1.      Introduction

The two groups had no significant differences in age, sex, body mass index, hemoglobin, left ventricular ejection fraction, SCr, eGFR, the incidence of hypertension, etc. The medications and hydration volumes used at the time of hospitalization were also not significantly different between the groups. Changes in Scr, GFR, and urine KIM-1 values before and after PCI are shown in (Table 2).

There were no significant differences in Scr and GFR before and after the PCI procedure in the control and PGE1 groups (P > 0.05). Urine KIM-1 levels 24 h, 48h after the procedure were significantly higher than those before the procedure in both groups.

1.1.  Multivariate Logistic Regression Analysis

 Multivariate logistic regression analysis showed that low eGFR and low left ventricular ejection fraction before PCI were independent predictors of CIN (Table 3).

During the entire study, all patients who did not appear with iodine allergy phenomenon, had not been observed in severe cardiac adverse events (revascularization, myocardial infarction, pulmonary edema, sudden death, etc.)

 2.      Discussion 

CIN is defined as renal impairment occurring after the administration of contrast materials. For the pathogenesis of CIN study, contrast medium caused renal hemodynamic changes, kidney ischemia hypoxia, and renal tubular cell injury, during this period produce the energy metabolism disorders, as well as the generation of oxygen, which can lead to acute renal injury [8]. L-carnitine palys a role as the inhibitor of free radical production processes and oxidative stress. The most important finding of this study is the demonstration of a significant decrease in the incidence of CIN by means of L-carnitine administration in patients with Diabetes Mellitus undergoing percutaneous coronary intervention. This study indicated that the antioxidant properties of L-carnitine might have contributed to the positive finding. On 48 h after the procedure, there was statistically significant difference compared with preoperative in serum creatinine and eGFR in control group, while not, in L-carnitine group (P < 0.05).

 Diabetes is one of the high-risk factors for CIN, but also is the common complication of CHD. The total incidence of CIN in diabetic population is approximately 5.7% ~ 29.4%, and when combined with renal insufficiency, the risk factors such as age, PCI, the incidence of CIN will be higher [9]. Diabetes affects the function of the vascular system. Endothelial dysfunction can be found in diabetes [10], it will reduce the ability of vessels to vasodilate in response to ischemia. Patients with diabetes are also at increased risk for coronary artery disease, hypertension, and congestive heart failure which may contribute to an increased risk of CIN by renal blood flow. This study suggests that the total incidence is not high, considering the possible reason of all the selected patients with normal renal function, conventional hydration, and without postoperative follow-up Scr 72 h.

 Currently, the only effective prevention measure for CIN is hydration therapy [11]. Hydration therapy, through correcting subclinical dehydration, reduces the viscosity of contrast agents and the resulting hyperosmolar state. It reduces tubulo-glomerular feedback, decreases renal vasoconstriction, increases urine volume to control renal tubular obstruction, reduces vasoconstrictor substances produced, reduces renal medullary ischemia, and can directly decrease tubular renal epithelial toxicity caused by contrast agents.  L-carnitine is in 1905 by two Russian scientists first discovered in muscle extract [12]. L-carnitine is an important medium of human body lipid metabolism, plays a role of carrier in the process of the oxidation of fatty acid used. It has been used as clinical medicine in the treatment of primary and secondary l-carnitine lack, especially for the late kidney dialysis patients. The present study showed that the L-carnitine can promote fatty acid oxidation, or a kind of effective oxygen free radical scavenger which has obvious protective effect in reducing oxidative stress and lipid peroxidation [13]. L-carnitine can effectively improve the drug caused by renal tubular necrosis, protect renal function [14]. Animal model, and find that the L-carnitine has a good effect in preventing of contrast-induced Nephropathy [5].

