Cardio-Renal SyndromeCRiSPSNCT03628443
Cardiorenal Risk Stratification Pilot Study
An observational study of Cardio-Renal Syndrome and Heart Failure, run by Coney Island Hospital, Brooklyn, NY at 1 site in United States.
Trial summary
This is prospective cohort study with the purpose of improving our understanding of morbidity and mortality risk in patients with heart failure and chronic kidney disease. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Cardio-Renal Syndrome, Heart Failure, Chronic Kidney Diseases
- What is being tested?
- Fibroblast Growth Factor 23
- How many people
- 100 participants
- Where
- 1 siteUnited States
- Study dates
- 19 Jul 2018to 31 Dec 2019
- Phase
- Observational
- 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 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Control Arm: People seen in the outpatient setting with congestive heart failure without renal impairment. Study Arm: People seen in the outpatient setting with congestive heart failure that have some form of renal impairment that did not start the study while on hemodialysis.
Who may be able to join
- Patients must have a diagnosis of congestive heart failure
Who cannot join
- Patients cannot be on hemodialysis at the study onset.
- Patients cannot have hyperphosphatemia defined as persistent serum phosphorus level>4.5mg/dL at study onset.
- Patients cannot be part of another study for the investigational treatment of heart failure or chronic kidney disease.
Trial locations and contacts
1 site in 1 country.
United States1 site, 1 recruiting
- Recruiting
Coney Island Hospital
Brooklyn, New York, 11235
Wesley A Romney, MD, 718-616-3779, romneyw@nychhc.org
Karen A Hultberg, 718-616-5627, karen.hultberg@nychhc.org
About this study
Official title: Cardiorenal Risk Stratification Pilot Study (CRiSPS): Using FGF-23 as a Risk Stratification Biomarker in Patients With Heart Failure and Chronic Kidney Disease as a Predictor of 1-year Morbidity and Mortality Risk
This is prospective cohort study with the purpose of improving our understanding of morbidity and mortality risk in patients with heart failure and chronic kidney disease.
Read the detailed description
The CDC reports that approximately 5.7 million adults in the U.S. have heart failure (HF), and NHANES reports that 26% of individuals 60 years-of-age and older have Chronic Kidney Disease. NHANES also reports that End-Stage Kidney Disease (ESKD) accounts for $40 billion in Medicare and Non-Medicare costs in 2009; 37% of those patients had a prior episode of HF. These figures demonstrate that the treatment of patients with HF and ESKD costs Americans almost $15 billion annually. A meta-analysis of 16 studies estimates that 63% of HF patients have some kidney impairment; a serum creatinine (Cr)>1.0mg/dL or Glomerular Filtration Rate (GFR)<90 ml/min. Among HF patients with even mildly decreased GFR, mortality increases significantly; those with none, any, and at least moderate CKD experienced a 24%, 38% and 51% 1-year mortality, respectively. In 2015, 66,713 patients were seen at our hospital. About 3% of those patients had a new diagnosis of CHF and at least 30% of those patients diagnosed with CHF had a dual diagnosis of CKD. This population alone accounted for 79,835 of visits in the same year. It is evident that there are both fiscal and ethical incentives, both locally and nationally, to understand how to mitigate disease progression in this population.
