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PubMed2006

Serum cystatin C for the prediction of glomerular filtration rate with regard to the dose adjustment of amikacin, gentamicin, tobramycin, and vancomycin.

Dosage regimes of aminoglycosides and vancomycin are modified according to the glomerular filtration rate (GFR). In 130 hospitalized patients who were administered amikacin, gentamicin, tobramycin, and vancomycin by intermittent intravenous infusion, we compared the predicted GFR values from the serum concentrations of creatinine (Cockcroft and Gault. Nephron. 1976;16:31-41) and cystatin C (Larsson et al. Scand J Clin Lab Invest. 2004;64:25-30) with respect to their relevance for proper dosage. In 83% and 67% of the cases, respectively, the serum levels of albumin and cholinesterase were below the corresponding lower limit of the reference range. The ratio of creatinine/cystatin C concentrations presented significant correlations with the predicted rate of creatinine production (r=0.762, P<0.001), serum albumin concentration (r=0.205, P<0.05), and catalytic serum concentrations of cholinesterase (r=0.207, P<0.05), gamma glutamyltransferase (r=-0.273, P<0.01), and alkaline phosphatase (r=-0.289, P<0.01). The GFR (mean+/-SD; median) predicted by the serum creatinine (84.0+/-35.1 mL/min/1.73 m; 82.6 mL/min/1.73 m) was significantly higher (P<0.001) than that predicted by the serum cystatin C (53.1+/-30.2 mL/min/1.73 m; 44.9 mL/min/1.73 m). The ratio between the GFR values predicted by creatinine and cystatin C had a highly significant negative correlation with the rate of creatinine production (r=-0.912, P<0.001). Furthermore, significant differences were found for the peak concentrations and clearances of amikacin and vancomycin estimated by means of the Abbottbase Pharmacokinetic Systems program, and using the GFR values predicted by the serum creatinine and cystatin C (P<0.005). In patients with hepatic dysfunction, the clearance of creatinine predicted by the Cockcroft-Gault formula leads to a significant overestimation of the GFR. Cystatin C seems to be a valid alternative as a GFR marker with regard to drug dose adjustment in these cases.

Adolescent↗
PubMed2001

Role of the single cysteine residue, Cys 3, of human and bovine cystatin B (stefin B) in the inhibition of cysteine proteinases.

Cystatin B is unique among cysteine proteinase inhibitors of the cystatin superfamily in having a free Cys in the N-terminal segment of the proteinase binding region. The importance of this residue for inhibition of target proteinases was assessed by studies of the affinity and kinetics of interaction of human and bovine wild-type cystatin B and the Cys 3-to-Ser mutants of the inhibitors with papain and cathepsins L, H, and B. The wild-type forms from the two species had about the same affinity for each proteinase, binding tightly to papain and cathepsin L and more weakly to cathepsins H and B. In general, these affinities were appreciably higher than those reported earlier, perhaps because of irreversible oxidation of Cys 3 in previous work. The Cys-to-Ser mutation resulted in weaker binding of cystatin B to all four proteinases examined, the effect varying with both the proteinase and the species variant of the inhibitor. The affinities of the human inhibitor for papain and cathepsin H were decreased by threefold to fourfold and that for cathepsin B by approximately 20-fold, whereas the reductions in the affinities of the bovine inhibitor for papain and cathepsins H and B were approximately 14-fold, approximately 10-fold and approximately 300-fold, respectively. The decreases in affinity for cathepsin L could not be properly quantified but were greater than threefold. Increased dissociation rate constants were responsible for the weaker binding of both mutants to papain. By contrast, the reduced affinities for cathepsins H and B were due to decreased association rate constants. Cys 3 of both human and bovine cystatin B is thus of appreciable importance for inhibition of cysteine proteinases, in particular cathepsin B.

Animals↗
PubMed1989

Absence of the cystatin C amyloid in the cerebral amyloid angiopathy, senile plaque, and extra-CNS amyloid deposits of aged Japanese.

