Background and objectives: Acute kidney injury (AKI) is a frequent complication of cardiopulmonary bypass (CPB). Serum creatinine (SCr), the current standard, is an inadequate marker for AKI since a delay occurs before SCr rises. Biomarkers that are sensitive and rapidly measurable could allow early intervention and improve patient outcomes. We investigated the value of serum cystatin C as an early biomarker for AKI after pediatric CPB.
Design, setting, participants, & measurements: We analyzed data from 374 prospectively enrolled children undergoing CPB. Serum samples were obtained before and at 2, 12, and 24 hours after CPB. Cystatin C was quantified by nephelometry. The primary outcome was AKI, defined as a 50% increase in SCr. Secondary outcomes included severity and duration of AKI, hospital length of stay, and mortality. A multivariable stepwise logistic regression analysis was used to assess predictors of AKI.
Results: One hundred nineteen patients (32%) developed AKI using SCr criteria. Serum cystatin C concentrations were significantly increased in AKI patients at 12 hours after CPB (P < 0.0001) and remained elevated at 24 hours (P < 0.0001). Maximal sensitivity and specificity for prediction of AKI occurred at a 12-hour cystatin C cut-off of 1.16 mg/L. The 12-hour cystatin C strongly correlated with severity and duration of AKI as well as length of hospital stay. In multivariable analysis, 12-hour cystatin C remained a powerful independent predictor of AKI.
Conclusion: Serum cystatin C is an early predictive biomarker for AKI and its clinical outcomes after pediatric CPB
Catherine D. Krawczeski*, Rene G. Vandevoorde, Thelma Kathman, Michael R. Bennett, Jessica G. Woo, Yu Wang, Rachel E. Griffiths*, and Prasad Devarajan
* The Heart Institute and the Divisions of Nephrology and Hypertension and Biostatistics and Epidemiology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio
Showing posts with label cystatin C. Show all posts
Showing posts with label cystatin C. Show all posts
Wednesday
Kidney Function Decline Increases Risk Of Heart Failure And Premature Death
ScienceDaily (Nov. 9, 2009) — cystatin C Research: Declining kidney function is linked to a higher risk of heart failure, heart attack, peripheral arterial disease, and early death in individuals with or without kidney disease, according to a pair of studies appearing in an upcoming issue of the Journal of the American Society Nephrology (JASN).
The findings indicate that poor kidney function may raise an individual's risk for cardiovascular complications. To evaluate heart health, clinicians should factor in not only their patients' current level of kidney function, but also changes in kidney function over time.
Chronic kidney disease (CKD) patients have an increased risk of developing and dying from cardiovascular disease, but the links between kidney function and heart health are not well understood. Michael Shlipak, MD (San Francisco VA Medical Center and University of California, San Francisco), Mark Sarnak, MD (Tufts-New England Medical Center), and their colleagues studied clinical information from individuals who were enrolled in the Cardiovascular Health Study, a community-based study of elderly people.
Using a new blood test of kidney function, called cystatin C , the researchers looked for links between changes in kidney function during a period of seven years with the incidence of heart failure, heart attack, stroke, and peripheral arterial disease (obstruction of large arteries in the arms and legs) during the subsequent eight years. Among 4,378 eligible participants in the study, those with rapid kidney decline (1,083 patients) demonstrated a 32% increased risk of experiencing heart failure, a 48% increased risk of having a heart attack, and a 67% increased risk of developing peripheral arterial disease. (They did not have an increased risk of suffering a stroke.)
Importantly, researchers identified an association between rapid kidney function decline and heart complications in patients with and without CKD. Treatments that slow the decline of kidney function and stabilize it in the normal range, before kidney disease develops, could have substantial health benefits.
In the second study, Kunihiro Matsushita, MD, PhD, Josef Coresh, MD, PhD (Johns Hopkins University), and their colleagues examined the effects of changes in kidney function in 13,029 participants of the Atherosclerosis Risk in Communities (ARIC) Study, a population-based sample of individuals aged 45 to 64 years. The researchers followed patients from 1987 to 2006, and monitored participants' kidney function at the start of the study, three years into the study, and nine years into the study. Investigators found that a large drop in kidney function over time -- regardless of the initial level of function -- increased one's risk of developing heart disease and of dying early. Patients whose kidney function dropped by more than 5.6% per year demonstrated a 30% increased risk of developing heart disease and a 22% increased risk of dying prematurely compared to patients with stable kidney function.
