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)

We compared the levels of transforming growth factor beta1 (TGF-beta1), vascular endothelial growth factor (VEGF) and other biochemical parameters in patients with type 1 diabetes mellitus with and without incipient diabetic nephropathy (iDN) and compared them with healthy control subjects. We also measured the effect of 3 and 6 months of ramipril treatment in diabetes patients with iDN. Compared with healthy controls, TGF-beta1 levels were increased in both groups of diabetes patients, whereas VEGF was only elevated in patients with iDN. Ramipril did not have a significant effect on TGF-beta1 or VEGF levels. We observed a significant decrease in microalbuminuria and cystatin C following ramipril treatment. Increased VEGF levels in patients with iDN suggest a role for this cytokine in the pathogenesis of diabetic nephropathy. Cystatin C would make a suitable marker for the screening and assessment of iDN, and for the evaluation of the therapeutic efficacy of drugs.
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PMID:The effect of ramipril therapy on cytokines and parameters of incipient diabetic nephropathy in patients with type 1 diabetes mellitus. 1759 66

In a clinic-based, cross-sectional study of 320 type 2 diabetic patients, we staged the level of diabetic nephropathy (normoalbuminuric, microalbuminuric and macroalbuminuric stage) and estimated GFR based on serum creatinine and cystatin C (CysC). Serum creatinine and CysC levels were 0.91+/-0.21 mg/dL and 0.87+/-0.26 mg/L, respectively. Correlation coefficients between CysC-GFR and each of the creatinine-based GFR measurements (MDRD-GFR, Cockcroft-Gault-GFR, and CLcr) were 0.589, 0.569, and 0.479 (p<0.001). Serum CysC was significantly lower in normoalbuminurics (0.83+/-0.22) than in microalbuminurics and macroalbuminurics (0.94+/-0.33 and 1.05+/-0.28; p=0.004 and p<0.001). Of the estimations of GFR, significant differences among the groups were found on CysC-GFR and CLcr. CysC-GFR (mL/min) was statistically lower in macroalbuminurics (79.5+/-30.5) than in normoalbuminurics (104.3+/-30.9, p=0.01). The logistic regression analyses showed that retinopathy, A1C, CysC, diabetic duration, and CysC-GFR were indicators to predict the development of microalbuminuria. Serum CysC seems to be more accurate serum marker than serum creatinine in evaluating a prognostic stage of type 2 diabetic nephropathy. Our study suggests that, in Korean type 2 diabetic patients, CysC-based GFR might be more valuable than creatinine-based GFR in the prediction of the microalbuminuric stage.
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PMID:The comparison of cystatin C and creatinine as an accurate serum marker in the prediction of type 2 diabetic nephropathy. 1782 97

Serum cystatin C (CysC) has been proposed as a potentially superior marker for the evaluation of renal function because it was more sensitive and accurate for the estimation of glomerular filtration rate (GFR) than other markers. We evaluated the clinical usefulness of CysC in diabetic nephropathy. The study was performed on 414 Japanese diabetic patients. We compared serum CysC levels with serum creatinine levels, urinary concentrations of albumin, transferrin and type IV collagen, and creatinine clearance (Ccr). Then, the correlation between serum CysC levels and high-sensitivity C-reactive protein (H-CRP) levels were examined. When the patients were classified by renal function, 19% of the patients were free from nephropathy, 49% had microalbuminuria, 28% had persistent proteinuria, and 4% had end stage renal disease. The serum CysC levels increased with the progression of nephropathy, and significantly higher in overt nephropathy, but not significant in early nephropathy. Serum CysC levels were well-correlated with H-CRP levels in the patients without nephropathy. These results indicate that serum CysC would be practical for the evaluation of renal function in diabetic patients with overt nephropathy but not early nephropathy and might be related with a risk for cardiovascular events in patients without nephropathy.
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PMID:Serum cystatin C in diabetic patients. Not only an indicator for renal dysfunction in patients with overt nephropathy but also a predictor for cardiovascular events in patients without nephropathy. 1798 Sep 29