Amyloid protein in Icelandic patients with hereditary cerebral amyloid angiopathy (CAA) is a variant of cystatin C. Immunoreactivities of the cystatin C and other amyloid proteins were investigated in CAA and other senile amyloid deposits in the Japanese sporadic aged cases including patients with dementia of Alzheimer type, and compared with those in Icelandic hereditary CAA. Compared with positive reaction of cystatin C in Icelandic hereditary CAA, no immunoreactivity of cystatin C was found in senile amyloid deposits of the Japanese aged including CAA. Immunoreactivity of the amyloid beta protein was negative in Icelandic hereditary CAA, for which CAA and senile plaque amyloid in the Japanese senile brains were positive. Our data suggest that the cystatin C amyloid would be present only in hereditary CAA, but not in the CAA and other senile amyloid deposits of the sporadic aged cases.

Aged↗
PubMed2005

Reduction of experimental human fibrosarcoma lung metastasis in mice by adenovirus-mediated cystatin C overexpression in the host.

Tumor cell invasion and metastasis are associated with degradation of components of the extracellular matrix by different proteinases. Among those, papain-like cysteine proteases, such as cathepsin B, seem to play an important role, as they are associated with poor clinical outcome in different cancers. In this study, we tested whether cystatin C, a natural extracellular inhibitor of papain-like cysteine proteases, can inhibit metastasis when overexpressed at the tumor-host interface. Local overexpression of cystatin C in liver and lungs of CD1 nu/nu mice was achieved by gene transfer with a novel adenoviral construct, which also led to the presence of 60 ng/mL of cystatin C in the serum. Three days after gene transfer, these mice were challenged by i.v. inoculation of lacZ-tagged human fibrosarcoma cells (HT1080lacZ-K15), leading to the formation of experimental lung and liver metastases. In this model, formation of experimental metastatic foci correlated with expression of cathepsin B in lungs, whereas there was no correlation with metastasis to the liver. In mice overexpressing cystatin C, the number of lung metastases was significantly reduced by 92%, as compared with mice receiving control adenovirus. The efficacy of extravasation of HT1080lacZ-K15 cells into the liver was not affected, indicating the independence of this process from the activity of cysteine-cathepsins. The present report is the first evidence of successful reduction of metastasis by inhibition of cysteine-cathepsins by cystatin C overexpression in the host microenvironment. Furthermore, organ-specific protease expression during tumor-host cell interactions could affect the success of antiproteolytic intervention against metastasis.

Adenoviridae↗
PubMed2003

Glomerular filtration rate estimation in patients with advanced chronic renal insufficiency based on serum cystatin C levels.

BACKGROUND: Cystatin C has an obvious advantage in the recognition of the initial stages of renal impairment. It is questionable whether cystatin C possesses the same benefit in follow-up of pre-dialysis patients. If cystatin C were also a sensitive marker of GFR in pre-dialysis patients, then it could be expected that, for the same degree of a decrease in GFR, the increase in S(cyst) would be higher than in S(cr) because of the significant increase in tubular secretion of creatinine in residual nephrons. The aim of this study was to evaluate whether S(cyst) in patients with GFR <or=40 ml/min/1.73 m(2) provides a more accurate estimate of GFR than S(cr) does. METHODS: The study was performed in 67 patients (mean age 41.5 +/- 7.6 years) with chronic renal insufficiency (GFR = 19.8 +/- 9.9 ml/min/1.73 m(2)) caused by various chronic renal diseases (predominantly by chronic glomerulonephritis and chronic interstitial nephritis). GFR was measured by inulin clearance under conditions of stabilized plasma concentrations and water loading. Creatinine clearance and serum cystatin C concentration (using immunonephelometry) were measured at the same time. For statistical evaluation, linear regression analysis, receiver-operating characteristic (ROC) curves analysis and the method of Bland and Altman were used. RESULTS: A significant correlation (r = 0.813, p < 0.001) was demonstrated between 1/S(cyst) and C(in) as well as between 1/S(cr) and C(in) (r = 0.815, p < 0.001). There were no significant differences between the regression coefficients and the intercepts of regression straight lines characterizing these relationships. ROC curves analysis using the cut-off values for C(in) = 20 ml/min/1.73 m(2) and C(in) = 10 ml/min/ 1.73 m(2) did not show significant differences of corresponding AUC values for S(cyst) and S(cr) although there was a trend for superiority of S(cyst) in comparison with S(cr). The multiples of upper reference values of S(cyst) and S(cr) in examined patients did not differ significantly. There was a highly significant linear correlation between C(in) and C(cr) in pre-dialysis patients (r = 0.921, p < 0.001). The regression coefficient of this relation (1.279) was significantly higher than 1.0 (p < 0.001) and the value of intercept (6.50 ml/min/1.73 m(2)) was significantly higher than zero (p < 0.001). The average of C(cr)/C(in) in patients with C(in) <10 ml/min/1.73 m(2) was 2.11 (+/- 0.29) and 1.72 (+/- 0.35) for those with C(in) 10-20 ml/min/1.73 m(2). CONCLUSIONS: The findings suggest that in patients with advanced chronic renal insufficiency (CRI) for the same decrease in GFR the increase of S(cyst) is not significantly higher than that of S(cr), although the tubular secretion of creatinine is significantly increased. Further studies (especially those focused on nonrenal elimination of cystatin C) are needed to elucidate the lack of difference between changes in S(cyst) and S(cr) in patients with CRI.

