Measurement of cystatin-C and creatinine in urine. Clin Chim Acta

Kyoto Medical Science Laboratory, 328 Furukawa-cho, Hazukashi Fushimi-ku, 612-8486, Kyoto, Japan.
Clinica Chimica Acta (Impact Factor: 2.82). 10/2002; 323(1-2):121-8. DOI: 10.1016/S0009-8981(02)00177-8
Source: PubMed


The concentration of serum cystatin-C (Cys-C) is highly correlated with creatinine (Cr), and is mainly determined by glomerular filtration; thus, Cys-C may be an index of the glomerular filtration rate (GFR). However, the kinetics of urinary Cys-C and Cr excretions are unclear. Thus, we investigated the kinetics of urinary Cys-C and Cr excretions, and examined whether the urinary Cys-C concentration can be used as a marker of renal function.
The urinary excretion of Cys-C and Cr was evaluated in 1670 healthy subjects and 217 patients with proteinuria. We also investigated the urinary Cys-C concentration in 52 patients with chronic renal failure.
There was a good correlation between the urinary concentrations of Cys-C and Cr in the healthy group. This relation was also observed in patients showing persistent proteinuria without tubular cell damage. The mean urinary Cr concentration increased with age, and it was affected by the muscle mass. In contrast, the urinary Cys-C concentration was not affected by the muscle mass, and the concentration remained constant for all ages. We further found that the ratio of Cys-C to Cr (CCR) is a good index of the state of Cys-C reabsorption in the proximal tubules.
The urinary CCR can be a marker of renal tubular dysfunction. In addition, when CCR was in the normal range, the urinary Cys-C concentration accurately reflected the glomerular filtration function.

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    • "Any process that impairs renal tubules affects cystatin C reabsorption. Therefore, AKI can be associated with elevated urinary cystatin C levels [77, 78]. Particularly it appears that elevated urinary cystatin C levels are an indication of tubular dysfunction [76]. "
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    ABSTRACT: Traditional diagnosis of acute kidney injury (AKI) depends on detection of oliguria and rise of serum creatinine level, which is an unreliable and delayed marker of kidney damage. Delayed diagnosis of AKI in the critically ill patient is related to increased morbidity and mortality, prolonged length of stay, and cost escalation. The discovery of a reliable biomarker for early diagnosis of AKI would be very helpful in facilitating early intervention, evaluating the effectiveness of therapy, and eventually reducing cost and improving outcome. Innovative technologies such as genomics and proteomics have contributed to the discovery of new biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (Cys C), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and liver-type fatty acid binding protein (L-FABP). The current status of the most promising of these novel AKI biomarkers, including NGAL, Cys C, KIM-1, L-FABP, and IL-18, is reviewed.
    Full-text · Article · Feb 2013 · Critical care research and practice
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    • "However, since creatinine is influenced by age, muscle mass and food intake, it has a disadvantage to reflect the glomerular filtration rate inaccurately. Therefore, there are continuing debates about other indicators to measure the glomerular filtration23,24). Cystatin-C (Cys-C) is widely being used now as an indicator to reflect the renal function relatively accurate without the limitation of age, muscle mass, and protein intakes compared to creatinine25). "
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    ABSTRACT: Kawasaki disease (KD) is a systemic vasculitis and affects many organ systems. It often presents sterile pyuria, microscopic hematuria, and proteinuria due to renal involvement. The aims of this study were to define clinical characteristics of acute KD patients with pyuria and to analyze meaning of pyuria in KD. The medical records and laboratory findings including serum and urine test of 133 patients with KD admitted to Yeungnam University Hospital from March 2006 to December 2010 were reviewed retrospectively. Forty patients had sterile pyuria and their clinical characteristics including age, gender and body weight were not significantly different with those who did not have pyuria. Fever duration after treatment was significantly longer in KD patients with pyuria. Erythrocyte sedimentation rate, C-reactive protein and serum concentration of alanine aminotransferase were significantly higher in patients with pyuria. Hyponatremia and coronary artery lesion were seen more often in patients with pyuria but there was no significant difference. Also serum blood urea nitrogen was significantly higher in KD patients with pyuria. Urine β(2)-microglobulin was elevated in both patients groups and showed no difference between two groups. We found more severe inflammatory reaction in KD patients with pyuria. We also found elevation of some useful parameters like β(2)-microglobulin that indicate renal involvement of KD through the urine test. Careful management and follow up will need for KD patients with pyuria and it is necessary in the future to study the specific parameters for renal involvement of KD.
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    • "In healthy subjects, cystatin C is almost freely filtered by the renal glomeruli and almost entirely reabsorbed in the proximal tubule like other low molecular weight proteins; there is no tubular secretion of cystatin C (12–14). Similar to the serum cystatin C, the urinary cystatin C level is not affected by age or muscle mass in healthy subjects or in proteinuric patients without renal tubular damage (15). On the other hand, increased urinary cystatin C has been recognized as a marker of renal tubular dysfunction (16,17). "
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    ABSTRACT: OBJECTIVE The aim of this study was to evaluate the association of urinary cystatin C, a tubular damage marker, with the progression of type 2 diabetic nephropathy.RESERCH DESIGN AND METHODS The baseline values of serum and urinary cystatin C were measured as primary parameters and those of urinary nonalbumin protein (NAP) were measured as secondary parameters. In this prospective observational study, a total of 237 type 2 diabetic patients were followed up for 29 months (13-44 months).RESULTSBoth the urinary cystatin C-to-creatinine ratio (CCR) and NAP-to-creatinine ratio (NAPCR) were significantly different according to the degree of albuminuria. Both markers had strongly positive correlations at baseline. After adjusting for several clinical factors, both urinary CCR and NAPCR had significant associations with the decline of the estimated glomerular filtration rate (eGFR) (r = 0.160, P = 0.021; r = 0.412, P < 0.001, respectively). Urinary CCR had positive correlations with the decline of eGFR in the subpopulation of patients with eGFR ≥60 mL/min/1.73 m(2). In patients with eGFR ≥60 mL/min/1.73 m(2) and normoalbuminuria, only urinary NAPCR showed a significant association with the decline of eGFR; urinary CCR did not. In multivariate regression analysis, the number of patients who progressed to chronic kidney disease stage 3 or greater was higher in those in the upper tertiles of both the urinary levels of cystatin C and NAP than in those in the lower tertiles.CONCLUSIONS The results of this study suggest that urinary cystatin C and NAP may be predictors of the progression of type 2 diabetic nephropathy.
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