Sequential Cystatin C Levels and Renal Impairment in Acute Heart Failure
| Status: | Completed |
|---|---|
| Conditions: | Renal Impairment / Chronic Kidney Disease, Cardiology |
| Therapuetic Areas: | Cardiology / Vascular Diseases, Nephrology / Urology |
| Healthy: | No |
| Age Range: | 18 - Any |
| Updated: | 4/2/2016 |
| Start Date: | November 2007 |
| End Date: | March 2013 |
| Contact: | Wilson W.H. Tang, MD |
| Email: | Tangw@ccf.org |
| Phone: | 216-444-2121 |
Renal Compromise after treatment of decompensated heart failure with diuretics is not
uncommon. The purpose of our study is to investigate the relationship between cystatin C and
worsening renal function in this setting. Cystatin C is a biomarker produced at a constant
rate by all cells that is a sensitive biomarker of renal function.Cystatin C and Plasma
amino terminal proB-type natriuretic peptide (NT-proBNP) levels will be obtained at baseline
and daily. Our goal is to enroll 100 subjects with an estimated 5 samples per each subject.
The time course of changes in cystatin C in relation to serum creatinine levels over time
will be plotted.
Our hypothesis is that sequential changes in cystatin C levels following initial treatment
with diuretic therapy in the setting of acute decompensated heart failure may provide early
insight into cardio-renal compromise. Understanding the natural history and time course of
the changes in sequential cystatin C levels may facilitate further studies to guide the
judicious use of diuretic therapy in acute decompensated heart failure, and to predict the
risk of subsequent development of worsening renal function. If serial testing of cystatin C
can provide accurate assessment and prediction of worsening renal function, clinical
applications of these observations can be evaluated in future prospective studies.
uncommon. The purpose of our study is to investigate the relationship between cystatin C and
worsening renal function in this setting. Cystatin C is a biomarker produced at a constant
rate by all cells that is a sensitive biomarker of renal function.Cystatin C and Plasma
amino terminal proB-type natriuretic peptide (NT-proBNP) levels will be obtained at baseline
and daily. Our goal is to enroll 100 subjects with an estimated 5 samples per each subject.
The time course of changes in cystatin C in relation to serum creatinine levels over time
will be plotted.
Our hypothesis is that sequential changes in cystatin C levels following initial treatment
with diuretic therapy in the setting of acute decompensated heart failure may provide early
insight into cardio-renal compromise. Understanding the natural history and time course of
the changes in sequential cystatin C levels may facilitate further studies to guide the
judicious use of diuretic therapy in acute decompensated heart failure, and to predict the
risk of subsequent development of worsening renal function. If serial testing of cystatin C
can provide accurate assessment and prediction of worsening renal function, clinical
applications of these observations can be evaluated in future prospective studies.
Inclusion Criteria:
- Hospital admission within 48 hours for ADHF, with an expected stay over 24 hours.
- Evidence of fluid overload, including jugular venous distention, pulmonary rales,
peripheral edema, and/or ascites receiving diuretic therapy
Exclusion Criteria:
- Heart failure due to congenital heart disease or critical aortic stenosis
(potentially different cardio-renal pathophysiology)
- Acute myocardial infarction or unstable acute coronary syndromes
- End-stage renal insufficiency on renal replacement therapy (already has underlying
advanced renal failure).
- Patients with active cancer (cystatin C has been shown to be produced by some tumors)
- Known exposure to nephrotoxic agents (such as contrast dye) or planned surgery during
hospitalization at the time of enrollment
- Hemoglobin < 9 mg/dL or clinically significant active bleeding.
- Unable to comply with protocol or unable to have informed consent
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