Current classification schemes for patients with HF and chronic kidney disease (CKD), cardiorenal syndrome, do not significantly alter management other than managing HF or CKD independently with respect to their individual severity. In CKD, worsening renal function often leads to poor phosphate (PO4) regulation where hyperphosphatemia is significantly associated as a predictor of mortality. Further characterizations of the factors that contribute to hyperphosphatemia implicates Fibroblast Growth Factor 23 (FGF-23) as a major hormone regulator of PO4 levels in the body. FGF-23 has repeatedly demonstrated its use as an independent predictor of mortality in ESKD as well as an independent predictor of worsening renal function in non-diabetic patients with mild CKD. FGF-23 achieves PO4 level control by downregulating PO4 reabsorption via transporters in kidney's proximal tubules as well as the small intestines through an incompletely understood mechanism. This action allows the increased filtration of PO4 without proximal tubule reabsorption as well as indirectly decreased uptake of dietary PO4. In ESKD, the PO4-lowering effects of FGF-23 diminish despite rising FGF-23 levels; this indicates that pathologic hyperphosphatemia represents a decompensated state of PO4 regulation. There are studies that suggest FGF-23 is not only implicated in the worsening of CKD, but the pleiotropic effects of FGF-23 remain to be understood as a factor in cardiovascular disease. Increased FGF-23 levels have been associated with left ventricular dysfunction and atrial fibrillation as well as worsening CKD. In one study, not a single patient with Group 5 CKD had an FGF-23 level lower than 40.2ρg/dL, and more than 70% of those patients had and FGF-23 level greater than 66.1ρg/dL.14 Despite this information, it is not currently known how FGF-23 may be used as a predictor of mortality or progression of CKD in patients with cardiorenal syndrome prior to end-stage renal disease. Significant results from this study may provide a predictable classification scheme based on FGF-23 levels that may be employed in future studies to guide treatment evaluation. The prospect of treatment to reduce morbidity and mortality is supported by studies demonstrating that PO4 binders lower FGF-23 levels, even in healthy volunteers. The study proposed here is an early step in evaluating options to reduce the number of patients that progress to ESRD with a parallel step towards a reduction in significant healthcare costs. Participants in this study will only be observed after they have granted their informed consent. There are no significant potential risks posed by this study as blood collected would be from routine lab vials for the participant population. If the study has significant findings, there are immediate benefits to the population studied and the greater society.
Participants after this study will be equipped with more knowledge to help them understand their risk factors and help them make better decisions about their own healthcare. The investigators hope to achieve a better understanding of what levels of FGF-23 are significantly associated with morbidity and mortality in patients with CHF and CKD. This information can help us answer how current clinicians may better stratify the risks of CHF and CKD; translating theoretical disease predictions into a preventative medicine model. The answer to this question may lay the foundation for treatment and prevention option studies based on FGF-23 levels in patients that are not currently on hemodialysis.
We hypothesize (1) that in participants with congestive heart failure and chronic kidney disease who are not on hemodialysis, worsening heart disease or worsening kidney disease is associated with a significantly elevated FGF-23 serum level AND (2) participants with congestive heart failure and chronic kidney disease who are not on hemodialysis, decreased survival is associated with a significantly elevated FGF-23 serum level.
- Being tested
- Fibroblast Growth Factor 23
- Keywords
- CKD, HFrEF, HFpEF, FGF23, Dialysis, Atherosclerosis, Coronary Artery Disease
- Medical subject headings
- Cardio-Renal Syndrome, Heart Failure, Renal Insufficiency, Chronic, Atherosclerosis, Coronary Artery Disease
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Fibroblast Growth Factor 23Diagnostic test
A sample of blood is tested for levels of fibroblast growth factor 23
| Study group | Role | What they receive |
|---|---|---|
| Heart Failure without Chronic Kidney Disease | This group has patients managed with all types of heart failure without concomitant chronic kidney disease. Receives: Diagnostic Test: Fibroblast Growth Factor 23 | |
| Heart Failure with Chronic Kidney Disease | This group has patients managed with all types of heart failure with concomitant chronic kidney disease, without evidence of sustained hyperphosphatemia. Receives: Diagnostic Test: Fibroblast Growth Factor 23 |
What is being measured
The primary outcome is the main question the study is designed to answer.