Physicians regularly monitor kidney function in elderly patients and patients with diabetes and hypertension to optimize the dose of prescription drugs excreted by the kidneys. This study indicates that physicians who detect a decline in patients' kidney function over time should view this as a sign of increased risk of heart disease and premature death.
"Our results suggest there may be clinical value in sequential kidney function data, often measured in routine care, even among individuals with mildly reduced kidney function," the authors wrote.
Dr. Shlipak's and Dr. Sarnak's co-authors include Ronit Katz, DPhil, Bryan Kestenbaum, MD, David Siscovick, MD (University of Washington); Linda Fried, MD (VA Pittsburgh Healthcare System); Anne Newman, MD (University of Pittsburgh); and Dena Rifkin, MD (Tufts-New England Medical Center). Dr. Matsushita's and Dr. Coresh's co-authors include Elizabeth Selvin, PhD, Lori Bash, PhD, Brad Astor, PhD (Johns Hopkins University), and Nora Franceschini, MD (University of North Carolina).
The findings indicate that poor kidney function may raise an individual's risk for cardiovascular complications. To evaluate heart health, clinicians should factor in not only their patients' current level of kidney function, but also changes in kidney function over time.
Chronic kidney disease (CKD) patients have an increased risk of developing and dying from cardiovascular disease, but the links between kidney function and heart health are not well understood. Michael Shlipak, MD (San Francisco VA Medical Center and University of California, San Francisco), Mark Sarnak, MD (Tufts-New England Medical Center), and their colleagues studied clinical information from individuals who were enrolled in the Cardiovascular Health Study, a community-based study of elderly people.
Using a new blood test of kidney function, called cystatin C , the researchers looked for links between changes in kidney function during a period of seven years with the incidence of heart failure, heart attack, stroke, and peripheral arterial disease (obstruction of large arteries in the arms and legs) during the subsequent eight years. Among 4,378 eligible participants in the study, those with rapid kidney decline (1,083 patients) demonstrated a 32% increased risk of experiencing heart failure, a 48% increased risk of having a heart attack, and a 67% increased risk of developing peripheral arterial disease. (They did not have an increased risk of suffering a stroke.)
Importantly, researchers identified an association between rapid kidney function decline and heart complications in patients with and without CKD. Treatments that slow the decline of kidney function and stabilize it in the normal range, before kidney disease develops, could have substantial health benefits.
In the second study, Kunihiro Matsushita, MD, PhD, Josef Coresh, MD, PhD (Johns Hopkins University), and their colleagues examined the effects of changes in kidney function in 13,029 participants of the Atherosclerosis Risk in Communities (ARIC) Study, a population-based sample of individuals aged 45 to 64 years. The researchers followed patients from 1987 to 2006, and monitored participants' kidney function at the start of the study, three years into the study, and nine years into the study. Investigators found that a large drop in kidney function over time -- regardless of the initial level of function -- increased one's risk of developing heart disease and of dying early. Patients whose kidney function dropped by more than 5.6% per year demonstrated a 30% increased risk of developing heart disease and a 22% increased risk of dying prematurely compared to patients with stable kidney function.
Physicians regularly monitor kidney function in elderly patients and patients with diabetes and hypertension to optimize the dose of prescription drugs excreted by the kidneys. This study indicates that physicians who detect a decline in patients' kidney function over time should view this as a sign of increased risk of heart disease and premature death.
"Our results suggest there may be clinical value in sequential kidney function data, often measured in routine care, even among individuals with mildly reduced kidney function," the authors wrote.
Dr. Shlipak's and Dr. Sarnak's co-authors include Ronit Katz, DPhil, Bryan Kestenbaum, MD, David Siscovick, MD (University of Washington); Linda Fried, MD (VA Pittsburgh Healthcare System); Anne Newman, MD (University of Pittsburgh); and Dena Rifkin, MD (Tufts-New England Medical Center). Dr. Matsushita's and Dr. Coresh's co-authors include Elizabeth Selvin, PhD, Lori Bash, PhD, Brad Astor, PhD (Johns Hopkins University), and Nora Franceschini, MD (University of North Carolina).