The aim is to review the tools for early detection of renal dysfunction after pediatric solid organ transplantation. Currently, the most widely used marker for detection of renal dysfunction involves measurement of GFR. Inulin clearance forms the "gold standard" method for measuring GFR; however, nuclear medicine methods ((51)Cr EDTA and (99)Tc DTPA isotope clearance studies) have replaced inulin clearance. The measurement of serum creatinine has a low sensitivity for the early detection of renal damage. The Schwartz formula using patient height and serum creatinine requires center-specific constants and has limitations associated with creatinine determination. These limitations may be overcome using a cystatin C-based GFR estimation. In diabetic nephropathy, and more recently in hemolytic uremic syndrome, microalbuminuria has been established as a useful screening tool for renal damage, while its predictive value in the transplantation setting needs to be established. All transplant recipients should be screened for hypertension. Early referral for ambulatory 24-h blood pressure monitoring and involvement of pediatric nephrologists should be considered. All pediatric solid organ transplant recipients receiving CNI should be screened regularly for high blood pressure and early evidence of renal damage using either GFR scans or cystatin C-based GFR estimations.
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PMID:How to monitor renal function in pediatric solid organ transplant recipients. 1817 36

Methods for assessment of chronic kidney disease (CKD) are advancing worldwide. To this end, the Subcommittee of Measures for Pediatric CKD in the Japanese Society for Pediatric Nephrology was started in 2006. This Subcommittee has embarked on a multidisciplinary study for determining the normal/usual baseline value of serum creatinine and cystatin C, and standardizing the method of inulin clearance in children. For adults, pharmacotherapies such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been shown to be effective in non-diabetic nephropathy. This same treatment for childhood CKD is generally adopted, but there is no corresponding evidence of similar efficacy. We believe a randomized controlled trial to that end should be undertaken.
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PMID:[Chronic kidney disease in children]. 1878 15

The onset of diabetic nephropathy is characterised by a rise in albumin excretion rate (AER) and/or a transient rise in glomerular filtration rate (GFR) (hyperfiltration). Without intervention AER increases exponentially and there is a linear decrease in GFR after onset of overt nephropathy. In overt nephropathy, AER is a predictor of decline in GFR and the early AER response to antihypertensive therapy correlates with long-term decline in GFR. AER can be measured by immunoassay or by other techniques including HPLC. However, HPLC assays result in higher levels of AER in normal subjects compared with immunoassayable AER. Recent data suggest that there are distinct albuminuric and non-albuminuric pathways to renal impairment in type 1 and type 2 diabetes. In type 2 diabetes, the non-albuminuric pathway may explain a decline in GFR to <60 ml/min/1.73 m(2) in approximately one in four subjects after accounting for the use of renin angiotensin system inhibitors. In established nephropathy (chronic kidney disease (CKD) stages 3 and 4), plasma cystatin C based estimates of GFR are marginally superior to creatinine based estimates. However, cystatin C clearly outperforms creatinine based estimates of GFR decline at GFR levels >60 ml/min/1.73 m(2) (CKD stages 1 and 2). Other potential markers of progression of diabetic nephropathy include transforming growth factor beta (TGFbeta) and connective tissue growth factor (CTGF). However, long-term studies are needed to define their roles as markers of progression. Diabetic nephropathy is likely to be more susceptible to intervention at an early stage and accurate estimation of GFR is already possible with cystatin C. However, improved formulas for estimating GFR based on using creatinine or other markers are still required, because this may still provide the most cost effective approach applicable to existing clinical practice.
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PMID:New and old markers of progression of diabetic nephropathy. 1893 92

Medications to treat hyperglycemia and hyperinsulinemia are expected to inhibit the accumulation of advanced glycation end-products in the diabetic kidney and improve renal function by inhibiting oxidative reactions. In this study, we examined the effect of pioglitazone, an insulin sensitizer, on diabetic nephropathy. Feed containing pioglitazone at 0.01 or 0.02% was given to Zucker-fatty rats for 27 weeks. Pioglitazone reduced plasma glucose, plasma insulin, and blood HbAlc levels. It also decreased plasma total cholesterol, triglyceride, phospholipid and cystatin C levels and inhibited the increase in urine of 8-hydroxydeoxyguanosine and in plasma of malondialdehyde. In the histopathological examinations, pioglitazone inhibited diffusive or nodular thickening of the mesangial matrix, atrophy of the proximal convoluted tubule, thickening of the basement membrane of the tubule, and mild cellular infiltration (mostly small lymphocytes) in the stroma. Furthermore, pioglitazone inhibited the mRNA expression of the receptor for advanced glycation end-products (RAGE) and that of transforming growth factor-beta. Long-term administration of pioglitazone improved hyperglycemia lipid profiles, hypercholesterolemia, and hyperinsulinemia and had a protective effect on diabetic nephropathy in Zucker-fatty rats.
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PMID:Pioglitazone improves obesity type diabetic nephropathy: relation to the mitigation of renal oxidative reaction. 1894 78

