to study inclusion
- Urinary albumin excretion (UACR) > 100 mg/g (early morning spot urine)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Linagliptinorally 5 mg/d for 4 weeks | Drug | Linagliptin |
| Placeboorally once a day for 4 weeks | Drug | Placebo |
Primary outcome
effect of linagliptin compared to placebo on basal production and release of nitric oxide (NO) from renal vasculature
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
The primary objective of the study is the change of renal plasma flow to LNMMA infusion from baseline (given in ml/min) to determine the effect of linagliptin compared to placebo on basal production and release of nitric oxide (NO) from renal vasculature.
10 secondary outcomes
effects of linagliptin compared to placebo on other renal hemodynamic parameters
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to placebo on urinary albumin creatinine ratio and tubular markers (e.g. NGAL).
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to placebo on markers of oxidative stress (e.g. isoprostanes) and inflammation (e.g. hsCRP).
Time frame: Changes from baseline after 4 weeks with linagliptin versus placebo
effect of linagliptin compared to placebo on metabolic parameters (fasting glucose, fasting insulin, triglycerides, total-, LDL- and HDL-cholesterol)
Time frame: Changes from baseline after 4 weeks of treatment with linaplitpin and placebo
effect of linagliptin compared to baseline on the change of renal plasma flow due to L-NMMA-infusion
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effects of linagliptin compared to baseline on other renal hemodynamic parameters
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
of linagliptin compared to baseline on urinary albumin creatinine ratio and tubular markers (e.g. NGAL)
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to baseline on markers of oxidative stress (e.g. isoprostanes) and inflammation (e.g. hsCRP).
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
effect of linagliptin compared to baseline on metabolic parameters (fasting glucose, fasting insulin, triglycerides, total-, LDL- and HDL-cholesterol)
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
determine the relationship between changes of renal endothelial function with metabolic changes and changes of isoprostanes
Time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Jan 2018.
- Background: PubMed 21270268Ott C, Schneider MP, Delles C, Schlaich MP, Schmieder RE. Reduction in basal nitric oxide activity causes albuminuria. Diabetes. 2011 Feb;60(2):572-6. doi: 10.2337/db09-1630.
- Background: PubMed 18090547Schlaich MP, Schmitt D, Ott C, Schmidt BM, Schmieder RE. Basal nitric oxide synthase activity is a major determinant of glomerular haemodynamics in humans. J Hypertens. 2008 Jan;26(1):110-6. doi: 10.1097/HJH.0b013e3282f1a93e.
- Background: PubMed 19100670Ritt M, Ott C, Raff U, Schneider MP, Schuster I, Hilgers KF, Schlaich MP, Schmieder RE. Renal vascular endothelial function in hypertensive patients with type 2 diabetes mellitus. Am J Kidney Dis. 2009 Feb;53(2):281-9. doi: 10.1053/j.ajkd.2008.10.041. Epub 2008 Dec 19.
- Results publication: PubMed 27586249Ott C, Kistner I, Keller M, Friedrich S, Willam C, Bramlage P, Schmieder RE. Effects of linagliptin on renal endothelial function in patients with type 2 diabetes: a randomised clinical trial. Diabetologia. 2016 Dec;59(12):2579-2587. doi: 10.1007/s00125-016-4083-4. Epub 2016 Sep 1.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Roland E Schmieder, MD principal investigator
University of Erlangen-Nürnberg
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 3 study testing Linagliptin in people with Type 2-diabetes, run by University of Erlangen-Nürnberg Medical School at 2 sites in Germany.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 22 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 12 Jan 2018. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in Germany. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 3 studies compare the treatment with the current standard treatment or a placebo in a large group, to confirm how well it works and watch for side effects.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
effect of linagliptin compared to placebo on basal production and release of nitric oxide (NO) from renal vasculature (time frame: Changes from baseline after 4 weeks of treatment with linagliptin and placebo). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01835678, which also lists 4 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 12 Jan 2018.