Glomerular filtration rate estimated by cystatin C among different clinical presentations
Glomerular filtration rate estimated by cystatin C among different clinical presentations
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DOI：
10.1038/sj.ki.5000073
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发表时间：
2006-01-01
影响因子：
19.6
通讯作者：
Larson, TS
中科院分区：
文献类型：
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作者：
Rule, AD;Bergstralh, EJ;Larson, TS
根据血清肌酐估算肾小球滤过率(GFR)并不适用于所有人群。胱抑素C已被提出作为评估肾小球滤过率的替代标记物。本研究的目的是比较胱抑素C和血肌酐在不同临床表现中评估肾小球滤过率的作用。从成年患者(n=460)获得胱抑素C和血肌酐水平，评估中包括通过硫代巴比妥酸清除法测量GFR。在测量肾小球滤过率时，提取医疗记录用于临床表现(健康的、原发的慢性肾脏疾病或移植受者)。使用以下变量对GFR进行建模：胱抑素C(或血清肌酐)、年龄、性别和临床表现。胱抑素C与肾小球滤过率的关系因临床表现而异。在相同的胱抑素C水平下，移植受者的肾小球滤过率比先天性肾病患者高19%(P<；0.001)。在先天性肾病患者中，胱抑素C和肾小球滤过率的相关性比健康人更强(P<；0.001统计交互作用)。因此，只对204例先天性肾病患者进行了半胱氨酸氨基转移酶C方程的推导。与肾小球滤过率的相关性(r(2)=0.853)略高于同一样本的血肌酐方程(r(2)=0.827)、肾脏疾病饮食修正方程(r(2)=0.825)或Cockcroft-Gault方程(r(2)=0.796)。胱抑素C和血肌酐方程之间的平均估计进一步改善了相关性(r(2)=0.891)。不应将半胱氨酸氨基转移酶C纯粹解释为GFR的标志。其他因素，可能是炎症或免疫抑制治疗，也会影响胱抑素C的水平。在认识到这一局限性的同时，胱抑素C可能会改善慢性肾脏疾病患者的GFR估计。
Glomerular filtration rate (GFR) estimates from serum creatinine has not been generalizable across all populations. Cystatin C has been proposed as an alternative marker for estimating GFR. The objective of this study was to compare cystatin C with serum creatinine for estimating GFR among different clinical presentations. Cystatin C and serum creatinine levels were obtained from adult patients (n = 460) during an evaluation that included a GFR measurement by iothalamate clearance. Medical records were abstracted for clinical presentation (healthy, native chronic kidney disease or transplant recipient) at the time of GFR measurement. GFR was modeled using the following variables: cystatin C (or serum creatinine), age, gender, and clinical presentation. The relationship between cystatin C and GFR differed across clinical presentations. At the same cystatin C level, GFR was 19% higher in transplant recipients than in patients with native kidney disease (P < 0.001). The association between cystatin C and GFR was stronger among native kidney disease patients than in healthy persons (P < 0.001 for statistical interaction). Thus, a cystatin C equation was derived using only patients with native kidney disease (n = 204). The correlation with GFR (r(2) = 0.853) was slightly higher than a serum creatinine equation using the same sample (r(2) = 0.827), the Modification of Diet in Renal Disease equation (r(2) = 0.825) or the Cockcroft-Gault equation (r(2) = 0.796). Averaged estimates between cystatin C and serum creatinine equations further improved correlation (r(2) = 0.891). Cystatin C should not be interpreted as purely a marker of GFR. Other factors, possibly inflammation or immunosuppression therapy, affect cystatin C levels. While recognizing this limitation, cystatin C may improve GFR estimates in chronic kidney disease patients.