Thursday
cystatin C and CRP:Change of glomerular filtration rate in healthy adults with aging
AIM: In order to determine the relationship between glomerular filtration rate (GFR) and age, the associated factors, and the accurate method of GFR in healthy adults, we conducted a cross-sectional study in community-dwelling adults in Beijing.
METHODS: Renal function of 201 clinically healthy subjects was determined using technetium-99 m-labelled diethylene triamine pentacetic acid ((99m)Tc-DTPA). Estimated GFR was calculated with the Cockcroft-Gault (CG) equation, abbreviated Modification of Diet in Renal Disease (MDRD) equation, and plasma clearance of creatinine (Ccr). Serum cystatin C, biomarkers of inflammatory and endothelial cells were analyzed as well. Protein intake, carotid artery intima-media thickness and plaque formation were assayed as well.
RESULTS: Glomerular filtration rate was negatively associated with age and the correlation coefficient for (99m)Tc-GFR, CG-GFR, MDRD-GFR, Ccr were -0.643, -0.736, -0.55 and -0.619, respectively (P < 0.001), while the correlation coefficient between cystatin C and age was 0.681 (P < 0.001). Estimated GFR were associated with measured GFR, and the correlation coefficient for Ccr, CG-GFR and MDRD-GFR were 0.813, 0.582 and 0.418, respectively (P < 0.001). The area under the receiver-operator curve of Ccr was larger, CG was smaller while MDRD was the smallest, and the difference was significant (P < 0.001). So a predicted equation was presented by cystatin C and C-reactive protein for the elderly.
CONCLUSION: In the clinically healthy adults, GFR declined with age. MDRD and CG equation are not suitable to estimate GFR in healthy adults. The predicted equation established by cystatin C and C-reactive protein may be more accurate.
Sun X, Chen Y, Chen X, Wang J, Xi C, Lin S, Liu X.
Institute of Nephrology of PLA, General Hospital of PLA, Beijing, China
METHODS: Renal function of 201 clinically healthy subjects was determined using technetium-99 m-labelled diethylene triamine pentacetic acid ((99m)Tc-DTPA). Estimated GFR was calculated with the Cockcroft-Gault (CG) equation, abbreviated Modification of Diet in Renal Disease (MDRD) equation, and plasma clearance of creatinine (Ccr). Serum cystatin C, biomarkers of inflammatory and endothelial cells were analyzed as well. Protein intake, carotid artery intima-media thickness and plaque formation were assayed as well.
RESULTS: Glomerular filtration rate was negatively associated with age and the correlation coefficient for (99m)Tc-GFR, CG-GFR, MDRD-GFR, Ccr were -0.643, -0.736, -0.55 and -0.619, respectively (P < 0.001), while the correlation coefficient between cystatin C and age was 0.681 (P < 0.001). Estimated GFR were associated with measured GFR, and the correlation coefficient for Ccr, CG-GFR and MDRD-GFR were 0.813, 0.582 and 0.418, respectively (P < 0.001). The area under the receiver-operator curve of Ccr was larger, CG was smaller while MDRD was the smallest, and the difference was significant (P < 0.001). So a predicted equation was presented by cystatin C and C-reactive protein for the elderly.
CONCLUSION: In the clinically healthy adults, GFR declined with age. MDRD and CG equation are not suitable to estimate GFR in healthy adults. The predicted equation established by cystatin C and C-reactive protein may be more accurate.
Sun X, Chen Y, Chen X, Wang J, Xi C, Lin S, Liu X.
Institute of Nephrology of PLA, General Hospital of PLA, Beijing, China
Wednesday
Cystatin C in cerebrospinal fluid as a biomarker of ALS.
