Chakraborty Debarati, Akbari Ayub, Knoll Greg A, Flemming Jennifer A, Lowe Catherine, Akbari Shareef, White Christine A
Division of Nephrology, Department of Medicine, Queen's University, Etherington Hall, 94 Stuart Street, Kingston, ON, K7L 2N6, Canada.
Division of Nephrology, Department of Medicine, University of Ottawa, Ottawa, ON, Canada.
BMC Nephrol. 2018 Apr 13;19(1):87. doi: 10.1186/s12882-018-0881-x.
Beta Trace Protein (BTP) is a promising marker of glomerular filtration rate (GFR). Equations to estimate GFR using BTP have been proposed. Very little is known about BTP's production and metabolism. It has been hypothesized that the liver metabolizes certain BTP isoforms. As such, hepatic dysfunction may influence serum levels independently of GFR. This would impact on the accuracy and precision of GFR estimates using BTP. The purpose of this study was to assess the impact of cirrhosis on serum BTP concentrations.
BTP, cystatin C (cysC) and creatinine (Cr) were measured in 99 cirrhotic subjects and in matched controls. BTP/cysC and Cr/cysC ratios were compared between cases and controls. This was repeated after stratification by Child Pugh category. Comparisons of ratios between Child Pugh category A and combined B and C case subjects were also performed.
There were no differences in BTP/cysC ratios between cases and controls for the entire cohort (0.80 vs 0.79) or for any of the Child Pugh categories (p > 0.10). There were significant differences between cases (1.09) and controls (0.73) for the BTP/Cr ratios (p < 0.001). The BTP/Cr ratio was higher in those with more advanced cirrhosis as compared to those with less severe cirrhosis (1.20 vs 1.03, p < 0.01). There were no differences in BTP/cysC ratios between those with less severe and more advanced cirrhosis (p = 0.25).
This study suggests that hepatic dysfunction does not influence serum BTP levels and argues against a significant role for the liver in BTP metabolism. Confirmation in a larger group of patients with advanced cirrhosis is required.
β-微量蛋白(BTP)是一种很有前景的肾小球滤过率(GFR)标志物。已有人提出使用BTP估算GFR的公式。关于BTP的产生和代谢,人们知之甚少。据推测,肝脏会代谢某些BTP异构体。因此,肝功能障碍可能会独立于GFR影响血清水平。这将影响使用BTP估算GFR的准确性和精确性。本研究的目的是评估肝硬化对血清BTP浓度的影响。
对99例肝硬化患者和匹配的对照组测定BTP、胱抑素C(cysC)和肌酐(Cr)。比较病例组和对照组的BTP/cysC和Cr/cysC比值。按Child Pugh分级分层后重复此操作。还对Child Pugh A级与B级和C级合并病例组之间的比值进行了比较。
整个队列中病例组和对照组的BTP/cysC比值无差异(0.80对0.79),任何Child Pugh分级的比值也无差异(p>0.10)。病例组(1.09)和对照组(0.73)的BTP/Cr比值有显著差异(p<0.001)。与肝硬化较轻者相比,肝硬化较严重者的BTP/Cr比值更高(1.20对1.03,p<0.01)。肝硬化较轻者和较严重者之间的BTP/cysC比值无差异(p=0.25)。
本研究表明肝功能障碍不会影响血清BTP水平,并反驳了肝脏在BTP代谢中起重要作用的观点。需要在更大一组晚期肝硬化患者中进行验证。