A head-to-head comparison of homocysteine and cystatin C as pre-procedure predictors for contrast-induced nephropathy in patients undergoing coronary computed tomography angiography

Cystatin C, but not urinary or serum NGAL, may be associated with contrast induced nephropathy after

“…This early increase in serum CysC following a kidney injury is also reported in studies that investigated renal toxicity after contrast medium administration (4)(5)(6)(13)(14)(15)(16)(17)(18). In all these investigations the peak of serum CysC was significantly associated with the development of CIN occurring 24-48 hours after PCIP.…”

Efficacy of alprostadil in preventing contrast‐induced nephropathy in patients undergoing percutaneous coronary intervention: A multicenter prospective randomized controlled trial

“…In addition, hyperhomocysteine was also associated with direct endothelial damage, decreased bioavailability of nitric oxide, generation of free radicals, increased oxidative stress, dysfunction of the vascular endothelium, and proliferation of vascular smooth muscle cells, which share the proposed pathophysiologic mechanisms of CIN [23]. Furthermore, several studies have demonstrated that hyperhomocysteinemia was independent predictor for CIN [24,25]. In our result, we found that blood homocysteine concentration 48 hr after PCI was significantly lower in the alprostadil group than that in the control group, suggesting that alprostadil may decreased the incidence of CIN by reducing homocysteine.…”

Preprocedure and Postprocedure Predictive Values of Serum β2-Microglobulin for Contrast-Induced Nephropathy in Patients Undergoing Coronary Computed Tomography Angiography

“…Then, 320-slice CCTA was performed by the standard procedure as described in previous literature. 7 Before CCTA examination, 500 mL oral fluid was given to each patient. After CCTA, patients took unrestrictively oral fluid as much as possible.…”

“…[2][3][4] However, previous studies demonstrated that sCr was not an ideal indicator of CIN, especially in subjects with normal sCr at baseline, which is an intrinsic flaw of sCr so-called creatinine blind range. 3,[5][6][7] Cystatin C, a cysteine protease inhibitor (molecular weight, 13.3 kd) that has a constant production rate irrespective of muscle mass and a plasma concentration determined by glomerular filtration alone, is considered to be a more sensitive predictor of CIN when compared with sCr. 3,6,7 Recently, β2-microglobulin, a subunit of the major histocompatibility class I complex (molecular weight, 11.8 kd), which is constantly shed from the cells during cellular turnover and freely filtrated by glomerular filtration, is also considered to be a sensitive biomarker of kidney injury.…”

“…3,[5][6][7] Cystatin C, a cysteine protease inhibitor (molecular weight, 13.3 kd) that has a constant production rate irrespective of muscle mass and a plasma concentration determined by glomerular filtration alone, is considered to be a more sensitive predictor of CIN when compared with sCr. 3,6,7 Recently, β2-microglobulin, a subunit of the major histocompatibility class I complex (molecular weight, 11.8 kd), which is constantly shed from the cells during cellular turnover and freely filtrated by glomerular filtration, is also considered to be a sensitive biomarker of kidney injury. 8,9 However, only 1 study investigated that baseline serum β2-microglobulin was a useful predictor of CIN, in which the number of participants (n = 96) was small, and the postprocedure value of β2-microglobulin was not evaluated.…”