Mortality
The occurrence of death
Measured: 1 year from sample date
Worsening Renal Function
Significant, persistently decreased in estimated glomerular filtration rate
Measured: 1 year from sample date
Worsening Cardiac Function
Decreased ejection fraction, newly documented structural abnormality
Measured: 1 year from sample date
End-Stage Renal Disease Progression
Progression of patient's health condition requiring the initiation of hemodialysis
Measured: 1 year from sample date
Secondary outcomes (8)
Hospitalizations
Number of times the patient was hospitalized
Measured: 1 year from sample date
Increased Medication Use
Number of medication changes during observation period, including for comirbidities
Measured: 1 year from sample date
Worsening Control of Co-Morbidities
Progression of other co-morbid conditions including, diabetes, dyslipidemia, and hypertension.
Measured: 1 year from sample date
Urgent visits
Number of times the patient visited the emergency department, urgent care, or walked into clinic.
Measured: 1 year from sample date
Myocardial Infarction
Myocardial infarction diagnosed during the trial period
Measured: 1 year from sample date
Coronary Artery Disease
Coronary artery disease diagnosed during the trial period
Measured: 1 year from sample date
Stroke
Stroke diagnosed during the trial period
Measured: 1 year from sample date
Arrhythmia
Arrhythmia diagnosed during the trial period
Measured: 1 year from sample date
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted14 Aug 2018
- Study start19 Jul 2018
- Primary completion31 Oct 2019 (estimated)
- Study completion31 Dec 2019 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for Cardio-Renal SyndromeStudies of the same condition, open and under way.
- 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 100 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Coney Island Hospital, Brooklyn, NY
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, George Juang, Coney Island Hospital, Brooklyn, NY
- Investigators
- George Juang, MD, Principal investigator, Coney Island Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03628443
- Sponsor's protocol ID
- 18-08-172-378(HHC)
- Acronym
- CRiSPS
- Status last verified
- Oct 2018
- First submitted
- 9 Aug 2018
- Last updated
- 16 Oct 2018
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Writing Group Members; Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, Das SR, de Ferranti S, Despres JP, Fullerton HJ, Howard VJ, Huffman MD, Isasi CR, Jimenez MC, Judd SE, Kissela BM, Lichtman JH, Lisabeth LD, Liu S, Mackey RH, Magid DJ, McGuire DK, Mohler ER 3rd, Moy CS, Muntner P, Mussolino ME, Nasir K, Neumar RW, Nichol G, Palaniappan L, Pandey DK, Reeves MJ, Rodriguez CJ, Rosamond W, Sorlie PD, Stein J, Towfighi A, Turan TN, Virani SS, Woo D, Yeh RW, Turner MB; American Heart Association Statistics Committee; Stroke Statistics Subcommittee. Executive Summary: Heart Disease and Stroke Statistics--2016 Update: A Report From the American Heart Association. Circulation. 2016 Jan 26;133(4):447-54. doi: 10.1161/CIR.0000000000000366. No abstract available.
PubMed 26811276Smith GL, Lichtman JH, Bracken MB, Shlipak MG, Phillips CO, DiCapua P, Krumholz HM. Renal impairment and outcomes in heart failure: systematic review and meta-analysis. J Am Coll Cardiol. 2006 May 16;47(10):1987-96. doi: 10.1016/j.jacc.2005.11.084. Epub 2006 Apr 24.
PubMed 16697315Prie D, Friedlander G. Genetic disorders of renal phosphate transport. N Engl J Med. 2010 Jun 24;362(25):2399-409. doi: 10.1056/NEJMra0904186. No abstract available.
PubMed 20573928Prie D, Urena Torres P, Friedlander G. Latest findings in phosphate homeostasis. Kidney Int. 2009 May;75(9):882-9. doi: 10.1038/ki.2008.643. Epub 2009 Feb 4.
PubMed 19190675Ferrari SL, Bonjour JP, Rizzoli R. Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. J Clin Endocrinol Metab. 2005 Mar;90(3):1519-24. doi: 10.1210/jc.2004-1039. Epub 2004 Dec 21.
PubMed 15613425Bogadel'nikov IV. [State of the kallikrein-kinin system in bacterial poisoning]. Zh Mikrobiol Epidemiol Immunobiol. 1978 Nov;(11):20-5. No abstract available. Russian.