Department of Neurology, Graduate School of Medicine, Hokkaido University, Sapporo City, Hokkaido, Japan. tujitti@jb3.so-net.ne.jp
Amyotrophic lateral sclerosis (ALS) is diagnosed on the basis of progressive symptoms in both the upper and lower motor neurons. Because there are no specific biomarkers for ALS, it is difficult to diagnose this disease in its early stages. Cerebrospinal fluid (CSF) samples were obtained from 14 patients in the early stages of ALS, from 13 with polyneuropathy, and from 16 with other neurological disorders. The concentration of cystatin C in the CSF was measured using a sandwich enzyme-linked immunosorbent assay (ELISA) kit. The concentration of cystatin C in the CSF was significantly lower in ALS patients than in the control subjects who were patients with polyneuropathy or other neurological diseases (patients with ALS, polyneuropathy, and other diseases exhibited 5.5 +/- 0.3, 6.7 +/- 0.4, and 6.9 +/- 0.3 mg/L cystatin C, respectively; ALS patients vs. control subjects: p = 0.014 and ALS patients vs. polyneuropathy patients: p = 0.024). Cystatin C may be a useful biomarker of ALS and can be used to distinguish between ALS and polyneuropathy.
Amyotrophic lateral sclerosis (ALS) is diagnosed on the basis of progressive symptoms in both the upper and lower motor neurons. Because there are no specific biomarkers for ALS, it is difficult to diagnose this disease in its early stages. Cerebrospinal fluid (CSF) samples were obtained from 14 patients in the early stages of ALS, from 13 with polyneuropathy, and from 16 with other neurological disorders. The concentration of cystatin C in the CSF was measured using a sandwich enzyme-linked immunosorbent assay (ELISA) kit. The concentration of cystatin C in the CSF was significantly lower in ALS patients than in the control subjects who were patients with polyneuropathy or other neurological diseases (patients with ALS, polyneuropathy, and other diseases exhibited 5.5 +/- 0.3, 6.7 +/- 0.4, and 6.9 +/- 0.3 mg/L cystatin C, respectively; ALS patients vs. control subjects: p = 0.014 and ALS patients vs. polyneuropathy patients: p = 0.024). Cystatin C may be a useful biomarker of ALS and can be used to distinguish between ALS and polyneuropathy.
Serum cystatin C level for better assessment of glomerular filtration rate in cystic fibrosis patients treated by amikacin.
BACKGROUND AND OBJECTIVE:
Monitoring of renal function in cystic fibrosis (CF) patients is essential. The dosage regimen of amikacin is regularly modified according to the patient's glomerular filtration rate (GFR). The aim of the study was to evaluate the use of
cystatin C (CyC) for monitoring amikacin therapy along with other markers of renal tubular and glomerular function, and damage [N-acetyl-beta-d glucosaminidase (NAG), creatinine level and creatinine clearance].
METHODS:
We compared the GFR, estimated from the serum concentrations of creatinine (Cockcroft-Gault formula) and cystatin C (CyC) (Grubb's formula). Seventy-one patients (mean age 12 years; range 4-28 years) with CF were treated by intermittent intravenous infusion of amikacin. Tubular nephrotoxicity was investigated by measurement of urine NAG/urine creatinine ratio (U-NAG/U-creatinine). Concentrations of all markers were measured before starting amikacin therapy and at days 3, 5, 7, 10 and 12. Fluorescence polarization analysis, turbidimetry, enzymatic phototometric creatinine deaminase method and fluorimetry were used for determination of serum amikacin, serum CyC, creatinine and urine NAG activity. Receiver operating characteristic (ROC) analysis was performed to assess the influence of GFR estimated from serum creatinine and serum CyC for the prediction of amikacin clearance during aminoglycoside therapy.
RESULTS:
Significant differences in the rate of U-NAG/U-creatinine were noted before and after treatment with amikacin (P < 0.001). Serum creatinine levels and creatinine clearance at the end of amikacin therapy (12th day) did not show any significant differences in comparison with the levels measured before the start of therapy (0th day). At days 5, 7, 10 and 12, serum CyC levels showed a significant elevation (P < 0.001), and cystatin C (CyC) clearance showed a significant decrease (P < 0.001) in comparison with the levels measured at day 0. The ratio of amikacin clearance/creatinine clearance decreased with therapy whereas the amikacin clearance/CyC and amikacin clearance/CyC clearance increased.