Adolescent↗
PubMed1999

Cystatin C as a determinant of fasting plasma total homocysteine levels in coronary artery disease patients with normal serum creatinine.

Serum creatinine, a surrogate for both renal function and homocysteine generation, is a determinant of fasting plasma total homocysteine levels in coronary artery disease (CAD) patients. We hypothesized that among stable-CAD patients with normal creatinine levels (ie, </=1.4 mg/dL), serum cystatin C, a more sensitive indicator of glomerular filtration rate, would better predict fasting total homocysteine levels in comparison with serum creatinine. Fasting plasma total homocysteine, folate, vitamin B(12), and pyridoxal 5'-phosphate levels, along with serum cystatin C, creatinine, and albumin levels, were determined in 164 consecutive stable-CAD patients (mean+/-SD age, 61+/-9 years; 78.7% men) whose serum creatinine level was </=1.4 mg/dL. All subjects were examined at least 3 to 4 months after the widespread availability of cereal grain flour products fortified with folic acid. General linear modeling with ANCOVA revealed that serum cystatin C (P<0.001), B(12) (P<0.001), age (P=0.002), albumin (P=0.008), and sex (P=0.024) were independent determinants of fasting total homocysteine levels. Cystatin C alone determined over half of the variability (ie, R(2)) in total homocysteine levels accounted for by these 5 independent regressors. In contrast, creatinine, folate, and pyridoxal 5'-phosphate were not independently predictive of fasting total homocysteine levels (P>0.2). Consistent with the impact of folic acid fortification of cereal grain flour in the general population, only 1 of the CAD subjects (0.6%) had a plasma folate level <3 ng/mL. We conclude that serum cystatin C levels may reflect subtle decreases in renal function that independently predict fasting total homocysteine levels among stable-CAD patients with normal serum creatinine.

Adult↗
PubMed2005

Cystatin C deficiency increases elastic lamina degradation and aortic dilatation in apolipoprotein E-null mice.

The pathogenesis of atherosclerosis and abdominal aortic aneurysm involves substantial proteolysis of the arterial extracellular matrix. The lysosomal cysteine proteases can exert potent elastolytic and collagenolytic activity. Human atherosclerotic plaques have increased cysteine protease content and decreased levels of the endogenous inhibitor cystatin C, suggesting an imbalance that would favor matrix degradation in the arterial wall. This study tested directly the hypothesis that impaired expression of cystatin C alters arterial structure. Cystatin C-deficient mice (Cyst C-/-) were crossbred with apolipoprotein E-deficient mice (ApoE-/-) to generate cystatin C and apolipoprotein E-double deficient mice (Cyst C-/-ApoE-/-). After 12 weeks on an atherogenic diet, cystatin C deficiency yielded significantly increased tunica media elastic lamina fragmentation, decreased medial size, and increased smooth muscle cell and collagen content in aortic lesions of ApoE-/- mice. Cyst C-/-ApoE-/- mice also showed dilated thoracic and abdominal aortae compared with control ApoE-/- mice, although atheroma lesion size, intimal macrophage accumulation, and lipid core size did not differ between these mice. These findings demonstrate directly the importance of cysteine protease/protease inhibitor balance in dysregulated arterial integrity and remodeling during experimental atherogenesis.

