ABSTRACT
The physiology and pathology of the heart and kidney are interdependent and interact with each other, and dysfunction of any one of them causes dysfunction of the other, namely cardiorenal syndrome, in which type I and type Ⅱ have the highest incidence rate and are the commonest in clinic. Traditional Chinese medicine has a long history of treating the cardiorenal syndrome. It believes that the disease is located in the heart and kidney, and Wenyang Yiqi, Huoxue Lishui and other methods shall be adopted to effectively improve the heart and kidney function of patients. However,the pathogenesis of cardiorenal syndrome is complicated, and the clinical manifestations are diverse, which makes it difficult to diagnose and treat in the early stage, and causes missing of the best intervention timing and a poor prognosis. Biomarkers play a vital role in predicting the occurrence and development of cardiorenal syndrome. Therefore, efforts shall be made to look for biomarkers with better specificity and sensitivity, accurately evaluate physiological and pathological changes in heart and kidney, so as to achieve early diagnosis and early intervention of cardiorenal syndrome, and improve the effect of disease diagnosis and treatment. At present, domestic and foreign scholars have studied and applied more markers mainly in renal tubular injury, including neutrophil gelatinase-associated lipocalin, kidney injury molecule-1 and urinary interleukin-18. In addition, other studies have found cell cycle arrest inducing factors, such as insulin-like growth factor binding protein 7, tissue inhibitor metallo proteinase-2, and fibroblast growth factor 23 associated with mineral metabolism. The increase of the content of these biomarkers in the body is earlier than the rise of serum creatinine, which can better predict the occurrence of early cardiorenal syndrome, and has a high application value and research value. After summarization of the biomarkers relating to type I and Ⅱ cardiorenal syndrome in domestic and foreign literatures, the research progress of several representative markers were reviewed to provide reference for related research.
ABSTRACT
Objective:To investigate the expression of HIF-1α in serum of rats with contrast induced nephropathy and its effect on renal tubular injury.Methods:45 SD rats were randomLy divided into three groups (n=15).The rats in the blank control group (group A)were treated with 12 h (Sodium Chloride Injection) for three 0.5 mL after fasting water for a period of about 15 minutes.Contrast nephropathy group (B group) rats after fasting 12 h,in the tail vein with 10 mg/kg injection ofindomethacin,15 minutes after the injection of 10 mg/kg nitro-L-arginine methyl ester (L-NAME),15 minutes after the injection ofiobitridol (3 G I/kg).Atorvastatin group (C group) rats in the first 3 days of the experiment started feeding atorvastatin calcium tablets,continuous feeding for 3 days,at a dose of 80 mg/kg/d,and fasting 12 h,making contrast nephropathy model,with the steps of contrast nephropathy group.The changes of renal function indexes (BUN,Cr),HIF-1α expression and renal tubular injury in three groups were observed and compared.Results:The level of BUN in rats with contrast induced nephropathy was lower than that in atorvastatin calcium group and blank control group,but the level of Scr was higher than that of atorvastatin calcium group and blank control group,the difference was statistically significant (P＜0.05).The level of BUN in atorvastatin calcium group was lower than that in blank control group,but Scr level was higher than that in blank control group,the difference was statistically significant (P＜0.05).Compared with the blank control group,the renal tubular injury in the rats with contrast induced nephropathy group was higher than that in atorvastatin calcium group and blank control group,the difference was statistically significant (P＜0.05).Compared with the control group,the expression of HIF-1 was significantly higher in rats with contrast induced nephropathy than that in atorvastatin calcium group and blank control group.The expression of HIF-1 was significantly higher than that in the control group (P＜0.05).Conclusions:It is suggested that the statins could prevent the contrast-induced nephropathy.However,the ending mechanism of statins should be further studied in the clinical practices.
ABSTRACT
A variety of kidney diseases have different degree of renal tubular injury,it even occur before the kidney damage.Since renal tubular injury still lack of effective therapy,it usually recovered by renal tubular epithelial cell itself.But the self-recover process is too long.If it is unable to spend this period,renal damage may not be reversible.So effective therapy is an emergency problem to be solved in clinical.