Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability to assess renal function in diabetes patients rapidly and early is of major importance. This study was designed to determine whether cystatin C can replace serum creatinine as the screening marker for reduced glomerular filtration rate (GFR) in type 2 diabetes patients. The study was performed on 51 type 2 diabetic patients. GFR was estimated by the plasma clearance of (99m)Tc-DTPA. The correlation between (99m)Tc-DTPA clearance and levels of serum cystatin C, serum creatinine, and creatinine clearance was determined. Sensitivity and specificity for the diagnosis of renal impairment (defined as GFR<68 ml/min) were calculated by a receiver operating characteristic (ROC) curve for serum cystatin C, serum creatinine, and creatinine clearance. The correlation coefficients with (99m)Tc-DTPA clearance were -0.744 for serum cystatin C, -0.658 for serum creatinine, and +0.625 for creatinine clearance (P<0.001). With a cutoff value of 68 mL/min, the area under the ROC curve (AUC) was 0.891 for cystatin C, 0.77 for creatinine, and 0.753 for creatinine clearance. The AUC was statistically different between serum cystatin C and creatinine clearance (P<0.05). The ROC plot indicates that cystatin C is superior to serum creatinine and creatinine clearance for detecting impaired GFR. Serum cystatin C appropriately reflects GFR in diabetes, and is more efficacious than serum creatinine and creatinine clearance in detecting reduced GFR in type 2 diabetes patients.
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PMID:Serum cystatin C assay for the detection of early renal impairment in diabetic patients. 1473 May 55

Glomerular filtration rate (GFR) is the best indicator of renal function. GFR is usually estimated by serum creatinine or the creatinine clearance calculated on urine collected over 24 hours or with the Cockcroft formula. These methods are however limited. Serum creatinine has a very poor sensitivity and urine collection is difficult. Cystatin C is a protease inhibitor produced in a constant manner by nucleated cells. This molecule is freely filtrated by the glomerule and quite completely catabolized in the proximal tubules. Its plasmatic concentration might thus be used to estimate GFR. Presently available data allow to conclude that plasmatic cystatin C is at least as good as serum creatinine to estimate GFR. It is less sensible to changes in body mass. Its determination appears more sensitive to detect early mild changes in GFR. Reference values are presently available for the different methods of determination. Cystatin C plasma level determination is more expensive than routine creatinine plasma determination. In the absence of very significant advantages, this might explain its limited use in daily clinical practice.
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PMID:[Cystatin C in the evaluation of renal function]. 1473 79

Prevention of contrast agent-induced nephropathy is of crucial importance for a number of diagnostic studies. N-Acetylcysteine (NAC) was recently reported to decrease serum creatinine levels in this setting, and its administration before radiocontrast medium administration has been widely recommended. The objective of this prospective study was to investigate whether there are effects of NAC on serum creatinine levels that are independent of alterations in GFR. Volunteers with normal renal function who did not receive radiocontrast medium were studied. Fifty healthy volunteers completed the study protocol. NAC was administered orally at a dose of 600 mg every 12 h, for a total of four doses. Surrogate markers of renal function, such as serum creatinine, urea, albumin, and cystatin C levels, were measured and estimated GFR (eGFR) was assessed immediately before the administration of NAC and 4 and 48 h after the last dose. There was a significant decrease in the mean serum creatinine concentration (P < 0.05) and a significant increase in the eGFR (P < 0.02) 4 h after the last dose of NAC. The cystatin C concentrations did not change significantly. In several studies, a protective effect of NAC on renal function after radiocontrast medium administration has been postulated. This is the first study to demonstrate an effect of NAC on creatinine levels and eGFR, surrogate markers of renal injury, without any effect on cystatin C levels. Before renoprotective effects of NAC against contrast agent-induced nephropathy are considered, the direct effects of NAC on creatinine levels, urea levels, and eGFR should be assessed.
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PMID:The value of N-acetylcysteine in the prevention of radiocontrast agent-induced nephropathy seems questionable. 1474 87