Animals↗
PubMed1999

Cystatin C deficiency in human atherosclerosis and aortic aneurysms.

The pathogenesis of atherosclerosis and abdominal aortic aneurysm involves breakdown of the elastic laminae. Elastolytic cysteine proteases, including cathepsins S and K, are overexpressed at sites of arterial elastin damage, but whether endogenous local inhibitors counterbalance these proteases is unknown. We show here that, whereas cystatin C is normally expressed in vascular wall smooth muscle cells (SMCs), this cysteine protease inhibitor is severely reduced in both atherosclerotic and aneurysmal aortic lesions. Furthermore, increased abdominal aortic diameter among 122 patients screened by ultrasonography correlated inversely with serum cystatin C levels. In vitro, cytokine-stimulated vascular SMCs secrete cathepsins, whose elastolytic activity could be blocked when cystatin C secretion was induced by treatment with TGF-beta(1). The findings highlight a potentially important role for imbalance between cysteine proteases and cystatin C in arterial wall remodeling and establish that cystatin C deficiency occurs in vascular disease.

Aorta↗
PubMed2000

Detection of immature dendritic cells in the enamel organ of rat incisors by using anti-cystatin C and anti-MHC class II immunocytochemistry.

Dendritic cells in the enamel organ of rat incisors were examined with immunocytochemistry using an anti-cystatin C antibody for immature dendritic cells and macrophages, OX6 for MHC Class II, ED1 for macrophages and dendritic cells, and ED2 for macrophages. Single cells positive for anti-cystatin C appeared in the enamel organ in zones at which ameloblasts secrete enamel matrix proteins. They were also present in transition and enamel maturation zones. In addition, ameloblasts, osteocytes, and osteoclasts were labeled by anti-cystatin C. ED1 and ED2 immunocytochemistry revealed that there was no macrophage population in the enamel organ of secretion, transition, or enamel maturation zone. A double labeling study showed that most anti-cystatin C-positive cells in the enamel maturation zone were also positive for OX6, whereas anti-cystatin C-positive and OX6-negative cells were prevalent in the secretion zone. The results suggest that immature dendritic cells penetrate the enamel organ of the secretion zone and begin to mature in the zones of transition and enamel maturation. (J Histochem Cytochem 48:1243-1255, 2000)

Ameloblasts↗
PubMed2001

Plasma levels of cystatin-C and mannose binding protein are not associated with risk of developing systemic atherosclerosis.

Cystatin-C, a cysteine protease inhibitor, and mannose binding lectin, an innate defense protein involved in microbial clearance, have both been hypothesized to mediate atherosclerotic plaque progression. Prospective data evaluating whether levels of these proteins are associated with incident cardiovascular disease are sparse. Employing a prospective, nested, case-control study design, baseline levels of cystatin-C and mannose binding protein were evaluated among 133 apparently healthy men who subsequently developed symptomatic peripheral arterial disease (cases) and among 133 age- and smoking-matched controls who remained free of reported vascular disease during 5 years of follow-up. Overall, median baseline levels of cystatin-C were virtually identical among case and control subjects (0.83 mg/l, p = 0.84), whereas median baseline levels of mannose binding protein among cases and controls were 2.32 mg/l and 2.20 mg/l respectively (p = 0.69). No evidence of association was found between either cystatin-C or mannose binding protein and the development of peripheral arterial disease in analyses evaluating for linear trends or for threshold effects (all p-values > 0.05). In contrast with prior retrospective and cross-sectional studies, no evidence was found that baseline levels of cystatin-C or mannose binding protein are associated with an increased risk of future arterial disease.