PubMed 364890Gutierrez OM, Mannstadt M, Isakova T, Rauh-Hain JA, Tamez H, Shah A, Smith K, Lee H, Thadhani R, Juppner H, Wolf M. Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N Engl J Med. 2008 Aug 7;359(6):584-92. doi: 10.1056/NEJMoa0706130.
PubMed 18687639Fliser D, Kollerits B, Neyer U, Ankerst DP, Lhotta K, Lingenhel A, Ritz E, Kronenberg F; MMKD Study Group; Kuen E, Konig P, Kraatz G, Mann JF, Muller GA, Kohler H, Riegler P. Fibroblast growth factor 23 (FGF23) predicts progression of chronic kidney disease: the Mild to Moderate Kidney Disease (MMKD) Study. J Am Soc Nephrol. 2007 Sep;18(9):2600-8. doi: 10.1681/ASN.2006080936. Epub 2007 Jul 26.
PubMed 17656479Ikee R, Tsunoda M, Sasaki N, Sato N, Hashimoto N. Emerging effects of sevelamer in chronic kidney disease. Kidney Blood Press Res. 2013;37(1):24-32. doi: 10.1159/000343397. Epub 2013 Mar 6.
PubMed 23486088Liu S, Quarles LD. How fibroblast growth factor 23 works. J Am Soc Nephrol. 2007 Jun;18(6):1637-47. doi: 10.1681/ASN.2007010068. Epub 2007 May 9.
PubMed 17494882Larsson T, Nisbeth U, Ljunggren O, Juppner H, Jonsson KB. Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Kidney Int. 2003 Dec;64(6):2272-9. doi: 10.1046/j.1523-1755.2003.00328.x.
PubMed 14633152Seiler S, Cremers B, Rebling NM, Hornof F, Jeken J, Kersting S, Steimle C, Ege P, Fehrenz M, Rogacev KS, Scheller B, Bohm M, Fliser D, Heine GH. The phosphatonin fibroblast growth factor 23 links calcium-phosphate metabolism with left-ventricular dysfunction and atrial fibrillation. Eur Heart J. 2011 Nov;32(21):2688-96. doi: 10.1093/eurheartj/ehr215. Epub 2011 Jul 6.
PubMed 21733911Tanaka S, Fujita S, Kizawa S, Morita H, Ishizaka N. Association between FGF23, alpha-Klotho, and Cardiac Abnormalities among Patients with Various Chronic Kidney Disease Stages. PLoS One. 2016 Jul 11;11(7):e0156860. doi: 10.1371/journal.pone.0156860. eCollection 2016.
PubMed 27400031
Study at a glance
From the registry record, last updated by the sponsor on 16 Oct 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Cardiorenal Risk Stratification Pilot Study (CRiSPS): Using FGF-23 as a Risk Stratification Biomarker in Patients With Heart Failure and Chronic Kidney Disease as a Predictor of 1-year Morbidity and Mortality Risk
- ClinicalTrials.gov ID
- NCT03628443
- Acronym / sponsor ID
- CRiSPS / 18-08-172-378(HHC)
- Keywords
- CKD, HFrEF, HFpEF, FGF23, Dialysis, Atherosclerosis, Coronary Artery Disease
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 100 participants (estimated)
- Lead sponsor
- Coney Island Hospital, Brooklyn, NYUniversity, hospital or other
- Study start
- 19 Jul 2018 (actual)
- Primary completion
- 31 Oct 2019 (estimated)
- Study completion
- 31 Dec 2019 (estimated)
- First posted
- 14 Aug 2018 (actual)
- 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.
This is prospective cohort study with the purpose of improving our understanding of morbidity and mortality risk in patients with heart failure and chronic kidney disease.