CONCLUSION: We showed that the rate of U-NAG/U-creatinine is a suitable marker for monitoring tubular nephrotoxicity in CF patients. Serum creatinine and estimated creatinine clearance are modest predictors of GFR in CF patients. cystatin C (CyC) appears to be a better marker of GFR than serum creatinine concentration or creatinine clearance in our study. Serum CyC levels and CyC clearance showed greater ability to predict amikacin clearance during therapy than creatinine clearance.
Monitoring of renal function in cystic fibrosis (CF) patients is essential. The dosage regimen of amikacin is regularly modified according to the patient's glomerular filtration rate (GFR). The aim of the study was to evaluate the use of
cystatin C (CyC) for monitoring amikacin therapy along with other markers of renal tubular and glomerular function, and damage [N-acetyl-beta-d glucosaminidase (NAG), creatinine level and creatinine clearance].
METHODS:
We compared the GFR, estimated from the serum concentrations of creatinine (Cockcroft-Gault formula) and cystatin C (CyC) (Grubb's formula). Seventy-one patients (mean age 12 years; range 4-28 years) with CF were treated by intermittent intravenous infusion of amikacin. Tubular nephrotoxicity was investigated by measurement of urine NAG/urine creatinine ratio (U-NAG/U-creatinine). Concentrations of all markers were measured before starting amikacin therapy and at days 3, 5, 7, 10 and 12. Fluorescence polarization analysis, turbidimetry, enzymatic phototometric creatinine deaminase method and fluorimetry were used for determination of serum amikacin, serum CyC, creatinine and urine NAG activity. Receiver operating characteristic (ROC) analysis was performed to assess the influence of GFR estimated from serum creatinine and serum CyC for the prediction of amikacin clearance during aminoglycoside therapy.
RESULTS:
Significant differences in the rate of U-NAG/U-creatinine were noted before and after treatment with amikacin (P < 0.001). Serum creatinine levels and creatinine clearance at the end of amikacin therapy (12th day) did not show any significant differences in comparison with the levels measured before the start of therapy (0th day). At days 5, 7, 10 and 12, serum CyC levels showed a significant elevation (P < 0.001), and cystatin C (CyC) clearance showed a significant decrease (P < 0.001) in comparison with the levels measured at day 0. The ratio of amikacin clearance/creatinine clearance decreased with therapy whereas the amikacin clearance/CyC and amikacin clearance/CyC clearance increased.
CONCLUSION: We showed that the rate of U-NAG/U-creatinine is a suitable marker for monitoring tubular nephrotoxicity in CF patients. Serum creatinine and estimated creatinine clearance are modest predictors of GFR in CF patients. cystatin C (CyC) appears to be a better marker of GFR than serum creatinine concentration or creatinine clearance in our study. Serum CyC levels and CyC clearance showed greater ability to predict amikacin clearance during therapy than creatinine clearance.
Tuesday
Estimating GFR using serum cystatin C alone and in combination with serum creatinine: a pooled analysis of 3,418 individuals with CKD.
Serum cystatin C was proposed as a potential replacement for serum creatinine in glomerular filtration rate (GFR) estimation. We report the development and evaluation of GFR-estimating equations using serum cystatin C alone and serum cystatin C, serum creatinine, or both with demographic variables.
STUDY DESIGN: Test of diagnostic accuracy.
SETTING & PARTICIPANTS: Participants screened for 3 chronic kidney disease (CKD) studies in the United States (n = 2,980) and a clinical population in Paris, France (n = 438).
REFERENCE TEST: Measured GFR (mGFR).
INDEX TEST: Estimated GFR using the 4 new equations based on serum cystatin C alone, serum cystatin C, serum creatinine, or both with age, sex, and race. New equations were developed by using linear regression with log GFR as the outcome in two thirds of data from US studies. Internal validation was performed in the remaining one third of data from US CKD studies; external validation was performed in the Paris study.
MEASUREMENTS: GFR was measured by using urinary clearance of iodine-125-iothalamate in the US studies and chromium-51-EDTA in the Paris study. Serum cystatin C was measured by using Dade-Behring assay, standardized serum creatinine values were used.
