| Objective: Acute kidney injury represents a critical and common problem in clinical medicine. Nowadays with the widely use of contrast medium in clinical practice, contrast induced nephropathy has emerged to be the third major cause of acute kidney injury. The lack of early diagnosis and treatment often result of irreverserible damage of kidney tissue. Serum creatinine, as a traditional marker, is difficult to detect kidney injury early and it cannot satisfy the clinical purpose of early detection. Therefore, it is urgent to find new surrogate as early diagnosis biomarker of AKI. In recent years,researchers have found a series of acute renal injury markers applied in genomics and proteomics,such as Neutrophil gelatinase-associated lipocalin,kidney injury molecule-1,interleukin-18,cystatinC and et a1.Neutrophil gelatinase-associated lipocalin (NGAL), a protein covalently bound to gelatinase from human neutrophils . NGAL is expressed in very low concentrations in numerous human tissues, including the kidney, the lung, the stomach, the colon. The NGAL gene expression is strongly induced after the injury of epithelial cell by ischemia, sepsis or nephrotoxins. In humans, increased NGAL expression has been demonstrated as early as 2 h after a cardiosurgical procedure, while increased NGAL concentrations in urine preceded increases in serum creatinine. In addition, NGAL has the ability of antiproteolysis, and is stable in the urine , so it is suitable to use as a biomarker of AKI.Cystatin C is an endogenous inhibitor of cysteine proteinases, produced by all nucleated cells of the body and released into the bloodstream at a constant rate. It is freely filtered by the glomerulus, and reabsorbed and catabolized , but not secreted in proximal tubular cells. Due to its complete filtration from the glomerulus, the assessment of serum cystatin C concentrations may be a accurate and sensitive marker of glomerular filtration.IL-18 is a proinflammatory cytokine, a mediator of inflammation and ischemic tissue damage in many organs. It may act as a neutrophilic attractant and plays an important role in the pathophysiology of sepsis. Experimental studies in animals revealed that IL-18 production is induced in proximal epithelial cell after the development of AKI. It is reported urine IL-18 levels were markedly increased in patients with established AKI but not in subjects with urinary tract infection, chronic kidney disease, nephritic syndrome. And a combination of IL-18 and NGAL will emerge as powerful tools for the early prediction and risk stratification of AKI after cardiac surgery.Kidney injury molecule-1(KIM-1) is a type 1 transmembrane glycoprotein. In a healthy kidney, KIM-1 is not detectable, whereas under experimental conditions, KIM-1 has been recognized, both in animals and in humans, as having the features of high expression in ischemic and toxic acute injury of proximal tubular cells. The extracellular ectodomain of KIM-1, detached by metalloproteinases and excreted into urine, is a quantitative marker of AKI. It is demonstrated KIM-1 levels in urine increase earlier than serum creatinine.The research of novel biomarkers applied in the contrast induced kidney injury has rarely been reported. It is worth further research how the biomarkers changes in the urine of patients with contrast induced acute kidney injury,and its role in the earlier diagnosis of acute renal injury. The purpose of the present study is to investigate the incidence of AKI after coronary artery angiography and percutaneous coronary intervention therapy prospectively and observe the change of urine concentration of NGAL, cystatinC, IL-18,KIM-1. Methord:During the period of November 2010 to December 2010, 36 inpatients of coronary heart disease who accept coronary artery angiography and percutaneous coronary intervention therapy in our hospital were enrolled to our study. Male were 20,female were 16, the mean age was 65.16±9.52 years. All patients was coronary atherosclerotic heart disease, stable angina or unstable angina. Nine patients were diabetic, 26 had a history of hypertension,and 10 had a history of hyperlipoidemia. Eleven were smoker, seven had a history of drinking. All patients had normal renal function before the operation. All patients used hypotensive contrast agent. Patient urine were collected at the time of pre-operation, post-2h, post-12h, post-24h. All urine samples were centrifuged at 2000 r.p.m. for 10 min and the supernatants are aliquoted and stored at ?80°C. To detect urine NGAL, cystatin C, IL-18,Kim-1 by ELISA method. Meanwhile, venous blood was collected at the time of post-12h, post-24h,and serum creatinine was detected by dry-slides method. Then to analyze the data using SPSS17.0 .Results: The surem creatinine, compared with pre-operation, at 24h and 48h after coronary artery angiography and/or percutaneous coronary intervention therapy didn't increase in 36 patients(p>0.05). There was a significant increase of urinary NGAL between post-operation and pre-operation (p<0.001), the peak concentration appeared at 2h after operation, was 75.985±51.570ng/ml, then it decreased since 12h after the operation.There was a significant increase of urinary KIM-1 at 12h and 24h after the operation, compared with pre-operation (p<0.001).Urinary NGAL and KIM-1 elevated after the operation, while serum creatinine did't change. It suggested urinary NGAL and KIM-1 is more sensitive than serum creatinine to show the kidney injury.The urinary cystatinC and IL-18 concentrations didn't increase after the angiography.Conclusion: Urinary NGAL and KIM-1 increased after the coronary artery angiography and/or percutaneous coronary intervention therapy in 36 patients, but serum creatinine didn't elevated. It suggested that the kidney had a transient kidney injury after the operation, and urinary NGAl and KIM-1were more sensitive than serum creatinine.Urinary cystatin C and IL-18 did't increase after the angiography. It may be associated with urine collection,storage and test method, and it need to be confirmed by further investigation.
|
PDF Full Text Request