Detailed description
The CDC reports that approximately 5.7 million adults in the U.S. have heart failure (HF), and NHANES reports that 26% of individuals 60 years-of-age and older have Chronic Kidney Disease. NHANES also reports that End-Stage Kidney Disease (ESKD) accounts for $40 billion in Medicare and Non-Medicare costs in 2009; 37% of those patients had a prior episode of HF. These figures demonstrate that the treatment of patients with HF and ESKD costs Americans almost $15 billion annually. A meta-analysis of 16 studies estimates that 63% of HF patients have some kidney impairment; a serum creatinine (Cr)>1.0mg/dL or Glomerular Filtration Rate (GFR)<90 ml/min. Among HF patients with even mildly decreased GFR, mortality increases significantly; those with none, any, and at least moderate CKD experienced a 24%, 38% and 51% 1-year mortality, respectively. In 2015, 66,713 patients were seen at our hospital. About 3% of those patients had a new diagnosis of CHF and at least 30% of those patients diagnosed with CHF had a dual diagnosis of CKD. This population alone accounted for 79,835 of visits in the same year. It is evident that there are both fiscal and ethical incentives, both locally and nationally, to understand how to mitigate disease progression in this population.
Current classification schemes for patients with HF and chronic kidney disease (CKD), cardiorenal syndrome, do not significantly alter management other than managing HF or CKD independently with respect to their individual severity. In CKD, worsening renal function often leads to poor phosphate (PO4) regulation where hyperphosphatemia is significantly associated as a predictor of mortality. Further characterizations of the factors that contribute to hyperphosphatemia implicates Fibroblast Growth Factor 23 (FGF-23) as a major hormone regulator of PO4 levels in the body. FGF-23 has repeatedly demonstrated its use as an independent predictor of mortality in ESKD as well as an independent predictor of worsening renal function in non-diabetic patients with mild CKD. FGF-23 achieves PO4 level control by downregulating PO4 reabsorption via transporters in kidney's proximal tubules as well as the small intestines through an incompletely understood mechanism. This action allows the increased filtration of PO4 without proximal tubule reabsorption as well as indirectly decreased uptake of dietary PO4. In ESKD, the PO4-lowering effects of FGF-23 diminish despite rising FGF-23 levels; this indicates that pathologic hyperphosphatemia represents a decompensated state of PO4 regulation. There are studies that suggest FGF-23 is not only implicated in the worsening of CKD, but the pleiotropic effects of FGF-23 remain to be understood as a factor in cardiovascular disease. Increased FGF-23 levels have been associated with left ventricular dysfunction and atrial fibrillation as well as worsening CKD. In one study, not a single patient with Group 5 CKD had an FGF-23 level lower than 40.2ρg/dL, and more than 70% of those patients had and FGF-23 level greater than 66.1ρg/dL.14 Despite this information, it is not currently known how FGF-23 may be used as a predictor of mortality or progression of CKD in patients with cardiorenal syndrome prior to end-stage renal disease. Significant results from this study may provide a predictable classification scheme based on FGF-23 levels that may be employed in future studies to guide treatment evaluation. The prospect of treatment to reduce morbidity and mortality is supported by studies demonstrating that PO4 binders lower FGF-23 levels, even in healthy volunteers. The study proposed here is an early step in evaluating options to reduce the number of patients that progress to ESRD with a parallel step towards a reduction in significant healthcare costs. Participants in this study will only be observed after they have granted their informed consent. There are no significant potential risks posed by this study as blood collected would be from routine lab vials for the participant population. If the study has significant findings, there are immediate benefits to the population studied and the greater society.
Participants after this study will be equipped with more knowledge to help them understand their risk factors and help them make better decisions about their own healthcare. The investigators hope to achieve a better understanding of what levels of FGF-23 are significantly associated with morbidity and mortality in patients with CHF and CKD. This information can help us answer how current clinicians may better stratify the risks of CHF and CKD; translating theoretical disease predictions into a preventative medicine model. The answer to this question may lay the foundation for treatment and prevention option studies based on FGF-23 levels in patients that are not currently on hemodialysis.