RESULTS: Mean mGFR, serum creatinine, and serum cystatin C values were 48 mL/min/1.73 m(2) (5th to 95th percentile, 15 to 95), 2.1 mg/dL, and 1.8 mg/L, respectively. For the new equations, coefficients for age, sex, and race were significant in the equation with serum cystatin C, but 2- to 4-fold smaller than in the equation with serum creatinine. Measures of performance in new equations were consistent across the development and internal and external validation data sets. Percentages of estimated GFR within 30% of mGFR for equations based on serum cystatin C alone, serum cystatin C, serum creatinine, or both levels with age, sex, and race were 81%, 83%, 85%, and 89%, respectively. The equation using serum cystatin C level alone yields estimates with small biases in age, sex, and race subgroups, which are improved in equations including these variables.
LIMITATIONS: Study population composed mainly of patients with CKD.
CONCLUSIONS: Serum cystatin C level alone provides GFR estimates that are nearly as accurate as serum creatinine level adjusted for age, sex, and race, thus providing an alternative GFR estimate that is not linked to muscle mass. An equation including serum cystatin C level in combination with serum creatinine level, age, sex, and race provides the most accurate estimates.
STUDY DESIGN: Test of diagnostic accuracy.
SETTING & PARTICIPANTS: Participants screened for 3 chronic kidney disease (CKD) studies in the United States (n = 2,980) and a clinical population in Paris, France (n = 438).
REFERENCE TEST: Measured GFR (mGFR).
INDEX TEST: Estimated GFR using the 4 new equations based on serum cystatin C alone, serum cystatin C, serum creatinine, or both with age, sex, and race. New equations were developed by using linear regression with log GFR as the outcome in two thirds of data from US studies. Internal validation was performed in the remaining one third of data from US CKD studies; external validation was performed in the Paris study.
MEASUREMENTS: GFR was measured by using urinary clearance of iodine-125-iothalamate in the US studies and chromium-51-EDTA in the Paris study. Serum cystatin C was measured by using Dade-Behring assay, standardized serum creatinine values were used.
RESULTS: Mean mGFR, serum creatinine, and serum cystatin C values were 48 mL/min/1.73 m(2) (5th to 95th percentile, 15 to 95), 2.1 mg/dL, and 1.8 mg/L, respectively. For the new equations, coefficients for age, sex, and race were significant in the equation with serum cystatin C, but 2- to 4-fold smaller than in the equation with serum creatinine. Measures of performance in new equations were consistent across the development and internal and external validation data sets. Percentages of estimated GFR within 30% of mGFR for equations based on serum cystatin C alone, serum cystatin C, serum creatinine, or both levels with age, sex, and race were 81%, 83%, 85%, and 89%, respectively. The equation using serum cystatin C level alone yields estimates with small biases in age, sex, and race subgroups, which are improved in equations including these variables.
LIMITATIONS: Study population composed mainly of patients with CKD.
CONCLUSIONS: Serum cystatin C level alone provides GFR estimates that are nearly as accurate as serum creatinine level adjusted for age, sex, and race, thus providing an alternative GFR estimate that is not linked to muscle mass. An equation including serum cystatin C level in combination with serum creatinine level, age, sex, and race provides the most accurate estimates.
Monday
NGAL (neutrophil gelatinase-associated lipocalin) and cystatin C: Are they good predictors of contrast nephropathy after percutaneous coronary interve
The aim of the study was to assess whether neutrophil gelatinase-associated lipocalin (NGAL) and Cystatin C could predict contrast-induced nephropathy in non-diabetic patients (n = 60, mean age 60 ± 11 years) with normal serum creatinine undergoing elective PCI. We found a significant rise in serum NGAL after 2, 4 and 8 h, and in urinary NGAL after 4, 8 and 24 h after PCI. Cystatin C rose significantly 8 and 24 h after the procedure. Prevalence of CIN was 10%. We found 90% sensitivity and 74% specificity of serum and 76% sensitivity and 80% specificity of urinary NGAL increase. NGAL may represent a sensitive early biomarkers of renal impairment after PCI.