Adult↗
PubMed2003

Cystatin C improves the detection of mild renal dysfunction in older patients.

BACKGROUND: Conventional estimates of glomerular dysfunction, including serum creatinine and creatinine clearance, are inadequate in older people. In this study we have compared the diagnostic accuracy of a novel test of kidney disease, cystatin C, against these markers in older patients with a range of renal function. METHODS: Fifty-three patients (mean age 79.6 years, range 69-92 years) with a variety of medical diagnoses were recruited via outpatient clinics. Exclusion criteria included active rheumatoid disease, known current malignancy, renal replacement therapy/renal transplantation and cognitive impairment. (51)Cr-EDTA was used as the reference method against which the other markers of glomerular filtration rate were compared using regression analyses. RESULTS: The best fit with glomerular filtration rate was given by Cockcroft and Gault calculated clearance (R(2) = 0.83), followed by serum cystatin C (R(2) = 0.79), serum creatinine (R(2) = 0.76) and creatinine clearance (R(2) = 0.73). The accuracy for glomerular filtration rate prediction was poor for all markers. Serum cystatin C detected nearly all patients with mild renal impairment whereas serum creatinine only detected half of these cases. Regression modelling predicted that the upper limit of normal for serum cystatin C would be exceeded as glomerular filtration rate fell below 64 mL/min/1.73 m(2), compared with 44 mL/min/1.73 m(2) for serum creatinine. CONCLUSION: Serum cystatin C is a simple and sensitive screening test for kidney dysfunction in older people.

Aged↗
PubMed2003

Measurement of renal function in kidney donors using serum cystatin C and beta(2)-microglobulin.

BACKGROUND: The usefulness of serum cystatin C and serum beta(2)-microglobulin (B2M) as markers of glomerular filtration rate (GFR) were compared in kidney donors before and after nephrectomy. METHODS: Blood samples were taken from 28 donors (15 women and 13 men) for serum creatinine, urea, cystatin C and B2M estimation a median of 7 days before and 10 days after nephrectomy. RESULTS: Estimated GFR decreased from a median of 86.2 mL/min/1.73 m(2) to 60.3 mL/min/1.73 m(2), a median decrease of 28.6%. Serum creatinine increased by 40% and urea by 30.4%; serum cystatin C increased by 31.2% and serum B2M increased by 65.6%. Using published data on biological variation, critical values were calculated. An increase in serum creatinine above 18 micro mol/L detected the decline in renal function in 26/28 (92.9%) subjects. Increases in serum B2M greater than a critical value of 0.94 mg/L detected 24/28 (85.7%) of these subjects, but the critical value of 0.59 mg/L for cystatin C detected only 8/28 (28.6%). CONCLUSION: Using critical values, serial measurement of serum creatinine was better than serum B2M in detecting reduced renal function. Because of its large intraindividual variation, serial serum cystatin C estimation was very poor in detecting reduced renal function.

Adult↗
PubMed2005

Simple cystatin C-based prediction equations for glomerular filtration rate compared with the modification of diet in renal disease prediction equation for adults and the Schwartz and the Counahan-Barratt prediction equations for children.

BACKGROUND: Serum creatinine is the most commonly used marker for estimation of glomerular filtration rate (GFR). To compensate for its drawbacks as a GFR marker, several prediction equations including several parameters are being used, with the Modification of Diet in Renal Disease (MDRD), Schwartz, and Counahan-Barratt equations being the ones most widely accepted for estimation of relative GFR in mL x min(-1) x (1.73 m(2))(-1). The present study analyzes whether these GFR prediction equations for adults and children might be replaced by simple prediction equations based on plasma concentrations of cystatin C. METHODS: Data from 536 patients (0.3-93 years), consecutively referred for determination of GFR by an invasive gold standard procedure, were used for the analysis. Calculations of bias (median percentage of error), correlation (adjusted R(2)), and percentage of estimates within 30% and 50% of measured GFR were used in the comparisons. RESULTS: A cystatin C-based prediction equation using only concentration in mg/L and a prepubertal factor: GFR [mL x min(-1) x (1.73 m(2))(-1)] = 84.69 x cystatin C (mg/L)(-1.680) x 1.384 (if a child <14 years) assessed GFR equally well or better than the simplified MDRD, the Schwartz, and the Counahan-Barratt prediction equations for the adult (> or =18 years) and juvenile groups of the investigated cohort. Age did not influence the cystatin C-based prediction equation for adults, whereas gender did, but with a factor close to unity (0.948 for females). CONCLUSION: A GFR prediction equation based solely on cystatin C (in mg/L) and a prepubertal factor might replace the simplified MDRD prediction equation for adults and the Schwartz and Counahan-Barratt prediction equations for children.