We hypothesize (1) that in participants with congestive heart failure and chronic kidney disease who are not on hemodialysis, worsening heart disease or worsening kidney disease is associated with a significantly elevated FGF-23 serum level AND (2) participants with congestive heart failure and chronic kidney disease who are not on hemodialysis, decreased survival is associated with a significantly elevated FGF-23 serum level.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Heart Failure without Chronic Kidney Disease | – | Diagnostic Test: Fibroblast Growth Factor 23This group has patients managed with all types of heart failure without concomitant chronic kidney disease. |
| Heart Failure with Chronic Kidney Disease | – | Diagnostic Test: Fibroblast Growth Factor 23This group has patients managed with all types of heart failure with concomitant chronic kidney disease, without evidence of sustained hyperphosphatemia. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Control Arm: People seen in the outpatient setting with congestive heart failure without renal impairment. Study Arm: People seen in the outpatient setting with congestive heart failure that have some form of renal impairment that did not start the study while on hemodialysis.
Key inclusion criteria (1 listed)
- Patients must have a diagnosis of congestive heart failure
Key exclusion criteria (3 listed)
- Patients cannot be on hemodialysis at the study onset.
- Patients cannot have hyperphosphatemia defined as persistent serum phosphorus level>4.5mg/dL at study onset.
- Patients cannot be part of another study for the investigational treatment of heart failure or chronic kidney disease.
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 |
|---|---|---|
| Fibroblast Growth Factor 23A sample of blood is tested for levels of fibroblast growth factor 23 | Diagnostic test | Heart Failure with Chronic Kidney Disease, Heart Failure without Chronic Kidney Disease |
Primary outcome
Mortality
Time frame: 1 year from sample date
The occurrence of death
Worsening Renal Function
Time frame: 1 year from sample date
Significant, persistently decreased in estimated glomerular filtration rate
Worsening Cardiac Function
Time frame: 1 year from sample date
Decreased ejection fraction, newly documented structural abnormality
End-Stage Renal Disease Progression
Time frame: 1 year from sample date
Progression of patient's health condition requiring the initiation of hemodialysis
8 secondary outcomes
Hospitalizations
Time frame: 1 year from sample date
Increased Medication Use
Time frame: 1 year from sample date
Worsening Control of Co-Morbidities
Time frame: 1 year from sample date
Urgent visits
Time frame: 1 year from sample date
Myocardial Infarction
Time frame: 1 year from sample date
Coronary Artery Disease
Time frame: 1 year from sample date
Stroke
Time frame: 1 year from sample date
Arrhythmia
Time frame: 1 year from sample date
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 16 Oct 2018.
- Background: PubMed 26811276Writing Group Members; Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, Das SR, de Ferranti S, Despres JP, Fullerton HJ, Howard VJ, Huffman MD, Isasi CR, Jimenez MC, Judd SE, Kissela BM, Lichtman JH, Lisabeth LD, Liu S, Mackey RH, Magid DJ, McGuire DK, Mohler ER 3rd, Moy CS, Muntner P, Mussolino ME, Nasir K, Neumar RW, Nichol G, Palaniappan L, Pandey DK, Reeves MJ, Rodriguez CJ, Rosamond W, Sorlie PD, Stein J, Towfighi A, Turan TN, Virani SS, Woo D, Yeh RW, Turner MB; American Heart Association Statistics Committee; Stroke Statistics Subcommittee. Executive Summary: Heart Disease and Stroke Statistics--2016 Update: A Report From the American Heart Association. Circulation. 2016 Jan 26;133(4):447-54. doi: 10.1161/CIR.0000000000000366. No abstract available.
- Background: PubMed 16697315Smith GL, Lichtman JH, Bracken MB, Shlipak MG, Phillips CO, DiCapua P, Krumholz HM. Renal impairment and outcomes in heart failure: systematic review and meta-analysis. J Am Coll Cardiol. 2006 May 16;47(10):1987-96. doi: 10.1016/j.jacc.2005.11.084. Epub 2006 Apr 24.
