Keiko Nakai1, Masayuki Kikuchi2, Keiko Fujimoto2, Yoshito Kaneko3, So Omori4, Kenji Nakai5, Akira Suwabe5. 1. Department of Laboratory Medicine, Iwate Medical University, 19-1 Uchimaru, Morioka, 020-8505, Japan. keikoyn@iwate-med.ac.jp. 2. Department of Clinical Laboratory, Iwate Medical University Hospital, Morioka, Japan. 3. Department of Diabetes and Metabolism, Iwate Medical University, Morioka, Japan. 4. Department of Urology, Iwate Medical University, Morioka, Japan. 5. Department of Laboratory Medicine, Iwate Medical University, 19-1 Uchimaru, Morioka, 020-8505, Japan.
Abstract
BACKGROUND: Serum levels of cystatin C have been proposed to be an ideal marker of the glomerular filtration rate (GFR). However, some reports have shown that serum levels of cystatin C increase independently of GFR. In this study, we evaluated the clinical utility of cystatin C in monitoring GFR, especially in patients with a malignancy. METHOD: Study subjects consisted of 82 patients with a malignancy, 39 patients with a non-malignancy, 31 healthy volunteers, and 206 patients with various degrees of renal function. We measured serum cystatin C, beta2-microglobulin (beta 2mG), and creatinine (CRE) levels in all patients. Serum CRP levels were measured in 21 patients with a malignancy and 28 patients with a non-malignancy whose creatinine clearance (Ccr) was > or =70 ml/min. Cystatin C, beta 2mG, and CRP were measured by immune nephelometry and CRE was measured by an enzyme assay. RESULTS: In patients with a malignancy, regression analysis yielded the equation: 1/cystatin C = 0.06 x Ccr + 0.710, correlation coefficient, r, of 0.33. The r was significantly lower than in patients with various degrees of renal function. There were no significant differences when the r performed on beta 2mG and CRE was compared between the same groups of patients. In 74 patients with a malignancy, in whom serum CRE levels were < or =1.1 mg/dl, increased levels of cystatin C were observed in 25 patients and increased levels of beta 2mG were observed in 39 patients. In comparing patients with a malignancy and a non-malignancy, the number of patients with an increased level of cystatin C, despite a Ccr > or = 70 ml/min (8/33) or a CRE < or = 1.1 mg/dl (13/41), was larger in the former group than the latter group, although the result was not statistically significant. Similarly, the number of patients with an increased level of beta 2mG, despite a Ccr > or = 70 ml/min or a CRE < or = 1.1 mg/dl was significantly larger in the former group compared to the latter group. Regression analysis between the serum levels of cystatin C and CRP in patients with a malignancy whose Ccr were > or =70 ml/min had a weak correlation (r = 0.31). CONCLUSION: The results of our study suggest that the serum levels of cystatin C are not always a reliable marker of the GFR in patients with a malignancy, probably in relation to its nature as a cysteine protease inhibitor.
BACKGROUND: Serum levels of cystatin C have been proposed to be an ideal marker of the glomerular filtration rate (GFR). However, some reports have shown that serum levels of cystatin C increase independently of GFR. In this study, we evaluated the clinical utility of cystatin C in monitoring GFR, especially in patients with a malignancy. METHOD: Study subjects consisted of 82 patients with a malignancy, 39 patients with a non-malignancy, 31 healthy volunteers, and 206 patients with various degrees of renal function. We measured serum cystatin C, beta2-microglobulin (beta 2mG), and creatinine (CRE) levels in all patients. Serum CRP levels were measured in 21 patients with a malignancy and 28 patients with a non-malignancy whose creatinine clearance (Ccr) was > or =70 ml/min. Cystatin C, beta 2mG, and CRP were measured by immune nephelometry and CRE was measured by an enzyme assay. RESULTS: In patients with a malignancy, regression analysis yielded the equation: 1/cystatin C = 0.06 x Ccr + 0.710, correlation coefficient, r, of 0.33. The r was significantly lower than in patients with various degrees of renal function. There were no significant differences when the r performed on beta 2mG and CRE was compared between the same groups of patients. In 74 patients with a malignancy, in whom serum CRE levels were < or =1.1 mg/dl, increased levels of cystatin C were observed in 25 patients and increased levels of beta 2mG were observed in 39 patients. In comparing patients with a malignancy and a non-malignancy, the number of patients with an increased level of cystatin C, despite a Ccr > or = 70 ml/min (8/33) or a CRE < or = 1.1 mg/dl (13/41), was larger in the former group than the latter group, although the result was not statistically significant. Similarly, the number of patients with an increased level of beta 2mG, despite a Ccr > or = 70 ml/min or a CRE < or = 1.1 mg/dl was significantly larger in the former group compared to the latter group. Regression analysis between the serum levels of cystatin C and CRP in patients with a malignancy whose Ccr were > or =70 ml/min had a weak correlation (r = 0.31). CONCLUSION: The results of our study suggest that the serum levels of cystatin C are not always a reliable marker of the GFR in patients with a malignancy, probably in relation to its nature as a cysteine protease inhibitor.
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