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changes of renal markers in patients with contrast-induced nephropathy after percutaneous coronary intervention
순천향대학교 병원, 순천향대학교 구미병원*
김도회*, 방덕원, 정진욱, 현민수, 김성구, 권영주
Keyword : contrast-induced nephropathy, cystatin C, kidney injury molecule-1 Background: Contrast-induced nephropathy (CIN) is a complication that is underestimated in clinical practice after cardiac catheterization. In the present study, we sought to investigate whether serum cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), urinary kidney injury molecule-1 (KIM-1) may be an early diagnostic marker of CIN after percutaneous coronary intervention (PCI). Methods and Results: In 51 stable angina patients undergoing primary PCI, serum creatinine (Cr) and cystatin C were measured at baseline and 24, 48 hours after PCI. Contrast-induced nephropathy was defined as a rise in Cr 0.5 mg/dl or 25% above baseline. Serum NGAL, Urinary KIM-1 were measured immediately before, and 4, 24 and 48 hours after PCI. Urinary creatinine concentration was also checked for correction of urinary KIM-1. CIN occurred in 4 patients(7.8%). Baseline BMI(body mass index) was higher in CIN patients than in those without CIN (30 ± 3 kg/m2 vs 24 ± 3 kg/m2, p=0.001). Total cholesterol, LDL cholesterol, triglyceride was higher in contrast-induced nephropathy patients(232 ± 82 mg/dl vs 166 ± 33 mg/dl, 131 ± 41 mg/dl vs 100 ± 26 mg/dl, 352 ± 383 mg/dl vs 148 ± 65 mg/dl respectively, p<0.05). Serum Cystatin C levels were higher at 24hr and 48hr in contrast-induced nephropathy patients than in those without CIN (p<0.05). Serum NGAL levels were not statistically different between two groups. However, serum NGAL levels were increased significantly after 4 hours and maximally after 24 hours. (p<0.05) Urinary KIM-1/urinary creatinine levels were not significantly different between two groups. Conclusions: In this study, BMI, total cholesterol, LDL cholesterol, triglyceride, 24hr serum creatinine, 24hr and 48hr cystatin C level was higher in contrast-induced nephropathy patients. But serum NGAL and urinary KIM-1 was not significantly different in contrast-induced nephropathy group. Further studies with larger sample sizes are needed to validate our findings.
 

Table. Time-course changes in serum cystatin C, NGAL and urinary KIM-1, IL-18 according to the presence of contrast induced nephropathy

 

 

Before PCI

After 4 h

After 24 h

After 48 h

CIN

(-)

Creatinine

Cystatin C

Serum NGAL

UKIM-1/UCr

0.84 ± 0.19

1.07 ± 0.37

99.6 ± 69.3

0.82 ± 0.66

0.83 ± 0.19

0.99 ± 0.34

153.2 ± 120*

1.28 ± 2.13

0.82 ± 0.20$

 1.11 ± 0.33$

156.5 ± 114*

0.85 ± 0.52

0.85 ± 0.23

1.06 ± 0.32$

140.6 ± 92.8*

0.86 ± 0.6

CIN

(+)

Creatinine

Cystatin C

Serum NGAL

UKIM-1/UCr

1.05 ± 0.3

1.45 ± 0.62

92.4 ± 38.6

1.27 ± 0.92

1.05 ± 0.19

1.5 ± 0.61

107.0 ± 47.7

1.27 ± 0.84

1.13 ± 0.28$

1.58 ± 0.79$

117.6 ± 56.0

1.40 ± 1.14

1.18 ± 1.40

1.62 ± 0.85$

216.3 ± 145.1

1.27 ± 0.63

Datas given are mean values ± SD CIN ; contrast induced nephropathy, NGAL ; neutrophil-gelatinase-associated lipocalcin, KIM-1 ; Kidney injury molecule-1, IL-18 ; interleukin-18, PCI ; percutaneous coronary intervention

* p < 0.05 vs. baseline, $ p<0.05 CIN(-) vs. CIN(+)



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