 In our study, CIN occurred in fourteen (19.2%) patients in the control group and three (6.9%) patients in the L-carnitine group. 24 hours ,48 hours after the procedure, the increase in urine KIM-1 levels in the L-carnitine group was significantly lower than that in the control group. Recent studies have suggested that KIM-1 is an early molecular marker, which reflects acute kidney injury, and its sensitivity is better than Scr [15,16] We conclude that L-carnitine is likely to decrease the incidence of CIN in patients with high-risk factors undergoing PCI. However, the mechanisms and efficacy of L-carnitine on the prevention of CIN after PCI need to be determined by a further multicenter, randomized, double-blind, large-scale, clinical prospective study.

Table 1: Baseline clinical characteristics of the patients in the two groups.

1.       Goldfarb S, Mccullough P A, Mcdermott J, Gay SB (2009) Contrast-induced acute kidney injury: specialty-specific protocols for interventional radiology, diagnostic computed tomography radiology, and interventional cardiology. Mayo Clin Proc 84: 170-179.

2.       Richenberg J (2012) How to reduce nephropathy following contrast-enhanced CT: a lesson in policy implementation. Clin Radiol 67: 1136-1145.

3.       Rundback J H, Nahl D, Yoo V (2011) Contrast-induced nephropathy. J Vasc Surg 54: 575-579.

4.       Berni A, Meschini R, Filippi S, Palitti F, De Amicis A, et al. (2008) L-carnitine enhances resistance to oxidative stress by reducing DNA damage in Ataxia telangiectasia cells. Mutat Res 650: 165-174.

5.       Boyacioglu M, Turgut H, Akgullu C, Eryilmaz U, Kum C, et al. (2014) The effect of L-carnitine on oxidative stress responses of experimental contrast-induced nephropathy in rats. J Vet Med Sci 76: 1-8.

6.       Ma YC, Zuo L, Chen JH, Luo Q, Yu XQ, et al. (2006) Modified glomerular filtration rate estimating equation for Chinese patients with chronic kidney disease. J Am Soc Nephrol 17: 2937-2944.

7.       Thomsen H S (2003) Guidelines for contrast media from the European Society of Urogenital Radiology. AJR Am J Roentgenol 181: 1463-1471.

8.       Geenen R W, Kingma H J, van der Molen A J (2013) Contrast-induced nephropathy: pharmacology, pathophysiology and prevention. Insights Imaging 4: 811-820.

9.       Solomon R (2007) Contrast-induced nephropathy: update with special emphasis on patients with diabetes. Curr Diab Rep 7: 454-458.

10.    Economides PA, Caselli A, Zuo CS, Sparks C, Khaodhiar L, et al. (2004) Kidney oxygenation during water diuresis and endothelial function in patients with type 2 diabetes and subjects at risk to develop diabetes. Metabolism 53: 222-227.

11.    Rosenstock JL, Gilles E, Geller AB, Panagopoulos G, Mathew S, et al. (2010) Impact of heart failure on the incidence of contrast-induced nephropathy in patients with chronic kidney disease. Int Urol Nephrol 42: 1049-1054.

12.    Kerner J and Hoppel C (1998) Genetic disorders of carnitine metabolism and their nutritional management. Annu Rev Nutr 18: 179-206.

13.    Arockia R P and Panneerselvam C (2001) Carnitine as a free radical scavenger in aging. Exp Gerontol 36: 1713-1726.

14.    Jafari A, Dashti-Khavidaki S, Khalili H, Lessan-Pezeshki M (2013) Potential nephroprotective effects of l-carnitine against drug-induced nephropathy: a review of literature. Expert Opin Drug Saf 12: 523-543.

15.    Malyszko J, Bachorzewska-Gajewska H, Poniatowski B, Malyszko JS, Dobrzycki S (2009) Urinary and serum biomarkers after cardiac catheterization in diabetic patients with stable angina and without severe chronic kidney disease. Ren Fail 31: 910-919.

16.    Vaidya VS, Ramirez V, Ichimura T, Bobadilla NA, Bonventre JV (2006) Urinary kidney injury molecule-1: a sensitive quantitative biomarker for early detection of kidney tubular injury. Am J Physiol Renal Physiol 290: F517-F529.