H. Bachorzewska-Gajewskaa, 1, J. Malyszkoa, b, , 1, E. Sitniewskaa, J.S. Malyszkoa, B. Poniatowskia, K. Pawlaka and S. Dobrzycki
ARTICLE
H. Bachorzewska-Gajewskaa, 1, J. Malyszkoa, b, , 1, E. Sitniewskaa, J.S. Malyszkoa, B. Poniatowskia, K. Pawlaka and S. Dobrzycki
ARTICLE
Friday
Serum Cystatin C and Increased Coronary Heart Disease Prevalence in US Adults Without Chronic Kidney Disease
Previous studies indicated that serum cystatin C, a marker of renal function, was associated with cardiovascular disease (CVD). However, few data about this association are available for persons without chronic kidney disease or albuminuria. Data from 4,991 subjects in the Third National Health and Nutrition Examination Survey with an estimated glomerular filtration rate ≥60 ml/min/1.73 m2 without micro- or macroalbuminuria were analyzed. Subjects were categorized into quartiles of serum cystatin C and compared for prevalence of CVD. CVD was defined as a history of myocardial infarction, angina, or stroke. After age standardization, prevalences of CVD from the lowest to highest quartile of serum cystatin C were 6.0%, 8.8%, 11.8%, and 16.7% (p-trend = 0.006). Also, age-standardized prevalences of myocardial infarction across quartiles of serum cystatin C were 1.9%, 4.4%, 6.6%, and 8.6%; age-standardized prevalences of angina were 2.4%, 4.4%, 4.2%, and 7.1%; and age-standardized prevalences of stroke were 2.5%, 1.6%, 3.5%, and 4.4% (each p-trend <0.05). Each 1-SD higher serum cystatin C level was associated with a multivariate prevalence ratio of CVD of 1.55 (95% confidence interval [CI] 1.13 to 2.13), and multivariate-adjusted prevalence ratios were 1.44 (95% CI 1.01 to 2.07), 1.64 (95% CI 1.02 to 2.64), and 1.65 (95% CI 1.06 to 2.56) for myocardial infarction, angina, and stroke, respectively. In conclusion, a graded association exists between higher serum cystatin C and increased CVD prevalence in patients without established chronic kidney disease.
Paul Muntner PhDa, , , Devin Mann MD, MSb, Jonathan Winston MDb, Sameer Bansilal MDc and Michael E. Farkouh MD, MScc
Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York, New York USA.
Department of Medicine, Mount Sinai School of Medicine, New York, New York USA.
The Zena and Michael A. Wiener Cardiovascular Institute and Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York, New York
Paul Muntner PhDa, , , Devin Mann MD, MSb, Jonathan Winston MDb, Sameer Bansilal MDc and Michael E. Farkouh MD, MScc
Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York, New York USA.
Department of Medicine, Mount Sinai School of Medicine, New York, New York USA.
The Zena and Michael A. Wiener Cardiovascular Institute and Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York, New York
Tuesday
Cystatin C and other cardiovascular markers in hypertension
BACKGROUND AND OBJECTIVE: The aim of the study was to assess the relationship of cystatine C to other cardiovascular risk factors in hypertension .
PATIENTS AND METHOD: Cross-sectional study in hypertensive outpatients with normal creatinine values (< 1.6 mg/dl for males and < 1.4 mg/dl for women). Cystatin C was analyzed by immunonephelometry.
RESULTS: 283 patients (47% male) were evaluated. Cystatin C values were 0.65 (0.27) mg/l (median, intercuartile range, percentile 70 = 0.76 mg/l), and were correlated to the estimated glomerular filtration rate (GFR) (ml/min/1.73 m2), C reactive protein , and urinary albumin excretion (UAE). In multiple regression analysis the GFR was the most significant factor and explained 38% of cystatine C variability. GFR, (odds ratio [OR] = 5.84; 95% confidence interval [CI], 2.27-15.03; p < 0.001), age (OR = 1.05; 95% CI, 1.02-1.08; p < 0.001), and CRP (OR = 2.03; 95% CI, 1.07-3.84; p = 0.03), but not UAE >= 30 mg/24 h, were independent factors related to the presence of high levels (> 0.76 mg/l) of cystatine C in a logistic regression analysis. 58% of patients with UAE >= 30 mg/24h had cystatin C values < 0,76 mg/l.