Adolescent↗
PubMed1998

Reference intervals for serum cystatin C and serum creatinine in adults.

The aim of this study was to establish reference intervals for cerum cystatin C and serum creatinine in adults. Blood samples were collected from 270 healthy blood donors (135 men and 135 women between 20 and 65 years old with 15 men and 15 women in each five-year-interval). Serum cystatin C was analyzed using an automated particle-enhanced immunoassay (DAKO Cystatin C PET kit) on the Cobas Mira S analyzer. Serum creatinine was analyzed using the Vitros Creatinine Slide, an enzymatic method on the Vitros 950 chemistry analyzer. The calculated reference intervals for serum cystatin C were 0.62-1.15 mg/l in women (median 0.84 mg/l, range 0.56-1.29 mg/l) and 0.51-1.25 mg/l in men (median 0.87 mg/l, range 0.42-1.39 mg/l). The Mann-Whithey U-test revealed no gender-related difference for cystatin C (p = 0.48). A common reference interval in women and men was calculated to be 0.54-1.21 mg/l (median 0.85 mg/l, range 0.42-1.39 mg/l). The non-parametric reference interval for serum creatinine was 57-95 mumol/l in women (median 72 mumol/l, range 44-105 mumol/l) and 69-111 mumol/l in men (median 89 mumol/l, range 58-123 mumol/l).

Adult↗
PubMed2002

Diagnostic efficiency of cystatin C and serum creatinine as markers of reduced glomerular filtration rate in the elderly.

This is a secondary analysis of data from a cross-sectional study to evaluate the diagnostic efficiency of cystatin C as a marker of the glomerular filtration rate in the elderly. Thirty patients (15 male, 15 female, mean age 75.4 +/- 7.1 years) attending a geriatric ward were enrolled. Exclusion criteria were previously diagnosed renal disease, dementia and heart failure (NYHA III or IV). Cystatin C in serum was determined by a particle-enhanced turbidimetric assay. Inulin clearance was assessed using a single-shot method. Also, Cockcroft-Gault formula was calculated. Twelve patients had a reduced glomerular filtration rate (<70 ml/min/ 1.73 m2). The mean values were 88.4 micromol/l (+/- 27.7) for serum creatinine, 1.57 mg/l (+/- 0.34) for cystatin C and 88.7 ml/min/1.73 m2 (+/- 34.6) for inulin clearance. Maximum efficiency was 0.73 for serum creatinine (cut-off limit 82 micromol/l), 0.67 for cystatin C (cut-off limit 1.63 mg/l) and 0.8 for Cockcroft and Gault estimation (cut-off limit 54 ml/min/1.73 m2). A receiver operating characteristics (ROC) analysis did not show any differences between the various methods. Therefore, cystatin C in serum may not improve the diagnostic efficiency in detecting a reduced glomerular filtration rate in the elderly. Furthermore, normal ranges for serum creatinine in the elderly might need to be adjusted.

Age Factors↗
PubMed2006

Variations in assay protocol for the Dako cystatin C method may change patient results by 50% without changing the results for controls.

