THE PATHOGENETIC MECHANISMS OF ACUTE KIDNEY INJURY AND CHRONIC KIDNEY DISEASE (A LITERATURE REVIEW)
Аim - compilation of scientific data on the pathogenetic mechanisms of acute kidney injury and chronic kidney disease. Although the general pathophysiological picture and the main clinical and laboratory signs of renal damage or comorbid conditions causing CKD have been established, the research of the gradual nephron death mechanisms are still very actual. To date it is unknown why kidney injury initially causes reversible changes, but with the passing of time irreversible acute renal insufficiency occurs or chronic process develops. Broadening pathogenesis knowledge is an important step toward improving early diagnosis and treatment of acute and chronic kidney injury for the maximal postponement of end-stage renal disease. We have analyzed available scientific literature for the past 5 years that allows formulating the modern concept of the general pattern and the key links in the mechanisms of kidney dysfunction and loss of nephrons homeostatic functions. The results, shown in our own experiments, demonstrate the influence of ATP-dependent potassium (KATP) channel activator flocalin on renal. Defined nephroprotective effects of flocalin on tubular and glomerular parts indicate the pathogenetic role of KATP channels and importance of their pharmacological activation during acute and chronic kidney injury. Conclusions. Regardless of its etiology acute injury of the nephrocytes proceeds through several mechanisms. The initial compensatory effects of these mechanisms can change to irreversible destructive influence that finally results in reduction in the number of the functioning nephrocytes, chronic kidney disease formation and terminal renal insufficiency. Despite intensive research of pathogenesis and continuous search for the new markers of acute and chronic kidney injury the causes of kidney pathology progression have not been fully disclosed yet. The important medical, social and economic aspects of renal diseases substantiate perspective of the key links further study that form a universal pathophysiological picture and facilitate the pathogenetic directions of pharmacological nephroprotection improvement.