CONCLUSIONS: In hypertensive patients, the GFR is the most important factor related to cystatine C values. Increased levels of cystatine C do not correspond to UAE augmentation.
Med Clin (Barc). 2008 Jan 19;130(1):1-5.Unidad de Hipertensión Arterial y Riesgo Vascular. Servicio de Medicina Interna. Hospital de Sagunto. Agencia Valenciana de Salud. Valencia. España
PATIENTS AND METHOD: Cross-sectional study in hypertensive outpatients with normal creatinine values (< 1.6 mg/dl for males and < 1.4 mg/dl for women). Cystatin C was analyzed by immunonephelometry.
RESULTS: 283 patients (47% male) were evaluated. Cystatin C values were 0.65 (0.27) mg/l (median, intercuartile range, percentile 70 = 0.76 mg/l), and were correlated to the estimated glomerular filtration rate (GFR) (ml/min/1.73 m2), C reactive protein , and urinary albumin excretion (UAE). In multiple regression analysis the GFR was the most significant factor and explained 38% of cystatine C variability. GFR, (odds ratio [OR] = 5.84; 95% confidence interval [CI], 2.27-15.03; p < 0.001), age (OR = 1.05; 95% CI, 1.02-1.08; p < 0.001), and CRP (OR = 2.03; 95% CI, 1.07-3.84; p = 0.03), but not UAE >= 30 mg/24 h, were independent factors related to the presence of high levels (> 0.76 mg/l) of cystatine C in a logistic regression analysis. 58% of patients with UAE >= 30 mg/24h had cystatin C values < 0,76 mg/l.
CONCLUSIONS: In hypertensive patients, the GFR is the most important factor related to cystatine C values. Increased levels of cystatine C do not correspond to UAE augmentation.
Med Clin (Barc). 2008 Jan 19;130(1):1-5.Unidad de Hipertensión Arterial y Riesgo Vascular. Servicio de Medicina Interna. Hospital de Sagunto. Agencia Valenciana de Salud. Valencia. España
Thursday
CST3 CYSTATIN C
GeneID: 1471
Cystatin 3 , usually called Cystatin C (also CST3 and Gamma trace) is a serum protein used mainly as a measure of glomerular filtration rate . It is a single 120-residue polypeptide belonging to the type 2 cystatin gene family. Studies have shown that Cystatin C allows a more precise testing of kidney function than creatinine.
The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors , while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and the kininogens. The type 2 cystatin proteins are a class of cysteine proteinase inhibitors found in a variety of human fluids and secretions, where they appear to provide protective functions. The cystatin locus on chromosome 20 contains the majority of the type 2 cystatin genes and pseudogenes. This gene is located in the cystatin locus and encodes the most abundant extracellular inhibitor of cysteine proteases , which is found in high concentrations in biological fluids and is expressed in virtually all organs of the body. A mutation in this gene has been associated with amyloid angiopathy . Expression of this protein in vascular wall smooth muscle cells is severely reduced in both atherosclerotic and aneurysmal aortic lesions, establishing its role in vascular disease.
Cystatin 3 , usually called Cystatin C (also CST3 and Gamma trace) is a serum protein used mainly as a measure of glomerular filtration rate . It is a single 120-residue polypeptide belonging to the type 2 cystatin gene family. Studies have shown that Cystatin C allows a more precise testing of kidney function than creatinine.
The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors , while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and the kininogens. The type 2 cystatin proteins are a class of cysteine proteinase inhibitors found in a variety of human fluids and secretions, where they appear to provide protective functions. The cystatin locus on chromosome 20 contains the majority of the type 2 cystatin genes and pseudogenes. This gene is located in the cystatin locus and encodes the most abundant extracellular inhibitor of cysteine proteases , which is found in high concentrations in biological fluids and is expressed in virtually all organs of the body. A mutation in this gene has been associated with amyloid angiopathy . Expression of this protein in vascular wall smooth muscle cells is severely reduced in both atherosclerotic and aneurysmal aortic lesions, establishing its role in vascular disease.
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