- Background: PubMed 20573928Prie D, Friedlander G. Genetic disorders of renal phosphate transport. N Engl J Med. 2010 Jun 24;362(25):2399-409. doi: 10.1056/NEJMra0904186. No abstract available.
- Background: PubMed 19190675Prie D, Urena Torres P, Friedlander G. Latest findings in phosphate homeostasis. Kidney Int. 2009 May;75(9):882-9. doi: 10.1038/ki.2008.643. Epub 2009 Feb 4.
- Background: PubMed 15613425Ferrari SL, Bonjour JP, Rizzoli R. Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. J Clin Endocrinol Metab. 2005 Mar;90(3):1519-24. doi: 10.1210/jc.2004-1039. Epub 2004 Dec 21.
- Background: PubMed 364890Bogadel'nikov IV. [State of the kallikrein-kinin system in bacterial poisoning]. Zh Mikrobiol Epidemiol Immunobiol. 1978 Nov;(11):20-5. No abstract available. Russian.
- Background: PubMed 18687639Gutierrez OM, Mannstadt M, Isakova T, Rauh-Hain JA, Tamez H, Shah A, Smith K, Lee H, Thadhani R, Juppner H, Wolf M. Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N Engl J Med. 2008 Aug 7;359(6):584-92. doi: 10.1056/NEJMoa0706130.
- Background: PubMed 17656479Fliser D, Kollerits B, Neyer U, Ankerst DP, Lhotta K, Lingenhel A, Ritz E, Kronenberg F; MMKD Study Group; Kuen E, Konig P, Kraatz G, Mann JF, Muller GA, Kohler H, Riegler P. Fibroblast growth factor 23 (FGF23) predicts progression of chronic kidney disease: the Mild to Moderate Kidney Disease (MMKD) Study. J Am Soc Nephrol. 2007 Sep;18(9):2600-8. doi: 10.1681/ASN.2006080936. Epub 2007 Jul 26.
- Background: PubMed 23486088Ikee R, Tsunoda M, Sasaki N, Sato N, Hashimoto N. Emerging effects of sevelamer in chronic kidney disease. Kidney Blood Press Res. 2013;37(1):24-32. doi: 10.1159/000343397. Epub 2013 Mar 6.
- Background: PubMed 17494882Liu S, Quarles LD. How fibroblast growth factor 23 works. J Am Soc Nephrol. 2007 Jun;18(6):1637-47. doi: 10.1681/ASN.2007010068. Epub 2007 May 9.
- Background: PubMed 14633152Larsson T, Nisbeth U, Ljunggren O, Juppner H, Jonsson KB. Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Kidney Int. 2003 Dec;64(6):2272-9. doi: 10.1046/j.1523-1755.2003.00328.x.
- Background: PubMed 21733911Seiler S, Cremers B, Rebling NM, Hornof F, Jeken J, Kersting S, Steimle C, Ege P, Fehrenz M, Rogacev KS, Scheller B, Bohm M, Fliser D, Heine GH. The phosphatonin fibroblast growth factor 23 links calcium-phosphate metabolism with left-ventricular dysfunction and atrial fibrillation. Eur Heart J. 2011 Nov;32(21):2688-96. doi: 10.1093/eurheartj/ehr215. Epub 2011 Jul 6.
- Kidney Disease Statistics for the United StatesLink provided by the sponsor.
- Individual participant dataSharing planned: No
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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.
George Juang, MD principal investigator
Coney Island Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Cardio-Renal Syndrome and Heart Failure, run by Coney Island Hospital, Brooklyn, NY at 1 site in United States.
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 1 inclusion and 3 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: status not confirmed, as of the sponsor's last update on 16 Oct 2018. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. 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. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Wesley A Romney, MD (718-616-3779, romneyw@nychhc.org), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Mortality (time frame: 1 year from sample date). The study lists 4 primary outcomes in all. 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 NCT03628443, which also lists 13 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 16 Oct 2018.