In the last 30 years the use of X-ray contrast media (RCM) has increased significantly during urography, angiography, computed tomography, and operating procedures. Every year the world uses about 60 million doses of PKM, but, despite the use of newer and less nephrotoxic drugs, the risk of contrast-induced nephropathy (CIN) is still significant, especially among patients with prior renal impairment. Contrast induced nephropathy is a major cause of acute renal injury and is a huge problema in clinical practice. So far, con-tradictions remain in the understanding of many aspects of CIN. Contrast-induced nephropathy is acute renal failure (ARF) occurs within 48-72 hours after intravenous administration of contrast sub-stances. Toxicity PKC determined their molecular structure and its ability to dissociate in aqueous solution into ions which consist of salts which dissociate into cations and anions. The contrast-induced nephropathy is manifested in the increase of serum creatinine of 44 mmol/L (0.5 mg / dl) or more and the same rise in serum creatinine of more than 25 % compared to baseline in the absence of other possible causes. ARF is a sudden and sustained reduction in glomerular filtration rate and urine volume, or both together. Thus renal dysfunction existing even more than 1 month can be regarded as acute renal dysfunction. Usually the development of acute renal failure occurs within 1-7 days. The criteria of sustainability is a dysfunction of its registration within 24 hours or more. The aim: to consider different approaches to the pathogenesis, risk factors and achievements in the prevention of contrast-induced nephropathy.

BACKGROUND: The work is devoted to the analysis of the elements the reactivity of grelin system in the model of psychogenic stress. In recent years, it has been shown that the ghrelin brain system is not limited only to the regulation of energy balance and eating behavior. Along with other peptide regulatory systems, it plays an important role in the mechanisms of stress, reward and addiction. Therefore, the elements of this system should be considered primarily as molecular targets of pharmacological action in order to correct the states of addiction and post-stress disorders. MATERIALS AND METHODS: To produce psychoemotional stress, we used an acute single traumatic situation in male Wistar rats. The animals were placed in the tiger python, one animal died as a result of its nutritional needs, the rest of the rats experienced the death of a partner. One week after exposure to python, the animals were decapitated, and the brain structures were isolated. Aliquots of the brain structures suspensions were examined for the content of desacyl ghrelin (DAG) using a highly sensitive enzyme-linked immunosorbent assay (ELISA). In another group, rats were decapitated on the 4th day after exposure to python, stomachs were removed, which were fixed in 10% formalin solution. In horizontal paraffin sections of the gastric mucosa, after staining with hematoxylin and eosin, the heights of superficial and dimple mucous cells, the height of the dimple stroma, the area of superficial, dimple mucocytes and stroma of the dimples, and the number of dead mucocytes were calculated. To clarify the differentiation of epithelial cells, they were stained with alcian blue RESULTS: DAG was detected in all studied brain structures: amygdala, hippocampus, and hypothalamus. The highest concentration of DAG was noted in the hypothalamus (p 0.05), which may serve as an indirect confirmation of the data on the presence of ghrelin-containing neurons in the nuclei of the hypothalamus. After exposure to stress, a sharp decrease in the level of DAG was observed in all studied brain structures (812 times, p 0.01): amygdala, hippocampus, and hypothalamus. It has been established that the experience of the stress of the death of a partner is expressed by erosive inflammation of the gastric mucosa, the death of many mucous cells, and an increase in mucus production in viable epithelial cells. CONCLUSION: Psychoemotional stress completely suppresses the content of desacyl ghrelin of the brain in rats, which may be based on both a disturbance of the central mechanisms of limbic regulation and a violation of peripheral mechanisms, in particular, reactive changes in the gastric mucosa.