The aim of our study was to measure renal function and growth in survivors of unilateral Wilms' tumour in 21 children and young adults (7 female). The mean age was 12.6 +/- 4.8 years, mean follow-up time was 7.01 +/- 4.25 years: seven of the group received irradiation (35 Gy). Blood pressure was normal in all patients. Three of them had elevated cystatin C and clearance of cystatin C below referenced normal value. The others had normal renal function tests (cystatin C, creatinine and cystatin clearance, B2 microglobulin, microalbuminuria, osmolality). Compared to the control we found higher cystatin C values in children treated before the age 3 years old (p=0.03) and in children treated more than 5 years before (p=0.03), and lower cystatin clearance in group treated before the age 3 years old (p=0,03). No difference between the irradiated and non-irradiated group was found. We observed a greater increase in volume (155.9% +/- 33.4) than in length (127.9% +/- 6.3). The highest rise of renal volume was in children treated more than 5 years before (174.6% +/- 22.3). In conclusion, our data suggest that after combined treatment for Wilms' tumour compensatory renal hypertrophy and a tendency progressive renal dysfunction takes place.
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PMID:[Renal function and size after complex treatment of Wilms' tumour]. 1496 43

Management of renal transplant patients requires periodic measurement of renal function, which is usually assessed by measuring the glomerular filtration rate (GFR). The most commonly used marker for GFR is serum creatinine, although muscle wasting and tubular secretion may lead to overestimation of the actual GFR. Serum concentrations of the low-molecular-weight proteins, cystatin C and beta(2)-microglobulin (B(2)M), may afford useful markers to determine a reduced GFR. We investigated whether these molecules provide reliable indicators of renal function in 75 renal transplant patients. Cystatin C and B(2)M correlated significantly with creatinine (r =.648, P <.05 and r =.578, P <.05, respectively). Inverse serum creatinine was superior to inverse cystatin C and inverse B(2)M when renal function equations were used (r =.95, P <.05, according to MDRD; r =.87, P <.05, according to Cockroft-Gault). Receiver operating characteristic (ROC) analysis was performed to quantitate the accuracy of the different markers to detect reduced GFR using a cutoff value of 70 mL/min. No significant difference between the areas under the ROC curves comparing cystatin C and B(2)M was observed; however, serum creatinine demonstrated a significantly greater value than cystatin C (.981 vs.724, P =.001). We conclude that serum creatinine is a more efficacious marker than serum cystatin C to assess renal function.
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PMID:Serum cystatin C as an index of renal function in kidney transplant patients. 1501 12

Glomerular filtration rate (GFR) and urine and serum concentrations of cystatin C and creatinine were measured in 40 boys and 42 girls. The fractional excretion of cystatin C (FE Cyst C) increased in proportion to the decrease in GFR. Since serum creatinine concentration (S-Creatinine) in the numerator of the fractional excretion equation and serum cystatin C concentration (S-Cystatin C) in the denominator have similar numerical values, they cancel out. The result is an equation in which the FE Cyst C is equal to the ratio of urinary cystatin C to urinary creatinine (u[cystatin-C/Cr]). The ratio of u[cystatin C/Cr] was compared with GFR. Using a receiving operating characteristic (ROC) plot, the data showed that a ratio of u[cystatin C/Cr]*100 that is > or =0.100 has a sensitivity of 90.0% for identification of children with GFR < or =60 ml/min per 1.73 m(2). The false-positive rate is 16.1%. The u[cystatin C/Cr] ratio is a reliable screening tool for detecting decreased GFR that does not require a serum sample.
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PMID:The ratio of urinary cystatin C to urinary creatinine for detecting decreased GFR. 1550 80

The Cockcroft Gault formula is often used to calculate the glomerular filtration rate (GFR) from plasma creatinine results. In Sweden this calculation is not usually done in the laboratory, but locally in the wards. These manual calculations could cause erroneous results. In several studies plasma cystatin C has been shown to be superior to plasma creatinine for estimation of GFR. One limitation of using cystatin C as a GFR marker is that there is no conversion formula transforming cystatin C expressed as mg/L to GFR expressed as mL/min. In this study plasma creatinine and cystatin C were compared with iohexol clearance. A stronger correlation (p < 0.0001) was found between cystatin C and iohexol clearance (r2 = 0.91) than between creatinine and iohexol clearance (r2 = 0.84). From the correlation data a formula was calculated to convert cystatin C expressed as mg/L to GFR (mL/min). The formulas y = 77.24x(-1.2623) (Dade Behring cystatin C calibration) or y = 99.43x(-1.5837) (DakoCytomation cystatin C calibration) are used to calculate GFR expressed in mL/min from the cystatin C value in mg/L and both results are reported to the referral doctor. These formulas can provide the clinicians with reliable and readily available GFR data based on single measurements of cystatin C concentrations.
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PMID:Calculation of glomerular filtration rate expressed in mL/min from plasma cystatin C values in mg/L. 1502 26