We initiated the present work to explore whether neutrophil gelatinase-associated lipocalin (NGAL) could be used to predict the progression of diabetic nephropathy in type-2 diabetic patients. Seventy-four type-2 diabetic patients were divided into normo-, micro- and macro-albuminuria groups according to their 24 h-urinary albumin excreting rate. Serum and urine NGAL, and other clinical parameters were detected. Patients were followed and measurements were repeated 1 year later. An increased tendency of urine NGAL and a decreased tendency of serum NGAL were detected, from normo-albuminuria group to macro-albuminuria group. Serum NGAL was found to rise after follow-up. Moreover, urine NGAL was found to be correlated positively with cystatin C, urea nitrogen, and serum creatinine (SCr), and inversely with glomerular filtration rate (GFR), while serum NGAL correlated negatively with cystatin C and urea nitrogen, at both baseline and follow-up levels. The results indicate that NGAL correlates closely with renal function. Both serum and urine NGAL are sensitive for predicting the progression of type-2 diabetic nephropathy but they may change differently. Serum NGAL may be more useful in early detection and urine NGAL may be more meaningful in renal function assessment.
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PMID:Changes of serum and urine neutrophil gelatinase-associated lipocalin in type-2 diabetic patients with nephropathy: one year observational follow-up study. 1939 Sep 97

This study was designed to evaluate the usefulness of serum cystatin C (CysC) as a marker of renal function in 83 patients with diabetic nephropathy, considering multiple factors including tubular function and body mass index. Serum CysC was assayed using a particle-enhanced nephelometric immunoassay and the glomerular filtration rate (GFR) was obtained by measuring the plasma disappearance of the isotope (99m)Tc-diethylenetriamine penta-acetic acid. By comparing the correlation of CysC and serum creatinine (SCr) with GFR, it was concluded that CysC may be a better indicator of GFR than SCr in diabetic patients, in both the early hypertransfusion stage and in the late renal dysfunction stage. CysC showed a slightly higher sensitivity for renal function evaluation than SCr in patients with renal tubular dysfunction and moderate to severe proteinuria. In addition, CysC was not affected by the metabolic index. Thus, CysC may serve as an ideal endogenous marker of GFR in patients with diabetic nephropathy.
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PMID:Evaluation of glomerular filtration rate using cystatin C in diabetic patients analysed by multiple factors including tubular function. 2051 62

Diabetic nephropathy is the kidney disease that occurs as a result of diabetes. Cardiovascular and renal complications share common risk factors such as blood pressure, blood lipids, and glycemic control. Thus, chronic kidney disease may predict cardiovascular disease in the general population. The impact of diabetes on renal impairment changes with increasing age. Serum markers of glomerular filtration rate and microalbuminuria identify renal impairment in different segments of the diabetic population, indicating that serum markers as well as microalbuminuria tests should be used in screening for nephropathy in diabetic older people. The American Diabetes Association and the National Institutes of Health recommend Estimated glomerular filtration rate (eGFR) calculated from serum creatinine at least once a year in all people with diabetes for detection of kidney dysfunction. eGFR remains an independent and significant predictor after adjustment for conventional risk factors including age, sex, duration of diabetes, smoking, obesity, blood pressure, and glycemic and lipid control, as well as presence of diabetic retinopathy. Cystatin-C (Cys C) may in future be the preferred marker of diabetic nephropathy due differences in measurements of serum creatinine by various methods. The appropriate reference limit for Cys C in geriatric clinical practice must be defined by further research. Various studies have shown the importance of measurement of albuminuria, eGFR, serum creatinine and hemoglobin level to further enhance the prediction of end stage renal disease.
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PMID:Renal function in diabetic nephropathy. 2153 27


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