BACKGROUND: Cystatin C is increasingly used as a glomerular filtration marker, but so far only a few companies produce most of the cystatin C reagents suited for turbidimetry or nephelometry use in clinical laboratories. METHODS: We studied different protocols for measuring cystatin C on an Architect ci8200 system using cystatin C reagents from Dako (Glostrup, Denmark). The results were compared with those obtained with Dade Behring reagents (Deerfield, IL, USA) on a BN ProSpec system. RESULTS: Differences in assay protocol on the same instrument with the Dako reagent yielded an up to 50% difference in glomerular filtration rate calculated from the cystatin C results when analyzing patient samples, but had no effect on the results for controls. There were also significant differences regarding linearity and kinetics between samples and controls/calibrators. CONCLUSIONS: The results indicate different reactivity of the Dako antibodies against calibrators and controls in comparison with patient samples, highlighting the importance of using controls and calibrators that do not differ from patient samples.

Calibration↗
PubMed2001

Homocysteine and cystatin C level changes in haemodialysed patients and connection with cerebro- and cardiovascular complications.

Plasma homocysteine and Cystatin C levels of 360 chronic haemodialysed patients were measured in fasting (191 men, mean age: 55.5 years; and 169 women, mean: 62.9 years). The patients were divided into subgroups: diabetes mellitus (34 men and 38 women 7 vs 8 IDDM). obliterative arteriosclerosis (68 men and 61 women), cardiovascular complications (75 men and 84 women) and stroke (16 men and 12 women), and after renal transplantation in chronic rejection (15 men and 5 female). Homocysteine was determined by IMx analyser from Abbott by FPIA method. Immunoturbidimetric method was used for quantification of Cystatin C (PETIA). The lowest Cystatin C concentration was found in diabetic patients (4.35 +/- 0.15 mg/l in men and 3.18 +/- 1.77 mg/l in women) and the highest one occurred in anuric and bilateral nephrectomised and transplanted chronic rejected patients (6.075 mg/l in men and 6.35 mg/l in women: p<0.001). The homocysteine levels (24.98 +/- 2.94 micromol/l in men and 23.88 +/- 1.76 micromol/l in women) exceeded the upper limit of reference range (<15.0 micromol/l). There was a significant difference in favour of subgroup of cardiovascular (27.25 micromol/l in men and 26.87 micromol/l in women) and stroke patients (27.16 micromol/l in men and 30.76 micromol/l in women p<0.001). Elevated levels were found in chronic rejected patients with accelerated arteriosclerotic events (25.94 micromol/l in men and 27.43 micromol/l in women). Good positive linear correlation was found between serum homocysteine and Cystatin C levels (r=0.2393 and 0.2252). The authors demonstrated hyperhomocysteinaemia associated with high Cystatin C concentration in four subgroups of haemodialysed patients (obliterative and accelerated arteriosclerosis, cardiovascular disease, and cerebrovascular complications and stroke).

Adolescent↗
PubMed1999

Serum cystatin C as a determinant of fasting total homocysteine levels in renal transplant recipients with a normal serum creatinine.

Serum creatinine, a surrogate for both renal function and homocysteine generation, is an important determinant of fasting plasma total homocysteine levels in stable renal transplant recipients. In this study, it is hypothesized that among stable renal transplant recipients with normal creatinine levels (i.e., < or = 1.5 mg/dl), serum cystatin C, a more sensitive indicator of GFR, would better predict fasting total homocysteine levels compared with serum creatinine. Fasting plasma total homocysteine, folate, vitamin B12, and pyridoxal 5'-phosphate levels, along with serum cystatin C, creatinine, and albumin levels, were determined in 28 consecutive renal transplant recipients (mean age 47 +/- 14 yr; 60.7% men) with stable allograft function, whose serum creatinine was < or = 1.5 mg/dl. General linear modeling with analysis of covariance revealed that serum cystatin C was independently predictive (partial R = 0.494; P = 0.023) of fasting total homocysteine levels after adjustment for age, gender, vitamin status, albumin, and creatinine levels. In contrast, creatinine levels were not predictive of fasting total homocysteine levels in this model (P = 0.110) or an identical model that excluded cystatin C (P = 0.131). Serum cystatin C levels may reflect subtle decreases in renal function that independently predict fasting total homocysteine levels among stable renal transplant recipients with a normal serum creatinine.

Adult↗