The search for whether endogenous markers of changes in glomerular filtration rate (GFR) by serum cystatin C assay and serum cystatin C compare with creatinine clearance by the Cockeroft-Gault formula and the evaluation of its clinical significance as a marker of GFR is important in clinical practice at present. Serum cystatin C was determined by sandwich enzyme immunoassay using a kit. Control blood samples were collected from 70 healthy subjects and 168 patients with various kidney diseases. Creatinine clearance (Cockeroft-Gault formula) as a measure of GFR, in 168 patients with various kidney diseases, depends on the creatinine clearance; GFR parameters were used to divide patients into two groups. The GFR was >80 mL/min in 38 patients (group A) and <80 mL/min in 130 patients (group B). The two groups were analyzed by correlation coefficient and diagnostic sensitivity and specificity were assessed by the receiver-operating characteristic (ROC) plots (area under the curve). Of the 70 healthy control individuals, the serum level of cystatin C was measured as normal value range and a reference interval of 1.05+/-0.18 micro g/mL (mean+/-1.96 SD, 95% confidence limits for the upper references limit is 1.4 microg/mL). In group A, serum cystatin C had no correlation to the creatinine clearance (r=0.171, P>0.05) and in group B, serum cystatin C was closely correlated to the creatinine clearance (r=-0.771, P<0.001). Diagnostic sensitivity and specificity were assessed by the ROC plots for serum cystatin C (area under the curve=0.8461, SE=0.057) and creatinine clearance (area under the curve=0.7642, SE=0.068). These data suggest that combined measurement of serum cystatin C is useful to estimate GFR, especially to detect the reduction of GFR. Further studies are required to evaluate the whether serum cystatin C as a more sensitive marker of early renal injury might be extremely useful, particularly in nonproteinuric or unapparent renal disease.
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PMID:Clinical value of serum cystatin C by ELISA for estimation of glomerular filtration rate. 1506 9

Progressive improvement in kidney transplant survival rates and reduction in acute rejection rates have ironically restricted our ability to evaluate newer therapy. Current short-term endpoints such as acute rejection rates have reduced utility in predicting long-term survival. Long-term graft survival is an ideal endpoint, but is limited by longer follow-up requirements and the large cohort of patients required for such studies. Newer short-term surrogate markers should be identified and these markers should correlate with long-term graft failure. Hence, identification of short-term surrogate markers is critical to test newer immunosuppressive strategies over current therapies, and should also predict long-term transplant outcome. Potential surrogate markers are clinical parameters such as renal function, renal histological findings of fibrosis and immunological markers. Post-transplant renal function estimated by serum creatinine within 1 year has been shown to correlate with long-term survival. Alternative evaluation of renal function such as clearance studies and cystatin C, which are more accurate, could potentially be useful in clinical trials. Renal histological indices such as fibrosis measured as Chronic Allograft Disease Index score or Banff score correlate with long-term graft survival. Immunological markers such as antidonor antibodies, levels of blood and urine cytokines, real time PCR, ELISPOT and microarrays are attractive surrogates to consider. Measurement of morbidity and mortality after transplantation is critical to further enhance long-term survival. Thus, there are many potential surrogate markers and these individually or in combination with conventional endpoints should be implemented in clinical trials and validated in long-term studies.
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PMID:Surrogate markers for long-term renal allograft survival. 1519 79

N-acetylcysteine (NAC) has been suggested to prevent radiocontrast-induced nephropathy (RCIN) in patients with a reduced renal function. However, clinical studies have not been demonstrating this effect consistently. Also, reviews and meta-analyses dealing with the question of prevention of RCIN by NAC have been controversial. Nearly all investigators used serum creatinine as surrogate end point of their trials, and changes in serum creatinine concentrations are thought to reflect the extent of renal injury as primary outcome. In a recent study, an effect of NAC on creatinine values and estimated glomerular filtration rate without any effect on cystatin C levels has been shown in volunteers with a normal renal function. Therefore, before renal protective effects of NAC in RCIN are proposed, any direct effects of NAC on creatinine, urea, and estimated glomerular filtration rate should be addressed. In future trials, the glomerular filtration rate should preferentially be measured directly, or at least additional markers of the renal function (e.g., serum cystatin C) have to be assessed. Furthermore, additional 'hard' end points, i.e., hospital morbidity, mortality, or dialysis dependency, should be considered in the design of future studies of RCIN.
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PMID:N-acetylcysteine in the prevention of radiocontrast-induced nephropathy: clinical trials and end points. 1525 11


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